The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
Enzyme activated in response to DNA DAMAGE involved in cell cycle arrest. The gene is located on the long (q) arm of chromosome 22 at position 12.1. In humans it is encoded by the CHEK2 gene.
Regulatory signaling systems that control the progression through the CELL CYCLE. They ensure that the cell has completed, in the correct order and without mistakes, all the processes required to replicate the GENOME and CYTOPLASM, and divide them equally between two daughter cells. If cells sense they have not completed these processes or that the environment does not have the nutrients and growth hormones in place to proceed, then the cells are restrained (or "arrested") until the processes are completed and growth conditions are suitable.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.
Genes that code for proteins that regulate the CELL DIVISION CYCLE. These genes form a regulatory network that culminates in the onset of MITOSIS by activating the p34cdc2 protein (PROTEIN P34CDC2).
A group of PROTEIN-SERINE-THREONINE KINASES which activate critical signaling cascades in double strand breaks, APOPTOSIS, and GENOTOXIC STRESS such as ionizing ultraviolet A light, thereby acting as a DNA damage sensor. These proteins play a role in a wide range of signaling mechanisms in cell cycle control.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
Phase of the CELL CYCLE following G1 and preceding G2 when the entire DNA content of the nucleus is replicated. It is achieved by bidirectional replication at multiple sites along each chromosome.
A type of CELL NUCLEUS division by means of which the two daughter nuclei normally receive identical complements of the number of CHROMOSOMES of the somatic cells of the species.
CELL CYCLE regulatory signaling systems that are triggered by DNA DAMAGE or lack of nutrients during G2 PHASE. When triggered they restrain cells transitioning from G2 phase to M PHASE.
The period of the CELL CYCLE preceding DNA REPLICATION in S PHASE. Subphases of G1 include "competence" (to respond to growth factors), G1a (entry into G1), G1b (progression), and G1c (assembly). Progression through the G1 subphases is effected by limiting growth factors, nutrients, or inhibitors.
The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
The cellular signaling system that halts the progression of cells through MITOSIS or MEIOSIS if a defect that will affect CHROMOSOME SEGREGATION is detected.
An autosomal recessive inherited disorder characterized by choreoathetosis beginning in childhood, progressive CEREBELLAR ATAXIA; TELANGIECTASIS of CONJUNCTIVA and SKIN; DYSARTHRIA; B- and T-cell immunodeficiency, and RADIOSENSITIVITY to IONIZING RADIATION. Affected individuals are prone to recurrent sinobronchopulmonary infections, lymphoreticular neoplasms, and other malignancies. Serum ALPHA-FETOPROTEINS are usually elevated. (Menkes, Textbook of Child Neurology, 5th ed, p688) The gene for this disorder (ATM) encodes a cell cycle checkpoint protein kinase and has been mapped to chromosome 11 (11q22-q23).
Penetrating, high-energy electromagnetic radiation emitted from atomic nuclei during NUCLEAR DECAY. The range of wavelengths of emitted radiation is between 0.1 - 100 pm which overlaps the shorter, more energetic hard X-RAYS wavelengths. The distinction between gamma rays and X-rays is based on their radiation source.
A subclass of dual specificity phosphatases that play a role in the progression of the CELL CYCLE. They dephosphorylate and activate CYCLIN-DEPENDENT KINASES.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
ELECTROMAGNETIC RADIATION or particle radiation (high energy ELEMENTARY PARTICLES) capable of directly or indirectly producing IONS in its passage through matter. The wavelengths of ionizing electromagnetic radiation are equal to or smaller than those of short (far) ultraviolet radiation and include gamma and X-rays.
The process by which a DNA molecule is duplicated.
An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase.
A large family of regulatory proteins that function as accessory subunits to a variety of CYCLIN-DEPENDENT KINASES. They generally function as ENZYME ACTIVATORS that drive the CELL CYCLE through transitions between phases. A subset of cyclins may also function as transcriptional regulators.
A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. p21 interacts with a range of CYCLIN-DEPENDENT KINASES and associates with PROLIFERATING CELL NUCLEAR ANTIGEN and CASPASE 3.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A microtubule structure that forms during CELL DIVISION. It consists of two SPINDLE POLES, and sets of MICROTUBULES that may include the astral microtubules, the polar microtubules, and the kinetochore microtubules.
Phosphoprotein with protein kinase activity that functions in the G2/M phase transition of the CELL CYCLE. It is the catalytic subunit of the MATURATION-PROMOTING FACTOR and complexes with both CYCLIN A and CYCLIN B in mammalian cells. The maximal activity of cyclin-dependent kinase 1 is achieved when it is fully dephosphorylated.
A cyclin subtype that is transported into the CELL NUCLEUS at the end of the G2 PHASE. It stimulates the G2/M phase transition by activating CDC2 PROTEIN KINASE.
The ability of some cells or tissues to survive lethal doses of IONIZING RADIATION. Tolerance depends on the species, cell type, and physical and chemical variables, including RADIATION-PROTECTIVE AGENTS and RADIATION-SENSITIZING AGENTS.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
An increased tendency of the GENOME to acquire MUTATIONS when various processes involved in maintaining and replicating the genome are dysfunctional.
Regulatory signaling systems that control the progression of the CELL CYCLE through the G1 PHASE and allow transition to S PHASE when the cells are ready to undergo DNA REPLICATION. DNA DAMAGE, or the deficiencies in specific cellular components or nutrients may cause the cells to halt before progressing through G1 phase.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Proteins obtained from the species SACCHAROMYCES CEREVISIAE. The function of specific proteins from this organism are the subject of intense scientific interest and have been used to derive basic understanding of the functioning similar proteins in higher eukaryotes.
A genus of ascomycetous fungi of the family Schizosaccharomycetaceae, order Schizosaccharomycetales.
A cyclin B subtype that colocalizes with MICROTUBULES during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.
Cell regulatory signaling system that controls progression through S PHASE and stabilizes the replication forks during conditions that could affect the fidelity of DNA REPLICATION, such as DNA DAMAGE or depletion of nucleotide pools.
That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.
Nocodazole is an antineoplastic agent which exerts its effect by depolymerizing microtubules.
A cell line derived from cultured tumor cells.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Established cell cultures that have the potential to propagate indefinitely.
Proteins obtained from the species Schizosaccharomyces pombe. The function of specific proteins from this organism are the subject of intense scientific interest and have been used to derive basic understanding of the functioning similar proteins in higher eukaryotes.
Interruptions in the sugar-phosphate backbone of DNA, across both strands adjacently.
A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
Product of the retinoblastoma tumor suppressor gene. It is a nuclear phosphoprotein hypothesized to normally act as an inhibitor of cell proliferation. Rb protein is absent in retinoblastoma cell lines. It also has been shown to form complexes with the adenovirus E1A protein, the SV40 T antigen, and the human papilloma virus E7 protein.
An increased tendency to acquire CHROMOSOME ABERRATIONS when various processes involved in chromosome replication, repair, or segregation are dysfunctional.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
The phosphoprotein encoded by the BRCA1 gene (GENE, BRCA1). In normal cells the BRCA1 protein is localized in the nucleus, whereas in the majority of breast cancer cell lines and in malignant pleural effusions from breast cancer patients, it is localized mainly in the cytoplasm. (Science 1995;270(5237):713,789-91)
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
A key regulator of CELL CYCLE progression. It partners with CYCLIN E to regulate entry into S PHASE and also interacts with CYCLIN A to phosphorylate RETINOBLASTOMA PROTEIN. Its activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P27 and CYCLIN-DEPENDENT KINASE INHIBITOR P21.
Proteins found in any species of fungus.
Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.
Large multiprotein complexes that bind the centromeres of the chromosomes to the microtubules of the mitotic spindle during metaphase in the cell cycle.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
A 50-kDa protein that complexes with CYCLIN-DEPENDENT KINASE 2 in the late G1 phase of the cell cycle.
3-Hydroxy-4-oxo-1(4H)-pyridinealanine. An antineoplastic alanine-substituted pyridine derivative isolated from Leucena glauca.
Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.
An alkylating agent in cancer therapy that may also act as a mutagen by interfering with and causing damage to DNA.
Enzymes that are involved in the reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule, which contained damaged regions.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
A family of cell cycle-dependent kinases that are related in structure to CDC28 PROTEIN KINASE; S CEREVISIAE; and the CDC2 PROTEIN KINASE found in mammalian species.
Protein kinases that control cell cycle progression in all eukaryotes and require physical association with CYCLINS to achieve full enzymatic activity. Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.
A cyclin subtype that has specificity for CDC2 PROTEIN KINASE and CYCLIN-DEPENDENT KINASE 2. It plays a role in progression of the CELL CYCLE through G1/S and G2/M phase transitions.
An antiviral antibiotic produced by Cephalosporium aphidicola and other fungi. It inhibits the growth of eukaryotic cells and certain animal viruses by selectively inhibiting the cellular replication of DNA polymerase II or the viral-induced DNA polymerases. The drug may be useful for controlling excessive cell proliferation in patients with cancer, psoriasis or other dermatitis with little or no adverse effect upon non-multiplying cells.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Compounds that inhibit cell production of DNA or RNA.
The chromosomal constitution of a cell containing multiples of the normal number of CHROMOSOMES; includes triploidy (symbol: 3N), tetraploidy (symbol: 4N), etc.
The cell center, consisting of a pair of CENTRIOLES surrounded by a cloud of amorphous material called the pericentriolar region. During interphase, the centrosome nucleates microtubule outgrowth. The centrosome duplicates and, during mitosis, separates to form the two poles of the mitotic spindle (MITOTIC SPINDLE APPARATUS).
A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.
The phase of cell nucleus division following PROMETAPHASE, in which the CHROMOSOMES line up across the equatorial plane of the SPINDLE APPARATUS prior to separation.
An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.
The relationship between the dose of administered radiation and the response of the organism or tissue to the radiation.
An early non-mammalian embryo that follows the MORULA stage. A blastula resembles a hollow ball with the layer of cells surrounding a fluid-filled cavity (blastocele). The layer of cells is called BLASTODERM.
Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Elements of limited time intervals, contributing to particular results or situations.
Enzymes that catalyze the release of mononucleotides by the hydrolysis of the terminal bond of deoxyribonucleotide or ribonucleotide chains.
Transport proteins that carry specific substances in the blood or across cell membranes.
A type of chromosomal aberration involving DNA BREAKS. Chromosome breakage can result in CHROMOSOMAL TRANSLOCATION; CHROMOSOME INVERSION; or SEQUENCE DELETION.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A large family of signal-transducing adaptor proteins present in wide variety of eukaryotes. They are PHOSPHOSERINE and PHOSPHOTHREONINE binding proteins involved in important cellular processes including SIGNAL TRANSDUCTION; CELL CYCLE control; APOPTOSIS; and cellular stress responses. 14-3-3 proteins function by interacting with other signal-transducing proteins and effecting changes in their enzymatic activity and subcellular localization. The name 14-3-3 derives from numerical designations used in the original fractionation patterns of the proteins.
The material of CHROMOSOMES. It is a complex of DNA; HISTONES; and nonhistone proteins (CHROMOSOMAL PROTEINS, NON-HISTONE) found within the nucleus of a cell.
The interval between two successive CELL DIVISIONS during which the CHROMOSOMES are not individually distinguishable. It is composed of the G phases (G1 PHASE; G0 PHASE; G2 PHASE) and S PHASE (when DNA replication occurs).
Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Proteins which maintain the transcriptional quiescence of specific GENES or OPERONS. Classical repressor proteins are DNA-binding proteins that are normally bound to the OPERATOR REGION of an operon, or the ENHANCER SEQUENCES of a gene until a signal occurs that causes their release.
Nucleoproteins, which in contrast to HISTONES, are acid insoluble. They are involved in chromosomal functions; e.g. they bind selectively to DNA, stimulate transcription resulting in tissue-specific RNA synthesis and undergo specific changes in response to various hormones or phytomitogens.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Highly conserved proteins that specifically bind to and activate the anaphase-promoting complex-cyclosome, promoting ubiquitination and proteolysis of cell-cycle-regulatory proteins. Cdc20 is essential for anaphase-promoting complex activity, initiation of anaphase, and cyclin proteolysis during mitosis.
A terminal section of a chromosome which has a specialized structure and which is involved in chromosomal replication and stability. Its length is believed to be a few hundred base pairs.
Deoxyribonucleic acid that makes up the genetic material of fungi.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Drugs used to potentiate the effectiveness of radiation therapy in destroying unwanted cells.
Cyclin-dependent kinase 4 is a key regulator of G1 PHASE of the CELL CYCLE. It partners with CYCLIN D to phosphorylate RETINOBLASTOMA PROTEIN. CDK4 activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P16.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus.
Nuclear antigen with a role in DNA synthesis, DNA repair, and cell cycle progression. PCNA is required for the coordinated synthesis of both leading and lagging strands at the replication fork during DNA replication. PCNA expression correlates with the proliferation activity of several malignant and non-malignant cell types.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals.
The orderly segregation of CHROMOSOMES during MEIOSIS or MITOSIS.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A single-stranded DNA-binding protein that is found in EUKARYOTIC CELLS. It is required for DNA REPLICATION; DNA REPAIR; and GENETIC RECOMBINATION.
In a prokaryotic cell or in the nucleus of a eukaryotic cell, a structure consisting of or containing DNA which carries the genetic information essential to the cell. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
A suspected industrial carcinogen (and listed as such by OSHA). Its N-hydroxy metabolite is strongly carcinogenic and mutagenic.
The period from onset of one menstrual bleeding (MENSTRUATION) to the next in an ovulating woman or female primate. The menstrual cycle is regulated by endocrine interactions of the HYPOTHALAMUS; the PITUITARY GLAND; the ovaries; and the genital tract. The menstrual cycle is divided by OVULATION into two phases. Based on the endocrine status of the OVARY, there is a FOLLICULAR PHASE and a LUTEAL PHASE. Based on the response in the ENDOMETRIUM, the menstrual cycle is divided into a proliferative and a secretory phase.
Penetrating electromagnetic radiation emitted when the inner orbital electrons of an atom are excited and release radiant energy. X-ray wavelengths range from 1 pm to 10 nm. Hard X-rays are the higher energy, shorter wavelength X-rays. Soft x-rays or Grenz rays are less energetic and longer in wavelength. The short wavelength end of the X-ray spectrum overlaps the GAMMA RAYS wavelength range. The distinction between gamma rays and X-rays is based on their radiation source.
Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein TUBULIN and are influenced by TUBULIN MODULATORS.
A nucleoside that substitutes for thymidine in DNA and thus acts as an antimetabolite. It causes breaks in chromosomes and has been proposed as an antiviral and antineoplastic agent. It has been given orphan drug status for use in the treatment of primary brain tumors.
Abnormal number or structure of chromosomes. Chromosome aberrations may result in CHROMOSOME DISORDERS.
A serine-threonine protein kinase that, when activated by DNA, phosphorylates several DNA-binding protein substrates including the TUMOR SUPPRESSOR PROTEIN P53 and a variety of TRANSCRIPTION FACTORS.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
The functional hereditary units of FUNGI.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.
The phase of cell nucleus division following METAPHASE, in which the CHROMATIDS separate and migrate to opposite poles of the spindle.
Complexes of enzymes that catalyze the covalent attachment of UBIQUITIN to other proteins by forming a peptide bond between the C-terminal GLYCINE of UBIQUITIN and the alpha-amino groups of LYSINE residues in the protein. The complexes play an important role in mediating the selective-degradation of short-lived and abnormal proteins. The complex of enzymes can be broken down into three components that involve activation of ubiquitin (UBIQUITIN-ACTIVATING ENZYMES), conjugation of ubiquitin to the ligase complex (UBIQUITIN-CONJUGATING ENZYMES), and ligation of ubiquitin to the substrate protein (UBIQUITIN-PROTEIN LIGASES).
A family of enzymes that catalyze the exonucleolytic cleavage of DNA. It includes members of the class EC 3.1.11 that produce 5'-phosphomonoesters as cleavage products.
An E3 ubiquitin ligase primarily involved in regulation of the metaphase-to-anaphase transition during MITOSIS through ubiquitination of specific CELL CYCLE PROTEINS. Enzyme activity is tightly regulated through subunits and cofactors, which modulate activation, inhibition, and substrate specificity. The anaphase-promoting complex, or APC-C, is also involved in tissue differentiation in the PLACENTA, CRYSTALLINE LENS, and SKELETAL MUSCLE, and in regulation of postmitotic NEURONAL PLASTICITY and excitability.
Production of new arrangements of DNA by various mechanisms such as assortment and segregation, CROSSING OVER; GENE CONVERSION; GENETIC TRANSFORMATION; GENETIC CONJUGATION; GENETIC TRANSDUCTION; or mixed infection of viruses.
That portion of the electromagnetic spectrum usually sensed as heat. Infrared wavelengths are longer than those of visible light, extending into the microwave frequencies. They are used therapeutically as heat, and also to warm food in restaurants.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
An indolocarbazole that is a potent PROTEIN KINASE C inhibitor which enhances cAMP-mediated responses in human neuroblastoma cells. (Biochem Biophys Res Commun 1995;214(3):1114-20)
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
Enzymes that catalyze the transfer of multiple ADP-RIBOSE groups from nicotinamide-adenine dinucleotide (NAD) onto protein targets, thus building up a linear or branched homopolymer of repeating ADP-ribose units i.e., POLY ADENOSINE DIPHOSPHATE RIBOSE.
A Rec A recombinase found in eukaryotes. Rad51 is involved in DNA REPAIR of double-strand breaks.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
An E3 UBIQUITIN LIGASE that interacts with and inhibits TUMOR SUPPRESSOR PROTEIN P53. Its ability to ubiquitinate p53 is regulated by TUMOR SUPPRESSOR PROTEIN P14ARF.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
A group of enzymes removing the SERINE- or THREONINE-bound phosphate groups from a wide range of phosphoproteins, including a number of enzymes which have been phosphorylated under the action of a kinase. (Enzyme Nomenclature, 1992)
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
A product of the p16 tumor suppressor gene (GENES, P16). It is also called INK4 or INK4A because it is the prototype member of the INK4 CYCLIN-DEPENDENT KINASE INHIBITORS. This protein is produced from the alpha mRNA transcript of the p16 gene. The other gene product, produced from the alternatively spliced beta transcript, is TUMOR SUPPRESSOR PROTEIN P14ARF. Both p16 gene products have tumor suppressor functions.
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
The degree of replication of the chromosome set in the karyotype.
Compounds that inhibit the activity of DNA TOPOISOMERASE I.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
An alkaloid isolated from the stem wood of the Chinese tree, Camptotheca acuminata. This compound selectively inhibits the nuclear enzyme DNA TOPOISOMERASES, TYPE I. Several semisynthetic analogs of camptothecin have demonstrated antitumor activity.
A quiescent state of cells during G1 PHASE.
Interruption or suppression of the expression of a gene at transcriptional or translational levels.
The presence of an uncomplimentary base in double-stranded DNA caused by spontaneous deamination of cytosine or adenine, mismatching during homologous recombination, or errors in DNA replication. Multiple, sequential base pair mismatches lead to formation of heteroduplex DNA; (NUCLEIC ACID HETERODUPLEXES).
A family of highly conserved serine-threonine kinases that are involved in the regulation of MITOSIS. They are involved in many aspects of cell division, including centrosome duplication, SPINDLE APPARATUS formation, chromosome alignment, attachment to the spindle, checkpoint activation, and CYTOKINESIS.
Enzymes that catalyze the hydrolysis of the internal bonds and thereby the formation of polynucleotides or oligonucleotides from ribo- or deoxyribonucleotide chains. EC 3.1.-.
The decrease in the cell's ability to proliferate with the passing of time. Each cell is programmed for a certain number of cell divisions and at the end of that time proliferation halts. The cell enters a quiescent state after which it experiences CELL DEATH via the process of APOPTOSIS.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Proteins that catalyze the unwinding of duplex DNA during replication by binding cooperatively to single-stranded regions of DNA or to short regions of duplex DNA that are undergoing transient opening. In addition DNA helicases are DNA-dependent ATPases that harness the free energy of ATP hydrolysis to translocate DNA strands.
Agents that inhibit PROTEIN KINASES.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Screening techniques first developed in yeast to identify genes encoding interacting proteins. Variations are used to evaluate interplay between proteins and other molecules. Two-hybrid techniques refer to analysis for protein-protein interactions, one-hybrid for DNA-protein interactions, three-hybrid interactions for RNA-protein interactions or ligand-based interactions. Reverse n-hybrid techniques refer to analysis for mutations or other small molecules that dissociate known interactions.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.
Cellular DNA-binding proteins encoded by the c-myc genes. They are normally involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Elevated and deregulated (constitutive) expression of c-myc proteins can cause tumorigenesis.
A nitrosoguanidine derivative with potent mutagenic and carcinogenic properties.
Process of generating a genetic MUTATION. It may occur spontaneously or be induced by MUTAGENS.
A broad category of carrier proteins that play a role in SIGNAL TRANSDUCTION. They generally contain several modular domains, each of which having its own binding activity, and act by forming complexes with other intracellular-signaling molecules. Signal-transducing adaptor proteins lack enzyme activity, however their activity can be modulated by other signal-transducing enzymes
The aggregation of soluble ANTIGENS with ANTIBODIES, alone or with antibody binding factors such as ANTI-ANTIBODIES or STAPHYLOCOCCAL PROTEIN A, into complexes large enough to fall out of solution.
Tumors or cancer of the human BREAST.
The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES.
Tumors or cancer of the COLON.
The rate dynamics in chemical or physical systems.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
Genes that inhibit expression of the tumorigenic phenotype. They are normally involved in holding cellular growth in check. When tumor suppressor genes are inactivated or lost, a barrier to normal proliferation is removed and unregulated growth is possible.
A type of CELL NUCLEUS division, occurring during maturation of the GERM CELLS. Two successive cell nucleus divisions following a single chromosome duplication (S PHASE) result in daughter cells with half the number of CHROMOSOMES as the parent cells.
Defective nuclei produced during the TELOPHASE of MITOSIS or MEIOSIS by lagging CHROMOSOMES or chromosome fragments derived from spontaneous or experimentally induced chromosomal structural changes.
A group of enzymes catalyzing the endonucleolytic cleavage of DNA. They include members of EC 3.1.21.-, EC 3.1.22.-, EC 3.1.23.- (DNA RESTRICTION ENZYMES), EC 3.1.24.- (DNA RESTRICTION ENZYMES), and EC 3.1.25.-.
A genotoxicological technique for measuring DNA damage in an individual cell using single-cell gel electrophoresis. Cell DNA fragments assume a "comet with tail" formation on electrophoresis and are detected with an image analysis system. Alkaline assay conditions facilitate sensitive detection of single-strand damage.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
A class of weak acids with the general formula R-CONHOH.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
A DNA repair pathway involved in correction of errors introduced during DNA replication when an incorrect base, which cannot form hydrogen bonds with the corresponding base in the parent strand, is incorporated into the daughter strand. Excinucleases recognize the BASE PAIR MISMATCH and cause a segment of polynucleotide chain to be excised from the daughter strand, thereby removing the mismatched base. (from Oxford Dictionary of Biochemistry and Molecular Biology, 2001)
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
Proteins prepared by recombinant DNA technology.
An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.
Hybridization of a nucleic acid sample to a very large set of OLIGONUCLEOTIDE PROBES, which have been attached individually in columns and rows to a solid support, to determine a BASE SEQUENCE, or to detect variations in a gene sequence, GENE EXPRESSION, or for GENE MAPPING.

Comparison of efficacy and toxicity profile between intraperitoneal and intravenous topotecan in human ovarian cancer xenografts. (1/1169)

OBJECTIVE: To compare the therapeutic and toxic profile of topotecan given intraperitoneally with intravenously in human ovarian cancer xenografted into athymic nude mice. METHOD: Eighty female Balb-c/nu-nu mice were randomized assigned into eight groups (n=10). Xenografts resulted from intramesentery injection of cultured human ovarian cancer cells SKOV3 in athymic mice. Onset of intraperitoneal treatment with either topotecan or cisplatin (7.5 mg/kg) was on day 7. Animals scheduled for topotecan i.p. received intraperitoneal application of topotecan (1.5 mg/kg x 2, 3.0 mg/kg x 2, 6.0 mg/kg x 2 or 10.0 mg/kg x 1). Animals scheduled for topotecan i.v. received intravenous administration of topotecan (6.0 mg/kg x 2 or 10.0 mg/kg x 1). Two weeks after drug application animals were killed. Tumor growth inhibition were assessed and compared with untreated mice and cisplatin intraperitoneally administered mice. Acute toxicity was determined by loss of body weight. Cell cycle division and apoptosis after drug administration was determined by flow cytometric analysis. RESULTS: In a panel of ten tumour xenografts, intraperitoneal topotecan was significantly more effective than intravenous administration. The toxicity profile suggested a better tolerability in terms of weight loss after intraperitoneal administration than cisplatin control. Topotecan 10.0 mg/kg i.p. per day (1 day) schedule was an optimal treatment for ovarian cancer and well tolerated by mice with no signs of acute toxicity. Topotecan and cisplatin induce cells G0-G1 arrest and apparent apoptosis. No significant difference among mice treated with topotecan intraperitoneally or intravenously or cisplatin was observed in term of apoptosis and cell cycle perturbation. CONCLUSION: The results may have implications for the future design of clinical studies on intraperitoneal application of topotecan. It suggests that apoptosis and cell cycle perturbation play an limited role in the mechanism of topotecan administration.  (+info)

Cigarette smoke extract inhibits the proliferation of alveolar epithelial cells and induces apoptosis. (2/1169)

Cigarette smoke extract (CSE) contains abundant oxidants and free radicals. Oxidative stress caused by cigarette smoking results in the destruction of the alveolar cell walls and emphysema. However, there exists discrepancy about how CSE works in the process. In the present study, we observed the effect of CSE on the cell growth of type II alveolar epithelial cell-derived A549 cell line, and provided molecular understanding of this effect. The MTT assay results showed that CSE decreased the cell viability of A549 cells in a dose- and time-dependent manner, and cell cycle was arrested in G(1)/S phase. Furthermore, CSE-induced apoptosis of A549 cells was verified by Hoechst 33258 staining, electron microscopy in morphology, and the appearance of DNA fragmentation and annexin V-FITC/propidium iodide (PI) staining assay at molecular level. It was found that CSE treatment resulted in the upregulation of Fas/APO-1 receptor and activation of caspase-3. CSE also initiated accumulation of intracellular reactive oxygen species, which was detected by laser confocal microscopy. Taken together, CSE could inhibit the cell growth and induce apoptosis of A549 cells through Fas receptor pathway. Oxidative stress caused by CSE may be the radical factor leading to apoptosis as well as cell growth inhibition in alveolar epithelial cells.  (+info)

Glycogen synthase kinase 3beta induces cell cycle arrest in a cyclin D1-dependent manner in human lung adenocarcinoma cell line A549. (3/1169)

The effect of glycogen synthase kinase 3beta (GSK3beta) has been repeatedly implicated in cell proliferation, but studies on the effect of GSK3beta in different cell lines with different stimuli have drawn different conclusions. To investigate the direct effect of GSK3beta on cell growth in human lung adenocarcinoma cell line A549, we changed its activity by transient transfection with two kinds of GSK3beta mutant plasmids, constitutively active form S9A-GSK3beta and dominant negative form KM-GSK3beta. Twenty-four hours later, cell counting, flow cytometry and Western blot detection were made respectively. The results showed that enhancing GSK3beta activity caused a decrease in cell number, as well as a higher percentage of cells at G(1) phase. Further, the expression of cyclin D1 was down-regulated by GSK3beta. Taken together, our observations suggest that GSK3beta may induce G(1) cell cycle arrest in a cyclin D1-dependent fashion and therefore possibly plays a growth-inhibitory role in A549 cells.  (+info)

Adenine nucleotide translocase 4 deficiency leads to early meiotic arrest of murine male germ cells. (4/1169)


Silencing CENPF in bovine preimplantation embryo induces arrest at 8-cell stage. (5/1169)


Silencing of the IKKepsilon gene by siRNA inhibits invasiveness and growth of breast cancer cells. (6/1169)


SR and SR-related proteins redistribute to segregated fibrillar components of nucleoli in a response to DNA damage. (7/1169)


Unliganded progesterone receptors attenuate taxane-induced breast cancer cell death by modulating the spindle assembly checkpoint. (8/1169)


Cyclic GMP (cGMP)-dependent protein kinase (protein kinase G [PKG]) is essential for microneme secretion, motility, invasion, and egress in apicomplexan parasites, However, the separate roles of two isoforms of the kinase that are expressed by some apicomplexans remain uncertain. Despite having identical regulatory and catalytic domains, PKGI is plasma membrane associated whereas PKGII is cytosolic in Toxoplasma gondii. To determine whether these isoforms are functionally distinct or redundant, we developed an auxin-inducible degron (AID) tagging system for conditional protein depletion in T. gondii. By combining AID regulation with genome editing strategies, we determined that PKGI is necessary and fully sufficient for PKG-dependent cellular processes. Conversely, PKGII is functionally insufficient and dispensable in the presence of PKGI. The difference in functionality mapped to the first 15 residues of PKGI, containing a myristoylated Gly residue at position 2 that is critical for membrane ...
A recent in-depth view of cell cycle regulation and cancer has provided novel samples of research at the Frontiers of Science. However, the number of foremost revealing information about both the topics has been derived from the intersection of these two fields.1-5 This review intends to introduce the basics of the cell cycle and its regulation at different checkpoints in relation to cancer. Cancer is broadly a result of unchecked cell multiplication due to abnormal activity of varied cell cycle proteins; therefore, cell cycle regulators are considered attractive targets in cancer therapy. Many cancers are uniquely linked with these proteins and are therefore selectively sensitive to their inhibition.6 After a long run of research on the physiological functions of cell cycle proteins and their relevance for cancer, these data recently got converted into the first approved cancer therapeutics, targeting the regulator of cell cycle.7 Here, we are reviewing the role of cell cycle proteins in ...
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Cell cycle analysis is commonly used in biomedical research studies and clinical diagnosis. It helps in distinguishing cells that are in different phases of cell cycle and used to determine the cellular response to biological stimulations and various drug
The cell membrane The DNA Hello, today we will be learning about the cell cycle. The cell cycle is a process that cells go through in order to divide.
Drag the Labels Onto the Diagram to Identify the Stages Of the Cell Cycle. - Drag the Labels Onto the Diagram to Identify the Stages Of the Cell Cycle. , Ponents Of Blood Article
The most recent publications in Cell Cycle Checkpoints and accross biochemistry, molecular biology, neuroscience, development, biotechnology and medicine.
CELL CYCLE CHECKPOINTS The cell cycle has regulatory points called checkpoint. A check point is one of several points in the eukaryotic cell cycle at which the progression of a cell to the next stage in the cell cycle can be halted until conditions are favourable (e.g. the DNA is repaired). These checkpoints occur near […]. ...
Great news, we have finally launched a website devoted to the Australian Cell Cycle community ! This site will serve as a hub for all the amazing cell cycle research that is performed in Australia. In addition, we will also be rebooting the Australian Cell Cycle Workshop (ACCW), with a tentative date of early April…
Cell cycle in somatic cells vs. ESCs. (a) Cell cycle regulation in somatic cells: mitogen signaling through MAPK path
Hva er Cell Cycle Analysis? Cellesyklus-analyse er en teknikk som brukes i biokjemisk forskning for å identifisere og analysere fasen av en biologisk celle. I løpet av sin levetid, passerer en celle gjennom en serie av sykliske faser som kollektivt er kjent som cellesyklusen. M
Cell cycle, the ordered sequence of events that occur in a cell in preparation for cell division. The cell cycle is a four-stage process in which the cell increases in size, copies its DNA, prepares to divide, and divides. Learn more about the cell cycle and the proteins that regulate its progression.
Introduction to Cell Cycle: The cell cycle is the process by which a cell replicates its genetic material and synthesized the other elements of the cell
Identify the correct order of phases for the cell cycle? I. G 2 ​ phase- growth and preparation for mitosis II. Mitosis III. G 1 ​ phase- cell growth IV. S pha
The cell cycle is the meticulous series of events that parent cells go through as they grow and divide their cellular material between two new daughter... read full [Essay Sample] for free
Hello.. It appears Im stuck on another question. Ive figured out 3/4 of it, but I cant seem to find ANYWHERE in my textbook, anything about the stages of the cell cycle and cancer. If you can help me, that would be great ...
Find right answers right now! Which of the following is a correct statement about the events of the cell cycle? More questions about Science & Mathematics, which
worksheets : Cells Alive Worksheet Beautiful Cells Alive Cell Cycle Worksheet Promotiontablecovers Cells Alive Worksheet ~ zachemig2018
Quiescence is a temporary cell cycle state where populations of cells rest and do not replicate, before they are activated and re-enter the cell cycle.
If you have a question about this talk, please contact Laura Blackburn.. Abstract not available. This talk is part of the Lectures in Cancer Biology and Medicine series.. ...
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We welcome your input and comments. Please use this form to recommend updates to the information in ZFIN. We appreciate as much detail as possible and references as appropriate. We will review your comments promptly ...
Welcome to the Australian Cell Cycle Community website. This page is dedicated to bringing together all of the amazing research related to the cell cycle that is performed throughout Australia.
The cell cycle is the life of a cell from the time it is first formed from a dividing parent cell until its own division into two cells. Cell division involves the distribution of identical DNA to two daughter cells. A dividing cell duplicates its DNA,...
The longest phase of the cell cycle is the Gap 1 phase, or G1 phase. During this phase, the cell gears up for cell division by amassing more organelles and getting larger....
Science 9 Chapter 5.1 The Cell Cycle and Mitosis Pg152-158 Notes Cell Replacement and Development -Cells continue to divide as you continue to grow. -
TY - CONF. T1 - Quality and yield improvement through modulation of cell cycle. AU - De Veylder, L.. AU - Beeckman, T.. AU - Beemster, G.. AU - Salmenkallio-Marttila, Marjatta. AU - Oksman-Caldentey, Kirsi-Marja. AU - Inze, D.. PY - 2001. Y1 - 2001. M3 - Conference article. SP - 13. EP - 14. ER - ...
See 13 Best Images of Cell Cycle And Mitosis Worksheet Answers. Inspiring Cell Cycle and Mitosis Worksheet Answers worksheet images. Cell Cycle Worksheet Answers Cell Cycle and Mitosis Worksheet Answer Key Cell Cycle Mitosis and Meiosis Test Answers Cell Cycle Worksheet Answer Key Cell Division Mitosis Worksheet and Answers
View Notes - Cell Cycle from BIOL 101 at UNC. Cell Cycle, Mitosis Meiosis Tuesday, February 10, 2009 10:19 AM 1. Cell Cycle aka Life of a Cell o Interphase Secreting Not dividing o Mitosis Nuclear
補充影片: Dave Morgan Honor Biology: 生物學特論 Lecture 12: Cell cycle and check point control Part 1 Honor Biology: 生物學特論 Lecture 12: Cell cycle and check point control Part 2 Honor Biology: 生物學特論 Lecture 12: Cell cycle and check point contr ...
View Notes - bild lecture week 5.2 from BIOLOGY bild 1 at UCSD. Review: Monday. Skip chapter 11. Review: PSII PSI NADPH Mitosis and Cell Cycle 1.) Cell Cycle a. Alternates between interphase and
2 of 4 of my cell cycle unit. Image Credits: Biology (Campbell) 9th edition, copyright Pearson 2011, & The Internet. Provided under the terms of a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. By David Knuffke.
Research groupsCell biology and Biotechnology Role of Hsp90 in cell cycle control and ageing Dr Andrés Garzón Villar. ..
Get all questions and answers of Cell Cycle And Cell Division of NEET1 Structures And Functions on TopperLearning. TopperLearnings Experts and Students has answered all of Cell Cycle And Cell Division of NEET1 Structures And Functions questions in detail.
Kinases Available in QuickScout™ Cell Cycle panel. The QuickScout™ Cell Cycle Panel mainly includes kinases which are directly involved in the cell-cycle, and their inhibition may interfere with cell proliferation. Contact us to learn more about this panel and how we can help you identify the clinical potential of your compounds.. ...
Class 11 Biology Notes for Cell Cycle and Cell Division - Get here the Notes, Question & Practice Paper of Class 11 Biology for topic Cell Cycle and Cell
Cell Cycle & Cell Division objective MCQs and Study Notes to help you in NEET Biology preparation. Get important Cell Cycle & Cell Division NEET MCQs, tips and important topics
The cell cycle constitutes a series of stages that allow a cell to double its cellular components and divide into two daughter cells. Cell cycle and division are crucial for development of a multicellular organism, as well as...
Shop for the cell cycle recombinant proteins you need here at ProSci Inc.! We stock a wide selection of proteins of all kinds. Visit us online today.
The cell cycle is a five-stage process that begins with the prophase stage and ends with the cytokinesis stage. In between the beginning and end stages, the dividing cell passes through the stages of...
Research groupsCell biology and Biotechnology Cell cycle in yeast Dr Juan Jiménez Martínez. UPOPrincipal Investigator ..
Thank you for your interest in spreading the word about Science Signaling.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
welcome Today I well be teaching and showing you the cell cycle DNA The first step of the cell cycle is Interphase it when the DNA in the cell makes a
Nutr Cancer 63: 435- 443. Jaganathan SK( 2011) Can escapes from developmental aspects of the suggest oil film? Med Hypotheses 76: 535- 537.
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How To Run a Recomp Cycle I hear this all the time I want to get bigger and rip up a bit Starting my cycle, looking to lean up and
Reece, Jane B. (2011). "12". The Cell Cycle (9th ed.). San Francisco: Pearson Education, Inc. May, Karen M; Kevin G. Hardwick ( ... 2006). "The spindle checkpoint". Journal of Cell Science. 119 (Pt 20): 4139-42. doi:10.1242/jcs.03165. PMID 17038540. Retrieved ... Forces exerted by protein "motors" associated with spindle microtubules move the chromosomes toward the centre of the cell. ... Prometaphase is the phase of mitosis following prophase and preceding metaphase, in eukaryotic somatic cells. In prometaphase, ...
Elledge SJ (December 1996). "Cell cycle checkpoints: preventing an identity crisis". Science. 274 (5293): 1664-1672. Bibcode: ... Kaldis P, Aleem E (2007). "Cell cycle sibling rivalry: Cdc2 vs. Cdk2". Cell Cycle. 4 (11): 1491-1494. doi:10.4161/cc.4.11.2124 ... Cell cycle, Proteins, EC 2.7.11, Cell cycle regulators). ... "Viral infections and cell cycle G2/M regulation". Cell Res. 15 ... ISBN 978-0-19-920610-0. Nasmyth K (April 1993). "Control of the yeast cell cycle by the Cdc28 protein kinase". Curr. Opin. Cell ...
See schematic of the role of DUBs in the cell cycle regulation. The spindle checkpoint (also referred to as the mitotic ... Downstream pathways of p53 act to either halt cell cycle progression in G1 or G2 phases of the cell cycle or promote cell-death ... New research into the mitotic checkpoint has revealed a novel role for USP44 in regulating cell cycle progression. The ERK ... Donehower LA (May 2014). "Phosphatases reverse p53-mediated cell cycle checkpoints". Proceedings of the National Academy of ...
Cell Cycle. 4 (7): 883-888. doi:10.4161/cc.4.7.1791. PMID 15970698. Ringshausen, Ingo; O'Shea, Clodagh C.; Finch, Andrew J.; ... O'Shea, Clodagh C.; Choi, Serah; McCormick, Frank; Stokoe, David (2 May 2005). "Adenovirus Overrides Cellular Checkpoints for ... doi:10.1016/j.cell.2015.07.058. PMC 4681434. PMID 26317467. Higginbotham, Jennifer M.; O'Shea, Clodagh C. (15 October 2015). ... Clodagh C. O'Shea is a professor of molecular and cell biology and current Wicklow Chair at the Salk Institute for Biological ...
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to ... After rapid chromatin remodeling, cell cycle checkpoints are activated to allow DNA repair to occur before the cell cycle ... It leads to a pause in cell cycle allowing the cell time to repair the damage before continuing to divide. Checkpoint Proteins ... and some genes are involved in both DNA damage repair and cell cycle checkpoint control, for example ATM and checkpoint kinase ...
"Checkpoint inhibition of the APC/C in HeLa cells is mediated by a complex of BUBR1, BUB3, CDC20, and MAD2". The Journal of Cell ... Defects in BUB3 in the cell cycle can contribute to the following diseases: hepatocellular carcinoma gastric cancer breast ... "Checkpoint inhibition of the APC/C in HeLa cells is mediated by a complex of BUBR1, BUB3, CDC20, and MAD2". The Journal of Cell ... Yu H (December 2002). "Regulation of APC-Cdc20 by the spindle checkpoint". Current Opinion in Cell Biology. 14 (6): 706-14. doi ...
It is used to understand cell cycle checkpoints. Researchers are working to find a way to use this gene to create anti-cancer ... If MCR 1 is not present in the cell these check points do not work properly. Yin L, Locovei AM, D'Urso G (October 2008). " ... The most common function is found during the cell cycle when mutations occur because it becomes activated without ... "Activation of the DNA damage checkpoint in mutants defective in DNA replication initiation". Mol. Biol. Cell. 19 (10): 4374-82 ...
βTrCP plays important roles in regulating cell cycle checkpoints. In response to genotoxic stress, it contributes to turn off ... Cell cycle regulators constitute a major group of βTrCP substrates. During S phase, βTrCP keeps CDK1 in check by promoting the ... thereby preventing cell cycle progression before the completion of DNA repair. During recovery from DNA replication and DNA ... "SCFbetaTrCP-mediated degradation of Claspin regulates recovery from the DNA replication checkpoint response". Molecular Cell. ...
βTrCP plays important roles in regulating cell cycle checkpoints. In response to genotoxic stress, it contributes to turn off ... Cell cycle regulators constitute a major group of βTrCP substrates. During S phase, βTrCP keeps CDK1 in check by promoting the ... thereby preventing cell cycle progression before the completion of DNA repair. During recovery from DNA replication and DNA ... "SCFbetaTrCP-mediated degradation of Claspin regulates recovery from the DNA replication checkpoint response". Molecular Cell. ...
Borlado LR, Méndez J (February 2008). "CDC6: from DNA replication to cell cycle checkpoints and oncogenesis". Carcinogenesis. ... Cdc6, or cell division cycle 6, is a protein in eukaryotic cells. It is mainly studied in the budding yeast Saccharomyces ... CDC6 is normally present at high levels during the G1 phase of the cell cycle. This is partly because the CDC6 gene is only ... of DNA replication and plays important roles in the activation and maintenance of the checkpoint mechanisms in the cell cycle ...
Lu X, Nannenga B, Donehower LA (2005). "PPM1D dephosphorylates Chk1 and p53 and abrogates cell cycle checkpoints". Genes Dev. ... and cell cycle control". Mol. Cell. Biol. 22 (4): 1094-105. doi:10.1128/MCB.22.4.1094-1105.2002. PMC 134641. PMID 11809801. Li ... Cell. 15 (4): 621-34. doi:10.1016/j.molcel.2004.08.007. PMID 15327777. Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The ... Cell Res. 288 (1): 35-50. doi:10.1016/S0014-4827(03)00130-7. PMID 12878157. Bernards R (2004). "Wip-ing out cancer". Nat. Genet ...
Callegari AJ, Kelly TJ (March 2007). "Shedding light on the DNA damage checkpoint". Cell Cycle. 6 (6): 660-6. doi:10.4161/cc. ... and α can work in concert to ensure that the genome is replicated efficiently with high accuracy in every cell cycle. However, ... Melanoma cells are commonly defective in postreplication repair of DNA damages that are in the form of cyclobutane pyrimidine ... Molecular Cell Biology. 6 (12): 943-53. doi:10.1038/nrm1781. PMID 16341080. S2CID 22853897. Brash DE, Seidman MM (January 2020 ...
The Start checkpoint is a major cell cycle checkpoint in yeast. The Start checkpoint ensures irreversible cell-cycle entry even ... Thus, larger cells spend less time in the Start checkpoint compared to smaller cells. Morgan, David. The Cell Cycle: Principles ... a cell cycle gene, showed great coexpression in STE5-8A cells relative to wild type cells. Thus, Cln1/2 inhibition of Far1 ... The transcription of several G1/S genes is essential for cells to proceed through the cell cycle. In budding yeast, the ...
Stabilization of p53 by CHK2 leads to cell cycle arrest in phase G1. Furthermore, CHK2 is known to phosphorylate the cell-cycle ... The CHEK2 gene encodes for checkpoint kinase 2 (CHK2), a protein that acts a tumor suppressor. CHK2 regulates cell division, ... In the fruit fly Drosophila, irradiation of germ line cells generates double-strand breaks that result in cell cycle arrest and ... "Chk2 regulates cell cycle progression during mouse oocyte maturation and early embryo development". Molecules and Cells. 37 (2 ...
E2F integrates cell cycle progression with DNA repair, and G2(M) checkpoints., Genes and Development 16 (2002) 245-56. Johnson ... V.R. Iyer, C.E. Horak, C.S. Scafe, D. Botstein, M. Snyder, P.O. Brown, Genomic binding sites of the yeast cell-cycle ... Then, the cells are lysed and the DNA is sheared by sonication or using micrococcal nuclease. This results in double-stranded ... Last, during the dry-lab portion of the cycle, gathered data are analyzed to either answer the initial question or lead to new ...
... as well as cell cycle checkpoints. To minimize somatic genetic alterations, checkpoint mechanisms stimulate a cell cycle halt ... RFC2 gene product required for a cell cycle checkpoint. RFC is a heteropentamer in budding yeast, it is encoded either by RFC1 ... RFC5 and RCF2 are also engaged in DNA damage checkpoints and DNA replication checkpoints. Replication factor C is an emergency ... The rfc3+ gene is completely separated from fission yeast for DNA damage to regulate checkpoints. The checkpoint signal is also ...
Yeast are a popular species for study because of the rapid cell cycle. Rb is one of the most studied checkpoint molecules. It ... In a healthy cell, checkpoints between phases permit a new phase to begin only when the previous phase is complete and ... Cyclins are molecules that manage the timing of cell cycle events. Cyclin dependent kinases pair up with cyclins to become ... Cyclins are named because they are created or destroyed at predetermined points within the cell cycle. Kinase inhibitors add ...
He proposed the existence of cell cycle checkpoints, tumor suppressor genes and oncogenes. He speculated that cancers might be ... During the same period, the idea that the body was made up of various tissues, that in turn were made up of millions of cells, ... He discovered a method to generate cells with multiple copies of the centrosome, a structure he discovered and named. He ... He suggested that mutations of the chromosomes could generate a cell with unlimited growth potential which could be passed on ...
One of the cell cycle checkpoints occurs during prometaphase and metaphase. Only after all chromosomes have become aligned at ... "The Cell Cycle". Kimball's Biology Pages. Archived from the original on 19 November 2012. Retrieved 9 December 2012. Media ... Metaphase accounts for approximately 4% of the cell cycle's duration.[citation needed] Preceded by events in prometaphase and ... is a stage of mitosis in the eukaryotic cell cycle in which chromosomes are at their second-most condensed and coiled stage ( ...
Checkpoints are eukaryotic DNA damage-inducible cell cycle arrests at G1 and G2. Checkpoint suppressor 1 suppresses multiple ... Mol Cell Biol. 17 (6): 3037-46. doi:10.1128/MCB.17.6.3037. PMC 232156. PMID 9154802. "Entrez Gene: CHES1 checkpoint suppressor ... Pati D, Keller C, Groudine M, Plon SE (Jun 1997). "Reconstitution of a MEC1-independent checkpoint in yeast by expression of a ... yeast checkpoint mutations including mec1, rad9, rad53 and dun1 by activating a MEC1-independent checkpoint pathway. ...
The BRCT domain is found predominantly in proteins involved in cell cycle checkpoint functions responsive to DNA damage, for ... "A superfamily of conserved domains in DNA damage-responsive cell cycle checkpoint proteins". FASEB J. 11 (1): 68-76. doi: ...
This protein is required for cell cycle progression through the S/M checkpoint. Three transcript variants encoding different ... The effect of NEDD8 inhibition may be greater for cancer cells than for normal cells if the cancer cells are already deficient ... "The amyloid precursor protein-binding protein APP-BP1 drives the cell cycle through the S-M checkpoint and causes apoptosis in ... "The amyloid precursor protein-binding protein APP-BP1 drives the cell cycle through the S-M checkpoint and causes apoptosis in ...
... fluoropyrimidines increase sensitivity by dysregulating S-phase cell cycle checkpoints in tumor cells. Gemcitabine progresses ... Tumor cells in a hypoxic environment may be as much as 2 to 3 times more resistant to radiation damage than those in a normal ... A radiosensitizer is an agent that makes tumor cells more sensitive to radiation therapy. It is sometimes also known as a ... One of the major limitations of radiotherapy is that the cells of solid tumors become deficient in oxygen. Solid tumors can ...
These proteins are key checkpoint proteins in the cell cycle. Cancer patients have a lowered expression of per1. Gery, et al. ... PER1 expression may have significant effects on the cell cycle. Cancer is often a result of unregulated cell growth and ... "The circadian gene per1 plays an important role in cell growth and DNA damage control in human cancer cells". Mol. Cell. 22 (3 ... Therefore, a cell's circadian clock may play a large role in its likelihood of developing into a cancer cell. PER1 is a gene ...
Lu LY, Yu X. CHFR is important for the survival of male premeiotic germ cells. Cell Cycle. 2015;14(21):3454-60. doi: 10.1080/ ... Erson AE, Petty EM (2004). "CHFR-associated early G2/M checkpoint defects in breast cancer cells" (PDF). Mol. Carcinog. 39 (1 ... Matsusaka T, Pines J (2004). "Chfr acts with the p38 stress kinases to block entry to mitosis in mammalian cells". J. Cell Biol ... J Cell Biol. 156 (2): 249-59. doi:10.1083/jcb.200108016. PMC 2199220. PMID 11807090. "Entrez Gene: CHFR checkpoint with ...
CK2s anti-apoptotic function is in the continuation of the cell cycle; from G1 to S phase and G2 to M phase checkpoints. This ... Having roles in cell cycle regulation may also indicate CK2's role in allowing cell cycle progression when normally it should ... 2020). "The Global Phosphorylation Landscape of SARS-CoV-2 Infection Cell". Cell. 182 (3): 685-712.e19. doi:10.1016/j.cell. ... Casein kinase 2 (EC is a serine/threonine-selective protein kinase that has been implicated in cell cycle ...
Cell Cycle. 9 (17): 3591-3601. doi:10.4161/cc.9.17.12832. PMID 20818157. Diril; Bisteau; Kitagawa (2016). "Loss of the ... it is required for its maintenance by sustaining spindle assembly checkpoint signaling. Suppression of protein phosphatase 2A ... The MASTL depleted cells are delayed by RNAi in G2 phase and show a decreased condensation of the chromosomes. RNAi cells which ... This is present in mainly mammalian cells like human, house mouse, cattle, monkey, etc. It is in the 10th chromosome of the ...
... a cell cycle checkpoint gene required for cell cycle arrest and DNA damage repair in response to DNA damage. This protein ... Cell cycle checkpoint protein RAD17 is a protein that in humans is encoded by the RAD17 gene. The protein encoded by this gene ... "Phosphorylation of serines 635 and 645 of human Rad17 is cell cycle regulated and is required for G1/S checkpoint activation in ... "The human checkpoint Rad protein Rad17 is chromatin-associated throughout the cell cycle, localizes to DNA replication sites, ...
"E2F integrates cell cycle progression with DNA repair, replication, and G(2)/M checkpoints". Genes & Development. 16 (2): 245- ... Al-Wahiby S, Wong HP, Slijepcevic P (October 2005). "Shortened telomeres in murine scid cells expressing mutant hRAD54 coincide ... November 2006). "Rad54 is dispensable for the ALT pathway". Genes to Cells. 11 (11): 1305-1315. doi:10.1111/j.1365-2443.2006. ... Pluth JM, Fried LM, Kirchgessner CU (March 2001). "Severe combined immunodeficient cells expressing mutant hRAD54 exhibit a ...
"E2F integrates cell cycle progression with DNA repair, replication, and G(2)/M checkpoints". Genes & Development. 16 (2): 245- ... The E2F family plays a crucial role in the control of cell cycle and action of tumor suppressor proteins and is also a target ... Lindeman GJ, Gaubatz S, Livingston DM, Ginsberg D (May 1997). "The subcellular localization of E2F-4 is cell-cycle dependent". ... This protein binds specifically to retinoblastoma protein pRB in a cell-cycle dependent manner. Alternative gene splicing is ...
Eukaryotic cells respond to damaged DNA by stimulating or impairing G1, S, or G2 phases of the cell cycle to initiate DNA ... "Estrogen receptor beta decreases survival of p53-defective cancer cells after DNA damage by impairing G₂/M checkpoint signaling ... the cycle progresses compared to an average cycle. - The ranges denoted Inter-cycle variability are more appropriate to use in ... Estradiol is produced by action of aromatase mainly in the Leydig cells of the mammalian testis, but also by some germ cells ...
Just as in animals, plant cells differentiate and develop into multiple cell types. Totipotent meristematic cells can ... Land plants are key components of the water cycle and several other biogeochemical cycles. Some plants have coevolved with ... 89 The DNA checkpoint kinase ATM has a key role in integrating progression through germination with repair responses to the DNA ... Cell division is also characterized by the development of a phragmoplast for the construction of a cell plate in the late ...
DNA damage checkpointsEdit. After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle ... After rapid chromatin remodeling, cell cycle checkpoints are activated to allow DNA repair to occur before the cell cycle ... and some genes are involved in both DNA damage repair and cell cycle checkpoint control, for example ATM and checkpoint kinase ... DNA damage checkpoint is a signal transduction pathway that blocks cell cycle progression in G1, G2 and metaphase and slows ...
Johnson, D.G. & Walker, C.L. (1999). „Cyclins and cell cycle checkpoints". Annu. Rev. Pharmacol. Toxicol. 39: 295-312. PMID ... Nicholas C. Price; Lewis Stevens (1999). Fundamentals of Enzymology: The Cell and Molecular Biology of Catalytic Proteins ( ...
There are three checkpoints in the cell cycle: the G1/S Checkpoint or the Start checkpoint in yeast; the G2/M checkpoint; and ... Within the cell cycle, there is a stringent set of regulations known as the cell cycle control system that controls the timing ... Complexes of cyclin that are active during other phases of the cell cycle are kept inactivated to prevent any cell-cycle events ... particularly important in the cell cycle because it determines whether a cell commits to division or to leaving the cell cycle ...
Nilsson I, Hoffmann I (2000). "Cell cycle regulation by the Cdc25 phosphatase family". Progress in Cell Cycle Research. 4: 107- ... Sanchez, Y; Wong C; Thoma R S; Richman R; Wu Z; Piwnica-Worms H; Elledge S J (Sep 1997). "Conservation of the Chk1 checkpoint ... Amini S, Khalili K, Sawaya BE (2004). "Effect of HIV-1 Vpr on cell cycle regulators". DNA Cell Biol. 23 (4): 249-60. doi: ... "Entrez Gene: CDC25C cell division cycle 25 homolog C (S. pombe)". Bulavin, D V; Higashimoto Y; Popoff I J; Gaarde W A; Basrur V ...
The BCR-ABL transcript encodes a tyrosine kinase, which activates mediators of the cell cycle regulation system, leading to a ... Yoshida K, Komatsu K, Wang HG, Kufe D (May 2002). "c-Abl tyrosine kinase regulates the human Rad9 checkpoint protein in ... suggesting a cell cycle function for ABL1. The ABL1 gene is expressed as either a 6- or a 7-kb mRNA transcript, with ... "A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl tyrosine kinase in the cell cycle". ...
... checkpoints are used by the cell to monitor and regulate the progress of the cell cycle. Checkpoints prevent cell ... Controlling the Cell Cycle The cell cycle & Cell death Transcriptional program of the cell cycle: high-resolution timing Cell ... This cyclin-Cdk driven cell cycle transitional mechanism governs a cell committed to the cell cycle that allows cell ... Using GFP to visualize the cell-cycle Science Creative Quarterly's overview of the cell cycle KEGG - Human Cell Cycle Archived ...
Moreover, galectin-9 contributed to tumorigenesis by tumor cell transformation, cell-cycle regulation, angiogenesis, and cell ... "Upregulation of Galectin-9 and PD-L1 Immune Checkpoints Molecules in Patients with Chronic Lymphocytic Leukemia". Asian Pacific ... "A modified version of galectin-9 induces cell cycle arrest and apoptosis of Burkitt and Hodgkin lymphoma cells". British ... an interaction with CD40 on T-cells induced their proliferation inhibition and cell death. Galectin-9 also has important ...
Cell. 150 (4): 685-696. doi:10.1016/j.cell.2012.07.018. PMC 3431020. PMID 22901803. Jiang, Yuhui; Li, Xinjian; Yang, Weiwei; ... the spindle assembly protein Bub3 to regulate chromosome segregation and mitotic checkpoint in metaphase, and myosin light ... "Mitochondria-Translocated PGK1 Functions as a Protein Kinase to Coordinate Glycolysis and the TCA Cycle in Tumorigenesis". ... "PKM2 regulates chromosome segregation and mitosis progression of tumor cells". Molecular Cell. 53 (1): 75-87. doi:10.1016/j. ...
... is frequently used in cell biology laboratories to synchronize the cell division cycle. Cells treated with ... The absence of microtubule attachment to kinetochores activates the spindle assembly checkpoint, causing the cell to arrest in ... Prolonged arrest of cells in mitosis due to nocodazole treatment typically results in cell death by apoptosis. Another standard ... For cell synchronization experiments, nocodazole is usually used at a concentration of 40-100 ng/mL of culture medium for a ...
... is a protein that slows cell division by slowing the progression of the cell cycle from the G1 phase to the S phase, thereby ... "Ribosomal protein L11 negatively regulates oncoprotein MDM2 and mediates a p53-dependent ribosomal-stress checkpoint pathway". ... p16 is an inhibitor of cyclin-dependent kinases (CDK). It slows down the cell cycle by prohibiting progression from G1 phase to ... Ivanchuk SM, Mondal S, Rutka JT (June 2008). "p14ARF interacts with DAXX: effects on HDM2 and p53". Cell Cycle. 7 (12): 1836-50 ...
... delays cell cycle transition and/or proliferation. In contrast, methylation of histone residues H3K4, H3K36, and H3K79 is ... "The Dot1 histone methyltransferase and the Rad9 checkpoint adaptor contribute to cohesin-dependent double-strand break repair ... stem cell maturation, cell lineage development, genetic imprinting, DNA methylation, and cell mitosis. The class of lysine- ... Kouzarides T (February 2007). "Chromatin modifications and their function". Cell. 128 (4): 693-705. doi:10.1016/j.cell.2007.02. ...
Cell Cycle. 8 (24): 4155-4167. doi:10.4161/cc.8.24.10316. PMC 2896895. PMID 19946220. Yao V, Berkman CE, Choi JK, O'Keefe DS, ... Also in trials for CRPC are : checkpoint inhibitor ipilimumab, CYP17 inhibitor galeterone (TOK-001), and immunotherapy PROSTVAC ... prostate cancer cell population harbors self-renewing long-term tumor-propagating cells that resist castration". Cell Stem Cell ... LNCaP cells express AR, but PC-3 and DU-145 cells express very little or no AR. The proliferation of LNCaP cells is androgen- ...
Cell Cycle. 10 (15): 2549-60. doi:10.4161/cc.10.15.16531. PMC 3180193. PMID 21701264. Liu B, Wang J, Chan KM, Tjia WM, Deng W, ... Pichierri P, Ammazzalorso F, Bignami M, Franchitto A (2011). "The Werner syndrome protein: linking the replication checkpoint ... Thus, in a population of cells comprising a tissue with replicating cells, mutant cells will tend to be lost. However, ... Mutations are replicated when the cell replicates. In a population of cells, mutant cells will increase or decrease in ...
Post SM, Tomkinson AE, Lee EY (2003). "The human checkpoint Rad protein Rad17 is chromatin-associated throughout the cell cycle ... "The human checkpoint Rad protein Rad17 is chromatin-associated throughout the cell cycle, localizes to DNA replication sites, ... Cell. Biol. 17 (4): 1817-23. doi:10.1128/mcb.17.4.1817. PMC 232028. PMID 9121429. Coll JM, Hickey RJ, Cronkey EA, Jiang HY, ... Ohta S, Shiomi Y, Sugimoto K, Obuse C, Tsurimoto T (2002). "A proteomics approach to identify proliferating cell nuclear ...
Ford HL, Kabingu EN, Bump EA, Mutter GL, Pardee AB (October 1998). "Abrogation of the G2 cell cycle checkpoint associated with ... Ford HL, Landesman-Bollag E, Dacwag CS, Stukenberg PT, Pardee AB, Seldin DC (July 2000). "Cell cycle-regulated phosphorylation ...
It is involved in coordinating the Chk1-directed DNA damage/cell cycle checkpoint response by regulating the stability of the ... Cell. 127 (3): 635-48. doi:10.1016/j.cell.2006.09.026. PMID 17081983. S2CID 7827573. Sulem P, Gudbjartsson DF, Stacey SN, ... Iron is an essential nutrient in cells, but high levels can be cytotoxic, so maintaining cellular levels is important. HERC2 ... Sturm RA, Larsson M (October 2009). "Genetics of human iris colour and patterns" (PDF). Pigment Cell & Melanoma Research. 22 (5 ...
The G1 checkpoint is controlled most directly by mitogens: further cell cycle progression does not need mitogens to continue. ... preventing the cells from replicating and dividing. Tumor cells that are resistant to anti-mitogens allow the cell cycle to ... Cell proliferation is often regulated by not only external mitogens but also by anti-mitogens, which inhibit cell cycle ... "Mitogen requirement for cell cycle progression in the absence of pocket protein activity". December 2005, Cancer Cell, Vol. 8, ...
The ablation of Numb in a cell leads to a decrease in TP53, causing impaired apoptosis and cell cycle checkpoint response. ... The pIIa cell divides to produce a bristle cell and a socket cell, while the pIIb cell divides to produce a neuron and a glial ... The other daughter cell becomes a progenitor cell to fill the lost role of the parent cell and maintain proliferation. In ... The posterior daughter cell is called the pIIa cell and the anterior daughter cell is called the pIIb. ...
Macy B, Wang M, Yu HG (2009). "The many faces of shugoshin, the "guardian spirit," in chromosome segregation". Cell Cycle. 8 (1 ... Shugoshin also acts as a spindle checkpoint component. It senses tension between sister chromatids during mitosis, and it ... Cell Cycle. 5 (10): 1094-101. doi:10.4161/cc.5.10.2747. PMID 16687935. Salic A, Waters JC, Mitchison TJ (2004). "Vertebrate ... doi:10.1016/j.cell.2004.08.016. PMID 15339662. S2CID 14339817. Xu Z, Cetin B, Anger M, Cho US, Helmhart W, Nasmyth K, et al. ( ...
Factors that contribute to genome stabilization include proper cell-cycle checkpoints, DNA repair pathways, and other actions ... Growth of cells depends both on cell-to-cell interactions and cell-to-extracellular matrix (ECM) interactions. Mechanisms of ... is arrest of the cell cycle in the G1 phase. Qualitative differences have been found between senescent cells and normal cells, ... p53 has an identified role, however, in regulating the cell cycle as well, which is an essential gatekeeper function. Van Gent ...
"Specific association of estrogen receptor beta with the cell cycle spindle assembly checkpoint protein, MAD2". Proc. Natl. Acad ... Cell. Biol. 20 (1): 402-15. doi:10.1128/MCB.20.1.402-415.2000. PMC 85095. PMID 10594042. Xie W, Hong H, Yang NN, Lin RJ, Simon ... Cell. Biol. 17 (5): 2735-44. doi:10.1128/MCB.17.5.2735. PMC 232124. PMID 9111344. Voegel JJ, Heine MJ, Tini M, Vivat V, Chambon ... Cell. Biol. 19 (9): 6164-73. doi:10.1128/MCB.19.9.6164. PMC 84548. PMID 10454563. Atkins GB, Hu X, Guenther MG, Rachez C, ...
... and/or cell cycle checkpoint control. It is suggested that this gene may itself be a tumor suppressor acting in the same ... Yu X, Baer R (June 2000). "Nuclear localization and cell cycle-specific expression of CtIP, a protein that associates with the ... Yu X, Baer R (2000). "Nuclear localization and cell cycle-specific expression of CtIP, a protein that associates with the BRCA1 ... Dick FA, Sailhamer E, Dyson NJ (May 2000). "Mutagenesis of the pRB pocket reveals that cell cycle arrest functions are ...
"Specific association of estrogen receptor beta with the cell cycle spindle assembly checkpoint protein, MAD2". Proceedings of ... However, ERβ has been found to have proliferative effects in some breast cell lines. Expression of ERα and ERβ in the mammary ... ERβ may inhibit cell proliferation and opposes the actions of ERα in reproductive tissue. ERβ may also have an important role ... ERβ also plays a role in regulating APOE, a risk factor for AD that redistributes lipids across cells. APOE expression in the ...
doi:10.1016/j.cell.2008.05.043. PMC 2591934. PMID 18662541. Ah Fong, A; Judelson, HS (2003). "Cell cycle regulator Cdc14 is ... "Vertebrate cells genetically deficient for Cdc14A or Cdc14B retain DNA damage checkpoint proficiency but are impaired in DNA ... cells deleted for the genes showed no defects in growth or mitosis, and a similar failure of a cell cycle defect was also shown ... "The CDC-14 phosphatase controls developmental cell-cycle arrest in C. elegans". Nat Cell Biol. 6 (8): 777-783. doi:10.1038/ ...
"Cytokinins and the plant cell cycle: Problems and pitfalls of proving their function". Plant Cell Proliferation in Growth and ... In eukaryotes, the cellular repair response to DNA damage is orchestrated, in part, by the DNA damage checkpoint kinase ATM. ... The idea that a plant does not impose efficiency demands on immature cells is that most immature cells are part of so-called ... Parallels to cell division - the theory, perhaps even more controversially, asserts that just as both auxin and cytokinin seem ...
The armed group reorganised itself in the late 1970s into a smaller, cell-based structure, which was designed to be harder to ... Picador, p. 53; ISBN 0-330-34243-6 The list included: Three permanent checkpoints: Boa Island (1991) Derryard (1991) The Irish ... cycle of sectarian killings with loyalist paramilitaries. The worst examples of this occurred in 1975 and 1976. In September ... The IRA then reemerged as a cell-structured organisation. The report also asserts that the government efforts by the 1980s were ...
Cell cycle and differentiation In vitro experiments using both human and mouse cell lines have shown that EVI1 prevents the ... By inhibiting an important checkpoint pathway for tumor suppression and growth control, overexpression or aberrant expression ... has also been shown in vitro to upregulate the cell cycle and block granulocytic differentiation of murine hematopoietic cells ... It has been observed that it not only induces apoptosis but can also inhibit the cell cycle, and has marked anti-angiogenesis ...
After the cell has split into its two daughter cells, the cell enters G1. DNA repair processes and cell cycle checkpoints have ... Cell cycle checkpoints are control mechanisms in the eukaryotic cell cycle which ensure its proper progression. Each checkpoint ... Biochemical switches in the cell cycle Cell cycle analysis G2-M DNA damage checkpoint Postreplication checkpoint Meiotic ... known as the cell cycle control system, which monitors and dictates the progression of the cell through the cell cycle. This ...
... tetrahydropersin in cancer cells and activity of related synthetic analogs.  Author: Field, Jessica J ; Kanakkanthara, Arun ; ...
Cell-cycle development is monitored by checkpoint pathways that pause the cell. * Post author By exposed ... Cell-cycle development is monitored by checkpoint pathways that pause the cell routine when tension arises to threaten the ... We discovered that checkpoint-defective alleles suppress the MMS awareness as well as the checkpoint recovery defect of cells. ... Furthermore induced degradation of checkpoint-functional Mrc1 rescues the checkpoint recovery defect of cells partially. We ...
The association of cell cycle checkpoint 2 variants and kidney function: Findings of the family blood pressure program and the ... The association of cell cycle checkpoint 2 variants and kidney function: Findings of the family blood pressure program and the ... The association of cell cycle checkpoint 2 variants and kidney function : Findings of the family blood pressure program and the ... The association of cell cycle checkpoint 2 variants and kidney function : Findings of the family blood pressure program and the ...
... cell cycle progression and DNA damage/replication DMA checkpoint activation in cells (Fig. ?(Fig.1A).1A). We obtained similar ... These findings lead to the proposal that caffeine inhibits cell cycle checkpoint activation mediated by Rad3 and related PIKKs ... Home / Delta Opioid Receptors / These findings lead to the proposal that caffeine inhibits cell cycle checkpoint activation ... These findings lead to the proposal that caffeine inhibits cell cycle checkpoint activation mediated by Rad3 and related PIKKs ...
Cell Cycle Checkpoint. The DNA damage checkpoint pathway enforces cell cycle arrest to allow timely repair in response to DNA ... Remarkably, different activators of Mec1/ATR are utilized during different parts of the cell cycle, the checkpoint clamp 9-1-1 ... We are studying which factors in the cell are responsible for recognizing damage in distinct stages of the cell cycle, and how ... Emerging data in our lab indicate that the replication checkpoint that functions in S phase in response to stalling of ...
Cell cycle involves duplication and division of cellular material between daughter cells & it is regulated by Cell Cycle ... ... 1) Cell Cycle Checkpoints - While moving through the cell cycle, the cells dont transition from one phase to another just ... This process of maintaining the standards occur through Cell Cycle Checkpoints and Cell Cycle Regulators. In fact, the ...
... in complex with the Mitotic checkpoint complex (APC/C-MCC) at 3.8 angstrom resolution ... Cell division cycle protein 27 homolog. F, H. 824. Homo sapiens. Mutation(s): 0 Gene Names: CDC27, ANAPC3, D0S1430E, D17S978E. ... Cell division cycle protein 23 homolog. C, P. 597. Homo sapiens. Mutation(s): 0 Gene Names: CDC23, ANAPC8. ... Cell division cycle protein 16 homolog. J, K. 620. Homo sapiens. Mutation(s): 0 Gene Names: CDC16, ANAPC6. ...
Human Gene Set: GOBP_MEIOTIC_CELL_CYCLE_CHECKPOINT_SIGNALING GSEA and MSigDB Need Your Support. We are preparing a grant ... For the Mouse gene set with the same name, see GOBP_MEIOTIC_CELL_CYCLE_CHECKPOINT_SIGNALING ... A signaling process that contributes to a meiotic cell cycle checkpoint that ensures accurate chromosome replication and ... segregation by preventing progression through a meiotic cell cycle until conditions are suitable for the cell to proceed to the ...
Cell cycle/Check point Kód: MC-CELL CYCLE Značka: Targetmol. Na vyžiadanie ...
Quantitative proteomics reveals the basis for the biochemical specificity of the cell-cycle machinery. Pagliuca FW, et al. Mol ... TOPBP1 interacting checkpoint and replication regulatorprovided by HGNC. Primary source. HGNC:HGNC:28704 See related. Ensembl: ... involved_in mitotic G2 DNA damage checkpoint signaling IBA Inferred from Biological aspect of Ancestor. more info ... involved_in mitotic G2 DNA damage checkpoint signaling ISS Inferred from Sequence or Structural Similarity. more info ...
Methods In Molecular Biology Volume 241 Cell Cycle Checkpoint Control Protocols «« 195. Methods In Molecular Biology Volume 231 ... 196 Methods In Molecular Biology Volume 241 Cell Cycle Checkpoint Control Protocols. Δημοσιεύτηκε από billpits , 20 Mar 2013 18 ... Methods In Molecular Biology Volume 241 Cell Cycle Checkpoint Control Protocols. by Howard B. Lieberman. © 2004 Humana Press ... The Cell - Evolution of the First Organism, Joseph Panno. *Inside the Cell, National Institute of General Medical Sciences-ΝΙΗ ...
... cell cycle progression and checkpoint regulation (MCPH1, CENPJ, CDK5RAP2; Thornton and Woods, 2009), centrosome maturation ( ... If cell division is perfectly symmetric, it produces two daughter cell neural precursors. If not, the daughter cell may fail to ... are present in deep cell layers, and are similar to those found in multipotent or pluripotent stem cells. In contrast, cells ... Group I.C: Cortical Dysgeneses With Abnormal Cell Proliferation. An important advance in understanding cell proliferation has ...
However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in ... Cell Cycle Checkpoints / genetics * Heat-Shock Proteins / genetics * Heat-Shock Proteins / metabolism ... In proliferating cells, MOF directly binds and maintains the expression of genes required for cell cycle progression. In ... However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in ...
DNA damage checkpoints are responsible for keeping the fidelity of genetic info by arresting cell cycle progression and ... Many research have identified a network of proteins which are involved throughout the DNA damage checkpoints response. Central ... In these cell cycle checkpoints result in inappropriate proliferation. ... DNA damage checkpoints are responsible for. Posted On June 3, 2021. In these cell cycle checkpoints result in inappropriate ...
The spindle checkpoint is the prime cell-cycle control mechanism that ensures sister chromatids are bioriented before anaphase ... 2011) Spindle checkpoint silencing requires association of PP1 to both Spc7 and kinesin-8 motors. Developmental Cell, Vol.20 ( ... The role of Klp5 and Klp6 in checkpoint silencing is specific to this class of kinesin and independent of their motor ... Spindle checkpoint silencing requires association of PP1 to both Spc7 and kinesin-8 motors ...
response to cell cycle checkpoint signaling. 7. response to DNA integrity checkpoint signaling. 7. ... positive regulation of response to DNA integrity checkpoint signaling +. 0. regulation of response to DNA damage checkpoint ... positive regulation of response to DNA integrity checkpoint signaling +. 0. regulation of response to DNA damage checkpoint ... regulation of DNA integrity checkpoint effector process; regulation of response to signal involved in DNA integrity checkpoint ...
... checkpoint) since damages of any phase can cause severe cell cycle defect. The cell cycle can proceed to the next phase ... cell cycle returns to the G1 stationary phase through a sequence of the S, G2 and M phases. During the cell cycle, a cell ... To construct a timing-robust Boolean model that preserves checkpoint conditions of the budding yeast cell cycle, we used a ... In particular, such models violate the M phase checkpoint condition so that it allows a division of a budding yeast cell into ...
However, the above cell cycle checkpoint genes other than hBUB1/hBUBR1 still largely remain functionally characterized in ... Therefore, it is too early to dismiss the roles of cell cycle checkpoint genes for the pathogenesis of CI simply because of the ... Therefore, it will be important to determine whether inactivation of cell cycle checkpoint genes other than hBUB1 and hBUBR1 ... Elledge S. J. Cell cycle checkpoints: preventing an identity crisis. Science (Wash. DC) ...
Cell cycle checkpoint inhibitor.. *Anticancer treatment drug ≤ 21 days (≤ 6 weeks for nitrosoureas or mitomycin C) or use of an ... Maximum concentration (Cmax) of adavosertib [ Time Frame: 2 hours post-dose on Day 5 of Cycles 1 and 2 (each cycle is 21 days ... For Programmed cell death-1 receptor (PD-1) /Programmed death-ligand 1 (PD-L1) inhibitors, a minimum of 28 days since last dose ... The subjects will receive oral adavosertib 300 mg, once daily on Days 1 to 5 and Days 8 to 12 of a 21-day treatment cycle. ...
Cell cycle checkpoints and cancer Org.: Dpt de Biochimie Friday 25 February 2005 11:15 seminar room 174, Sciences II Dr Nicolas ...
Calcitriol inhibited the growth of CSCs derived from anaplastic thyroid cancer cells. It may also exert a pro-differentiation ... Keywords: Calcitriol; cancer stem-like cells; growth; thyroid carcinoma. MeSH terms * Cell Cycle Checkpoints / drug effects* ... As revealed by cell cycle analysis, calcitriol induced G2/M phase arrest in thyro-sphere cells derived cells from HTh74, HTh74R ... SW1736 and C643 cell lines was investigated by cell viability assays. In stem-enriched cells derived from thyro-spheres cell ...
Dive into the research topics of A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA ... A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage. ...
The Cell Cycle: Cyclins and Checkpoints. View QuickTime Movie. p53s Role in the Cell ... A term used to describe cancer cells that divide rapidly and have little or no resemblance to normal cells. ... A normal series of events in a cell that leads to its death. Also called programmed cell death. ... In an electrochemical cell, the electrode at which the oxidation half-reaction occurs. ...
... cells exit mitosis via mitotic slippage. In microtubule (MT) poisons, slippage requires cyclin B ... When the spindle assembly checkpoint (SAC) cannot be satisfied, ... Checkpoint controls delay cell cycle progression in response to ... Cell line-specific differences in the control of cell cycle progression in the absence of mitosis. Proc. Natl. Acad. Sci. USA. ... Cell line-specific differences in the control of cell cycle progression in the absence of mitosis. Proc. Natl. Acad. Sci. USA. ...
Cell Cycle Checkpoints. Rajendran P, Kidane AI, Yu T-W, Dashwood W-M, Bisson WH, Löhr CV, Ho E, Williams DE, Dashwood RH. 2013 ... Cell Line. Henderson MC, Siddens LK, Krueger SK, J Stevens F, Kedzie K, Fang WK, Heidelbaugh T, Nguyen P, Chow K, Garst M et al ... Carcinoma, Squamous Cell. Wang R, Chen Y-S, Dashwood W-M, Li Q, Löhr CV, Fischer K, Ho E, Williams DE, Dashwood RH. 2017. ... Cell Line, Tumor. Watson GW, Wickramasekara S, Fang Y, Maier CS, Williams DE, Dashwood RH, Perez VI, Ho E. 2016. HDAC6 activity ...
Cell cycle checkpoint signaling through the ATM and ATR kinases.. Genes Dev. 2001; 15: 2177-2196. View in Article *Scopus (1652 ... dependent up-regulation of DNAM-1 and NKG2D ligands on multiple myeloma cells by therapeutic agents results in enhanced NK-cell ... Checkpoint activation in response to double-strand breaks requires the Mre11/Rad50/Xrs2 complex. ... Identification of PVR (CD155) and nectin-2 (CD112) as cell surface ligands for the human DNAM-1 (CD226) activating molecule. ...
  • Background: Recent experimental evidence suggests that DNA damage and cell cycle regulatory proteins are involved in kidney injury and apoptosis. (
  • Although, if unrepairable, the cell will program its own death (apoptosis). (
  • As revealed by cell cycle analysis, calcitriol induced G2/M phase arrest in thyro-sphere cells derived cells from HTh74, HTh74R and C643 but did not affect apoptosis. (
  • The current review indicates that EOs and their constituents act by multiple pathways and mechanisms involving apoptosis, cell cycle arrest, antimetastatic and antiangiogenic, increased levels of reactive oxygen and nitrogen species (ROS/RNS), DNA repair modulation, and others to demonstrate their antiproliferative activity in the cancer cell. (
  • These findings suggest that FCP induced G2/M arrest and apoptosis of A549 cells. (
  • Natural substances exert their anti-cancer activity by modulating cell cycle progression and inducing apoptosis-regulatory proteins ( 8 , 9 ). (
  • Apoptosis is a type I programmed cell death that is characterized by distinct phenotypes from necrosis, including membrane blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation and apoptotic body formation ( 10 , 11 ). (
  • In addition, B-cell lymphoma (Bcl)-2 family proteins are important for apoptosis regulation, which could be either proapoptotic, such as Bcl-2-associated X protein (Bax) or Bcl-2 homologous antagonist/killer, or antiapoptotic, such as Bcl-2 and Bcl-extra large (Bcl-xL) ( 13 ). (
  • Following DNA damage, cells activate a complex DNA-damage-response (DDR) signaling network to arrest the cell cycle, repair DNA and, if the extend of damage is beyond repair capacity, induce apoptosis. (
  • Pappano WN , Zhang Q, Tucker LA, Tse C, Wang J. Genetic inhibition of the atypical kinase Wee1 selectively drives apoptosis of p53 inactive tumor cells. (
  • Cell cycle and apoptosis were determined by flow cytometry. (
  • In addition, the siRNA could markedly arrest the cell cycle at the G2/M checkpoint and induce cellular apoptosis in a dose-dependent manner. (
  • TBBE and TBWE inhibited the proliferation of breast (MCF-7), cervical (HeLa) and brain (U87) cancer cells by inducing G2/M arrest while TBEE caused apoptosis. (
  • Chao JI, Kuo PC, Hsu TS (2004) Down-regulation of survivin in nitric oxide induced cell growth inhibition and apoptosis of the human lung carcinoma cells. (
  • Ghate NB, Chaudhuri D, Sarkar R et al (2013) An antioxidant extract of tropical lichen, Parmotrema reticulatum , induces cell cycle arrest and apoptosis in breast carcinoma cell line MCF-7. (
  • Checkpoint kinase 2 (Chk2) is one of the critical kinases governing the cell cycle checkpoint, DNA damage repair, and cell apoptosis in response to DNA damaging signals. (
  • The physiological effects of PLK2 cross talk with TAp73 on cell cycle progress and apoptosis were observed by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling assays. (
  • Inhibiting PLK2 in TAp73-enriched cells strengthened the effects of the DNA-damaging drug on both G1 phase arrest and apoptosis. (
  • We have reported that combination of BRAFi or MEKi with the expression of wild-type INK4A or a CDK4 inhibitor (CDK4i) significantly suppresses growth and enhances apoptosis in melanoma cells [ 1 - 3 ]. (
  • Eukaryotic cells respond to DNA damages by activating the ATM-CHK2 and/or ATR-CHK1 pathway, whose function is to regulate cell cycle progression, to promote damage repair and to control apoptosis. (
  • This phenomenon was associated with the abrogation of the G2/M cell cycle checkpoint with changes in the expression pCDK1 and cyclin B1, and cell entry in mitosis, followed by the induction of apoptosis. (
  • siRNA-mediated knockdown against CDCA1 and KNTC2, both frequently overexpressed in colorectal and gastric cancers, suppresses cell proliferation and induces apoptosis. (
  • In addition, mechanisms such as mutagenic repair or dimer bypass, recombinational repair, cell-cycle checkpoints, apoptosis and certain alternative repair pathways are also operative in various organisms. (
  • Gain-of-function studies using mature miR-27a were performed to investigate cell proliferation and apoptosis in the Hep2 cells. (
  • Both miR-27a and knockdown of PLK 2 caused the increase of the cell viability and colony formation and inhibition of the late apoptosis in the Hep2 cell lines. (
  • Moreover, miR-27a but not PLK2 also repressed the early apoptosis in the Hep2 cells. (
  • In this study, we demonstrated that miR-27a, a frequently up-regulated miRNA in LSCC, could induce cell proliferation and repress apoptosis in the Hep2 cells. (
  • If checkpoint control events are not completed correctly, cancer cells may commit suicide by a process of programmed cell death called apoptosis. (
  • Aberrant expression of circadian clock genes could have important consequences on the transactivation of downstream targets that control the cell cycle and on the ability of cells to undergo apoptosis. (
  • I have identified a meiotic checkpoint that responds to defects in homolog synapsis, independent of a DNA damage/recombination checkpoint, and activates apoptosis to avoid the generation of aneuploid gametes. (
  • Survivin expression has been described to be cell cycle-dependent and restricted to the G2-M checkpoint, where it inhibits apoptosis in proliferating cells. (
  • Phosphorylated E2F-1 can reside in discrete nuclear structures and induce apoptosis, suggesting a unique role for E2F-1 in DNA repair and checkpoint functions. (
  • Thus, this study was performed to elucidate whether mitochondria and caspase cascades are involved in the modulation of apoptosis and cell cycle arrest in curcumin-treated NPC-TW 076 human nasopharyngeal carcinoma cells. (
  • The effects of curcumin on cell cycle arrest and apoptosis were measured by flow cytometry, and caspase-3 activity, apoptosis-associated protein levels and its regulated molecules were studied by flow cytometric assay and immunoblots. (
  • Curcumin-induced apoptosis was accompanied with upregulation of the protein expression of Bax and downregulation of the protein levels of Bcl-2, resulting in dysfunction of mitochondria and subsequently led to cytochrome c release and sequential activation of caspase-9 and caspase-3 in NPC-TW 076 cells in a time-dependent manner. (
  • These findings revealed that mitochondria, AIF caspase-3-dependent pathways play a vital role in curcumin-induced G2/M phase arrest and apoptosis of NPC-TW 076 cells in vitro. (
  • Plays a role in terminally differentiated hair cells development of the cochlea and induces cells apoptosis. (
  • Regulates numerous cellular processes, such as cell cycle progression, apoptosis and transcription, as well as viral infection. (
  • Sayed M, Pelech S, Wong C, Marotta A, Salh B. Protein kinase CK2 is involved in G2 arrest and apoptosis following spindle damage in epithelial cells. (
  • Shin S, Lee Y, Kim W, Ko H, Choi H, Kim K. Caspase-2 primes cancer cells for TRAIL-mediated apoptosis by processing procaspase-8. (
  • The effects of KNTC1 on HCC cells proliferation, migration, apoptosis and tumor formation was analyzed by MTT assay, colony formation assay, wound-healing assay, transwell migration assay, annexin V assay in vitro and in nude mouse models in vivo. (
  • Lv‑shKNTC1 cells showed reduced proliferation ability, increased apoptosis and decreased migration ability. (
  • If there is extensive damage, it triggers programmed cell death, also known as apoptosis . (
  • Analysis of the cell cycle and apoptosis regulators revealed that C-1305 strongly elevated phosphorylation of CDK1 at the inhibitory sites (Thr 14 /Tyr 15 ) in HL-60 cells. (
  • Dysfunction of splicing factors often result in abnormal cell differentiation and apoptosis, especially in neural tissues. (
  • Curcumin can induce apoptosis in a variety of tumor cells and has also prevented tumor initiation and growth in experimental models. (
  • But it is not clear why curcumin selectively targets tumor cells, although it has been suggested that it affects signaling pathways that regulate cell growth and survival and thus preferably will induce apoptosis in highly proliferating cells. (
  • The telomere gene sequences at the ends of chromosomes solve this problem by 'taking the hit' - telomere gene loss of about 50 nucleotides and subsequent telomere shortening occur with every cell replication until the telomeres reach certain critical lengths that first result in senescence and finally result in the death of the cell (apoptosis). (
  • Effects of brevilin A on cell viability were determined by MTT assay, and cell cycle and apoptosis were detected by flow cytometry. (
  • The molecular mechanism of cell cycle regulation and apoptosis were investigated via Western blot. (
  • Brevilin A induced cell cycle arrest at G2/M and induced apoptosis. (
  • Cell cycle checkpoints are control mechanisms in the eukaryotic cell cycle which ensure its proper progression. (
  • Each checkpoint serves as a potential termination point along the cell cycle, during which the conditions of the cell are assessed, with progression through the various phases of the cell cycle occurring only when favorable conditions are met. (
  • Progression through these checkpoints is largely determined by the activation of cyclin-dependent kinases by regulatory protein subunits called cyclins, different forms of which are produced at each stage of the cell cycle to control the specific events that occur therein. (
  • As the eukaryotic cell cycle is a complex process, eukaryotes have evolved a network of regulatory proteins, known as the cell cycle control system, which monitors and dictates the progression of the cell through the cell cycle. (
  • Those complexes, in turn, activate different downstream targets to promote or prevent cell cycle progression. (
  • The three pocket proteins are Retinoblastoma (Rb), p107, and p130, which bind to the E2F transcription factors to prevent progression past the G1 checkpoint. (
  • We recently recognized a previously uncharacterized linkage between the replication stress response and the SCF ubiquitin-proteasome pathway (Kile and Koepp 2010) a system that is better known for its part in protein turnover during cell-cycle progression (Ang and Harper 2005). (
  • Introduction The ability to rapidly delay cell cycle progression in response to environmental and genotoxic insults, is essential for the maintenance of genomic integrity and/or cell viability. (
  • In this study, we have investigated the effect of caffeine on Cdc25 stability, cell cycle progression and DNA damage/replication DMA checkpoint activation in cells (Fig. (
  • A signaling process that contributes to a meiotic cell cycle checkpoint that ensures accurate chromosome replication and segregation by preventing progression through a meiotic cell cycle until conditions are suitable for the cell to proceed to the next stage. (
  • In proliferating cells, MOF directly binds and maintains the expression of genes required for cell cycle progression. (
  • DNA damage checkpoints are responsible for keeping the fidelity of genetic info by arresting cell cycle progression and facilitating DNA repair pathways. (
  • They are serine threonine kinases that sense DNA damage and phosphorylate quite a few proteins that regulate cell cycle progression and DNA repair pathways [2]. (
  • Checkpoint controls delay cell cycle progression in response to conditions that, if uncorrected, generate genetic instability. (
  • DNA damage checkpoints are biochemical pathways that transiently block cell cycle progression while the DNA contains damage. (
  • A checkpoint is one of several points in the eukaryotic cell cycle at which the progression of a cell to the next stage in the cycle can be halted until conditions are favorable. (
  • 3) Inhibition of CDK 4 and 6 will prevent the phosphorylation of retinoblastoma protein, thereby blocking cell cycle progression from G1 to S phases. (
  • We demonstrated that a novel monoclonal antibody developed by our collaborators, sensitized tumors to therapy and inhibited tumor progression by promoting the retention of iron in the tumor cells. (
  • Blocks cell cycle progression by preventing spindle assembly checkpoint activation. (
  • Transduced p16INK4a peptides inhibit hypophosphorylation of the retinoblastoma protein and cell cycle progression prior to activation of Cdk2 complexes in late G1. (
  • It is concluded that cyclin D:Cdk4/6 activity is required for early G1 phase cell cycle progression up to, but not beyond, activation of cyclin E:C DK2 complexes at the restriction point and is thus nonredundant with cyclin Cdk2 in late G1. (
  • Inhibition of pRb phosphorylation and cell cycle progression by an antennapedia-p16(INK4A) fusion peptide in pancreatic cancer cells. (
  • Human ANAPC15 is a component of the anaphase promoting complex/cyclosome (APC/C), a cell cycle-regulated E3 ubiquitin ligase that controls progression through mitosis and the G1 phase of the cell cycle. (
  • The bifurcated spindle checkpoint blocks cell cycle progression at metaphase by monitoring unattached kinetochores and inhibits mitotic exit in response to the incorrect orientation of the mitotic spindle. (
  • CST has a diverse catalog of antibodies and assays to study cell cycle progression and checkpoint control. (
  • Orderly progression through the cell cycle is driven by the periodic oscillations in the activity of cyclin-dependent kinases (CDKs) [ 1 ]. (
  • Among the cyclins that play a crucial role in cell-cycle progression, is cyclin F. It is most similar to cyclin A, both in terms of amino acid sequence and the cyclic pattern of expression during the cell cycle [ 3 ]. (
  • In normal cells, a complex set of interacting proteins tightly regulates progression through the phases of the cell cycle. (
  • This cancer-like progression is exclusively driven by a population of parasite stem cells (germinative cells) that have to be eliminated for an effective cure of the disease. (
  • Melanoma inhibitory activity (MIA), an extracellular protein highly expressed by malignant melanoma cells, plays an important functional role in melanoma development, progression, and metastasis. (
  • PPM1G regulates cell cycle progression. (
  • Aneuploidy has catastrophic effects on cells and organisms, and plays a key role in the surprisingly high frequency of human birth defects, and in cancer initiation and progression. (
  • RNA interference in tissue culture cells, live analysis of chromosome segregation after antibody injection into early embryos, and observations of flies with CENP-A null mutations demonstrated that CENP-A is required for all chromosome movements during mitosis and for normal cell cycle progression. (
  • In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. (
  • Over a quarter of all DUBs, representing four different families, have been shown to play roles either in the unidirectional progression of the cell cycle through specific checkpoints, or in the DNA damage response and repair pathways. (
  • identified that targeted knockdown of kinetochore protein D40 can prevent neoplasm cell progression[15]. (
  • Reactivated after successful DNA repair through WIP1-dependent signaling leading to CDC25A/B/C-mediated dephosphorylation and restoring cell cycle progression. (
  • Non-small cell lung cancer (NSCLC): Participants whose tumors have a known sensitizing epidermal growth factor receptor (EGFR) mutation must also have experienced disease progression (during or after treatment) or have an intolerance to treatment with an EGFR tyrosine kinase inhibitor(s). (
  • Spindle Assembly Checkpoint (at the end of Metaphase, before entering Anaphase). (
  • In response to DNA damage, the protein kinase Chk1 is phosphorylated and inhibits mitotic entry by phosphorylating Wee1 and Cdc25 to prevent activation of Cdc2 [11].The spindle assembly checkpoint blocks chromosome segregation until all the chromosomes are attached for the mitotic spindle. (
  • The activation of Mad2, a spindle assembly checkpoint protein prevents the association of APC with Slp1/Cdc20 and blocks the cells during metaphase until all of the chromosomes are adequately attached towards the mitotic spindle [12]. (
  • Failure of the spindle assembly checkpoint machinery may rapidly result in aneuploidy that is frequently observed in many types of human cancer cells. (
  • SAC, spindle assembly checkpoint. (
  • When the spindle assembly checkpoint (SAC) cannot be satisfied, cells exit mitosis via mitotic slippage. (
  • DNA topoisomerase 2 α (TOP2A), cell division cycle protein homolog 20 (CDC20), mitotic checkpoint serine/threonine protein kinase BUB1 (BUB1) and mitotic spindle assembly checkpoint protein MAD2A (MAD2L1) exhibited the highest degree of interaction in the PPI network. (
  • The results indicated that DNA topoisomerase 2α (TOP2A), cell division cycle protein 20 homolog (CDC20), mitotic checkpoint serine/threonine kinase BUB1 (BUB1) and mitotic spindle assembly checkpoint MAD2A (MAD2L1) may be potential biomarkers and therapeutic targets in lung adenocarcinomas. (
  • it is not required for APC/C activity itself, but promotes the turnover of CDC20 and MCC on the APC/C, thereby participating to the responsiveness of the spindle assembly checkpoint. (
  • Perturbation of Spc25 expression affects meiotic spindle organization, chromosome alignment and spindle assembly checkpoint in mouse oocytes. (
  • We have also demonstrated that failure to form a kinetochore, due to depletion of CENP-A, results in the activation of a cell cycle checkpoint early in mitosis, prior to the time of a previously identified checkpoint known as the Spindle Assembly Checkpoint (SAC). (
  • During mitosis, functions as a component of the p53/TP53-dependent spindle assembly checkpoint (SAC) that maintains cyclin-B-CDK1 activity and G2 arrest in response to spindle damage. (
  • The eukaryotic spindle assembly checkpoint (SAC) monitors microtubule attachment to kinetochores and prevents anaphase onset until all kinetochores are aligned on the metaphase plate. (
  • The spindle assembly checkpoint (SAC) is critical for preventing the onset of anaphase until all chromosomes are aligned on the metaphase plate. (
  • The mitotic checkpoint, or spindle assembly checkpoint (SAC), is the major cell-cycle control mechanism that delays the onset of anaphase during mitosis. (
  • and the M (mitosis) phase, during which the duplicated chromosomes (known as the sister chromatids) separate into two daughter nuclei, and the cell divides into two daughter cells, each with a full copy of DNA. (
  • During the normal cell cycle, Cdc25 localizes predominantly in the nucleus from late G2 until the onset of mitosis. (
  • 2008)]. These pathways affect processes-alterations of cell cycle length, spindle positioning or DNA repair efficiency-that affect neurogenesis and, in particular, the cell cycle phases of mitosis (Supplementary Table 1). (
  • In M phase, the chromosomes need to be properly aligned and the spindles need to be oriented towards the daughter cell (M-metaphase checkpoint), and the cell should be correctly divided into two, before the end of mitosis (M-telophase checkpoint). (
  • To determine if MTs accelerate slippage, we followed mitosis in human RPE-1 cells exposed to various spindle poisons. (
  • The duration of mitosis in Eg5 inhibitors, which induce monopolar spindles without disrupting MT dynamics, was the same as in cells lacking MTs. (
  • Finally, compared with cells lacking MTs, exit from mitosis is accelerated over a range of spindle poison concentrations that allow MT assembly because the SAC becomes satisfied on abnormal spindles and not because slippage is accelerated. (
  • As for most checkpoints, satisfaction of the SAC is not required for exiting mitosis: normal (and many cancer) cells that enter mitosis in spindle poisons ultimately exit mitosis and enter the next G1 as tetraploid cells ( Rieder and Maiato, 2004 ). (
  • Other lesions induce potentially harmful mutations in the cell's genome, which affect the survival of its daughter cells after it undergoes mitosis . (
  • passage through the G2 checkpoint triggers the separation of chromatids during mitosis. (
  • During mitosis, genomic integrity is maintained by the proper coordination of mitotic events through the spindle checkpoint. (
  • The G 2 -specific genes include MEC3 (for mitosis entry checkpoint), RAD9, RAD17, and RAD24. (
  • We conclude that the checkpoint in budding yeast consists of overlapping S-phase and G 2 -phase pathways that respond to incomplete DNA replication and/or DNA damage and cause arrest of cells before mitosis. (
  • Weinert, TA, Kiser, GL & Hartwell, L 1994, ' Mitotic checkpoint genes in budding yeast and the dependence of mitosis on DNA replication and repair ', Genes and Development , vol. 8, no. 6, pp. 652-665. (
  • In the budding yeast Saccharomyces cerevisiae, a cell cycle checkpoint coordinates mitosis with bud formation. (
  • We herein describe the characterization of EmPlk1, encoded by the gene emplk1 , which displays significant homologies to members of the Plk1 sub-family of Polo-like kinases that regulate mitosis in eukaryotic cells. (
  • Correct execution of cell division requires duplication of all genetic material during S-phase followed by its precise partitioning between two daughter cells during mitosis. (
  • Our group described the role of non-proteolytic ubiquitin signaling in the regulation of essential kinases during mitosis of human cells. (
  • Using our expertise in cell biology, we aim at discovering novel essential pathways that regulate equal partitioning of genetic material and cellular organelles during mitosis and re-assembly of nuclear pore complexes after successful completion of cell division. (
  • When activated, the encoded protein is known to inhibit CDC25C phosphatase, preventing entry into mitosis, and has been shown to stabilize the tumor suppressor protein p53, leading to cell cycle arrest in G1. (
  • In addition to furthering our understanding of developmental biology in fruit flies, this discovery is highly relevant to cancer research, where Myt1 is being scrutinized for its role in 'checkpoint' mechanisms that govern entry into mitosis," said Shelagh Campbell, professor emerita in the Faculty of Science and member of the research team. (
  • Kinetochore associated 1 (KNTC1) encodes a kinetochore component in Rod-Zwilch-ZW10 (RZZ) complex which is essential for the segregation of sister chromatids during mitosis and participates in the spindle checkpoint. (
  • It was reported that KNTC2 was essential to maintain the normal process of cell mitosis [10] and was up-regulated in many tumor tissues, such as HCC, colon cancer, gastric cancer and pancreatic cancer[11-14]. (
  • Following interphase, the cell enters mitosis or meiosis, which leads to cell division (cytokinesis) and the beginning of a new cell cycle in each of the daughter cells. (
  • The cell cycle is a 4-stage process consisting of Gap 1 (G1), Synthesis, Gap 2 (G2) and mitosis. (
  • In this part of interphase, the cell synthesizes mRNA and proteins in preparation for subsequent steps leading to mitosis. (
  • G1 is an intermediate phase occupying the time between the end of cell division in mitosis and the beginning of DNA replication during S phase. (
  • G2 phase, Gap 2 phase, or Growth 2 phase, is the third subphase of interphase in the cell cycle directly preceding mitosis. (
  • G2 phase is a period of rapid cell growth and protein synthesis during which the cell prepares itself for mitosis. (
  • This last stage is all about prepping the cell for mitosis or meiosis. (
  • G2 phase is where the cell grows again, and prepares for mitosis. (
  • Definition - The phase of the cell cycle that includes mitosis and cytokinesis. (
  • Required in higher cells for entry into S-phase and mitosis. (
  • There are 3 different types of cell divisions seen both in eukaryotes and prokaryotes which are: amitosis, mitosis, and meiosis. (
  • As suggested in previous studies, AgNPs could either directly interact with DNA via oxidative damage [ 11 ] and interfere in the interphase at the DNA level and mitosis at the chromosomal level, or interact with the nucleoprotein and mitotic spindle apparatus to disturb cell cycle checkpoints [ 12 ]. (
  • In these cell cycle checkpoints result in inappropriate proliferation. (
  • Calcitriol inhibited proliferation of anaplastic thyroid carcinoma cells with a more pronounced effect on doxorubicin-resistant HTh74R cells, and it significantly reduced the capacity to form stem cell-derived spheres and decreased the size of these spheres that consist of CSCs and their progenitor cells. (
  • 2017. Divergent roles of p120-catenin isoforms linked to altered cell viability, proliferation, and invasiveness in carcinogen-induced rat skin tumors. . (
  • Nibrin's role in regulating cell division and cell growth (proliferation) is thought to lead to the problems with the immune system that are seen in affected individuals. (
  • A lack of functional nibrin results in less immune cell proliferation. (
  • The aim of this study was to determine the global transcriptome profile of three passages of dermal autologous fibroblasts from a male volunteer, focusing on the processes of the cell cycle and cell proliferation status to estimate the optimal passage of the tested cells with respect to their reimplantation. (
  • Detailed microarray analysis of the fibroblast genes indicated that the cell population of the third passage exhibited the highest number of upregulated genes involved in the cell cycle and cell proliferation. (
  • It is found among several proteins that bind directly to retinoblastoma protein, which regulates cell proliferation. (
  • Activation of cyclin-dependent kinase 4 (CDK4) and cyclin-dependent kinase 6 (CDK6) have been implicated in cell proliferation and resistance to therapy. (
  • FCP displayed concentration-dependent inhibition on A549 cells proliferation. (
  • Differentially inhibits human colon carcinoma cell proliferation. (
  • DDR genes are among the most commonly mutated genes in human cancer and it is believed that these lesions promote a „mutator-phenotype" that fuels the runaway proliferation of cancer cells. (
  • The regulation of cell cycle and proliferation has been extensively studied in the last few years and a consensus paradigm of cell cycle regulation has been developed [1,2]. (
  • Li Y, Liu D, Zhou Y, Li Y, Xie J, Lee RJ, Cai Y, Teng L. Silencing of Survivin Expression Leads to Reduced Proliferation and Cell Cycle Arrest in Cancer Cells. (
  • Cell proliferation was measured by MTT assay. (
  • Our data showed that the novel survivin-targeted siRNA could efficiently knockdown the expression of survivin and inhibit cell proliferation. (
  • However, these fractions did not inhibit the proliferation of lung (A549) and liver (HepG2) cancer cells. (
  • I need help or guide on cell proliferation assays. (
  • The aim of the present study was to investigate the impact of RV on MMC-mediated inhibition of colorectal cancer cell proliferation and to assess the potential mechanisms for such effects. (
  • Materials and Methods: Primary cell lines generated from resected colorectal tumor specimens were treated with RV, MMC or RV+MMC and cell proliferation and gene expression analyses were performed. (
  • Results: Suppression of cell proliferation by RV+MMC was significantly greater than individual treatments. (
  • The current study was designed to assess the capacity of a widely used natural product, resveratrol (RV), to increase the effectiveness of a chemotherapy agent, mitomycin C (MMC), in inhibiting the proliferation of human colorectal cancer cells. (
  • Dose-dependent inhibition of proliferation index Ki-67, cell cycle, and stem-cell-related markers were observed. (
  • The clinical efficacy of BRAFi and MEKi therapy is believed to rely on a functional retinoblastoma (RB) axis to inhibit cell proliferation. (
  • Disruptions to the cell cycle that governs proliferation are a root cause of many diseases, most notably cancer. (
  • Furthermore, low concentrations of BI 2536 eliminated the germinative cell population from mature metacestode vesicles in vitro , yielding parasite tissue that was no longer capable of proliferation. (
  • Since germinative cells are decisive for parasite proliferation and metastasis formation within the host, BI 2536 and related compounds are very promising compounds to complement benzimidazoles in AE chemotherapy. (
  • We herein describe a novel, druggable parasite enzyme, EmPlk1, that specifically regulates germinative cell proliferation. (
  • Bs6 is a potent inhibitor of the Kv1.3 channel which plays an important role during the activation and proliferation of memory T-cells (TEM), which play an important role in autoimmune diseases. (
  • However, ubiquitylation of substrate proteins can also result in non-proteolytic events and plays important functions in many biological processes including cell proliferation. (
  • The majority of the downregulated genes play a role in cell cycle and proliferation. (
  • While it is recognized that the Wnt/ß-catenin pathway orchestrates hepatocyte proliferation in both homeostasis and injury, little is known about the importance of β-catenin in biliary epithelial cell (BEC) plasticity. (
  • Cell proliferation, radiosensitivity, tamoxifen cytotoxicity, cell cycle analysis, and DNA damage response were evaluated using live cell imaging, clonogenic survival assay and immunocytochemistry. (
  • Compared to the eukaryotic cell cycle, the prokaryotic cell cycle (known as binary fission) is relatively simple and quick: the chromosome replicates from the origin of replication, a new membrane is assembled, and the cell wall forms a septum which divides the cell into two. (
  • The cell cycle checkpoints play an important role in the control system by sensing defects that occur during essential processes such as DNA replication or chromosome segregation, and inducing a cell cycle arrest in response until the defects are repaired. (
  • Consistent with the data showing hyperactivation of Rad53 in cells DNA replication is definitely sluggish in cells in the presence of MMS (Blake 2006). (
  • In response to stalled replication, activates the replication or S-M checkpoint. (
  • The DNA damage checkpoint pathway enforces cell cycle arrest to allow timely repair in response to DNA damage and replication stress. (
  • In particular, such models violate the M phase checkpoint condition so that it allows a division of a budding yeast cell into two before the completion of its full DNA replication and synthesis. (
  • The replication of damaged DNA before cell division can lead to the incorporation of wrong bases opposite damaged ones. (
  • Both the initiation and inhibition of cell division are triggered by events external to the cell when it is about to begin the replication process. (
  • In this study we found that Rad53 protein variants in which alanine and/or aspartate replace the threonine residues 354 and/or 358 do not retain kinase activity and do not undergo auto-phosphorylation, leading to defect in the checkpoint response and iper-sensitivity to DNA damage and DNA replication stress agents. (
  • We further found that the protein level of Sml1, which is the physiological inhibitor of ribonucleotide reductase, remains high during DNA replication in rad53-T358D cells, suggesting that an inadequate pool of dNTPs in checkpoint defective cells causes the accumulation of spontaneous DNA breaks. (
  • This process includes mechanisms to ensure errors are corrected while cell replication occurs, and if the correction cannot be performed, cells enter into the apoptotic process ( 15 ). (
  • When something goes awry during the cell cycle - for example, if DNA gets broken during replication - checkpoint mechanisms put the cycle on pause so that the cell can repair the damage before dividing. (
  • The cell-cycle roles of the RAD and MEC genes were examined by combination of rad and mec mutant alleles with 10 cdc mutant alleles that arrest in different stages of the cell cycle at the restrictive temperature and by the response of rad and mec mutant alleles to DNA damaging agents and to hydroxyurea, a drug that inhibits DNA replication. (
  • Claspin would then continue to associate with replication fork machinery where it can serve as a checkpoint sensor protein. (
  • We have previously elucidated how chromatin regulation affects transcription, DNA replication, S phase checkpoint and recombination using budding yeast as a model organism. (
  • However, replication of the native RPE phenotype becomes more difficult because these cells lose their specialized phenotype after multiple passages. (
  • These results suggested that, the up-regulated p21 and down-regulated CyclinD1 , CyclinE , CDK6 and CDK2 genes, which can induce the arrest of cell cycle G1 and thus provide sufficient time for DNA repair and ensure the accuracy of DNA replication, contribute to the long-time adaptation of M. baileyi to hypoxic environments. (
  • Acts as component of the MCM2-7 complex (MCM complex) which is the putative replicative helicase essential for 'once per cell cycle' DNA replication initiation and elongation in eukaryotic cells. (
  • If the checkpoint mechanisms detect problems with the DNA, the cell cycle is halted, and the cell attempts to either complete DNA replication or repair the damaged DNA. (
  • To enable this mitotic role, centrosomes undergo a complex replication cycle that is intimately linked to the cell division cycle. (
  • Here, we also catalogue and discuss DUBs that have been linked to centrosome replication or function, including centrosome clustering, a mitotic survival strategy unique to cancer cells with supernumerary centrosomes. (
  • Which phase of the cell cycle does replication take place? (
  • During this time, the cell grows in preparation for DNA replication, and certain intracellular components, such as the centrosomes undergo replication. (
  • Inactivated by PKR/EIF2AK2- and WEE1-mediated phosphorylation upon DNA damage to stop cell cycle and genome replication at the G2 checkpoint thus facilitating DNA repair. (
  • They consist of repeats of a six nucleotide sequence and specialized telomere-binding proteins that form a stable T-loop structure, essentially capping the chromosome ends and protecting the genome from degradation during replication and the cell cycle. (
  • Thus, these terminal genes are vulnerable to deletion with each replication, threatening loss of codons with each cell cycle. (
  • The main mechanism of action of the cell cycle checkpoints is through the regulation of the activities of a family of protein kinases known as the cyclin-dependent kinases (CDKs), which bind to different classes of regulator proteins known as cyclins, with specific cyclin-CDK complexes being formed and activated at different phases of the cell cycle. (
  • The E2F gene family is a group of transcription factors that target many genes that are important for control of the cell cycle, including cyclins, CDKs, checkpoint regulators, and DNA repair proteins. (
  • WDR62, ASPM and STIL are spindle pole proteins, suggesting that focused spindle poles are of great significance in neural progenitor cell division. (
  • Many research have identified a network of proteins which are involved throughout the DNA damage checkpoints response. (
  • Initially, exosomes were proposed to eliminate cellular waste, but it has been proven that they also play a key role in the intercellular communication between adjacent as well as distal cells through the horizontal transfer of lipids, proteins and nucleic acids. (
  • The goal of our research is to purify the human checkpoint proteins, characterize these proteins biochemically, and reconstitute the DNA damage checkpoint in vitro. (
  • Growth factor proteins arriving at the dividing cell's plasma membrane can trigger the cell to begin dividing. (
  • negative regulator molecules, such as tumor suppressor proteins, monitor cellular conditions and can halt the cycle until specific requirements are met. (
  • Regulation of cell cycle control and other cellular pathways by 14-3-3 proteins. (
  • In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. (
  • Migration through constrictions can clearly rupture nuclei and mis-localize nuclear proteins but damage to DNA remains uncertain as does any effect on cell cycle. (
  • Moreover, TBBE and TBWE treated MCF-7, HeLa and U87 cells showed upregulation of p53 and p21 proteins. (
  • If stabilized, these proteins maintain the cells in the phase just before division (G2/M arrest) by binding to and repressing the genes essential for cell division to proceed. (
  • thus, it functions as a regulator of a wide variety of downstream proteins, including tumor suppressor proteins p53 and BRCA1, checkpoint kinase CHK2, checkpoint proteins RAD17 and RAD9, and DNA repair protein NBS1. (
  • Studying the dynamic nature and contribution of cytoskeletal and ECM proteins to cell structure and motility can provide insight into cell migration in the tumor microenvironment, metastasis, and neurodegeneration. (
  • Maintaining homeostasis requires cells to regulate the translation, stability and degradation of thousands of proteins simultaneously. (
  • Proteins involved in cell cycle control and checkpoint initiation (e.g. (
  • The identification and characterization of proteins that interact with factors required for PC function will provide insight into how this locus activates the checkpoint when unsynapsed. (
  • The ARPE-19 cells cultured for 4 months developed a phenotype characteristic of native RPE and expressed proteins, mRNAs, and miRNAs characteristic of the RPE. (
  • Cell division is regulated by a variety of proteins at all stages of cell cycle. (
  • Kinetochores possesses complex multi-subunit structure that consist of more than 100 different proteins in human cells[9], which is imperative in maintaining the normal division of cell sister chromatid and maintaining chromosomal stability. (
  • In higher eukaryotes, cytoplasmic dynein is involved in silencing the SAC by removing the checkpoint proteins Mad2 and the Rod-Zw10-Zwilch complex (RZZ) from aligned kinetochores (Howell, B.J., B.F. McEwen, J.C. Canman, D.B. Hoffman, E.M. Farrar, C.L. Rieder, and E.D. Salmon. (
  • Consequently, alterations of epigenetic regulators and histone marks are frequently observed in cancer and numerous compounds have been reported to be effective against cancer cells by inhibiting epigenetic proteins and reversing the effect of epigenetic modifications [ 7 , 8 ]. (
  • In proliferating cells, CDK1-mediated FOXO1 phosphorylation at the G2-M phase represses FOXO1 interaction with 14-3-3 proteins and thereby promotes FOXO1 nuclear accumulation and transcription factor activity, leading to cell death of postmitotic neurons. (
  • G1 is now termed as the first growth phase as it involves the synthesis of other components of the cell such as RNA (Ribose Nucleic Acid), membranes, and proteins which lead to the growth of cytoplasm and nucleus of the daughter cells to get their mature size. (
  • Proteins like kinases and cyclins are critical for the cell cycle. (
  • FIR20 cells displayed increased radioresistance and population doubling time, reduced accumulation of DNA damage response proteins following irradiation, and a core radioadaptive signature of significantly differentially expressed mRNAs (DEMs) and circRNAs (DECs). (
  • It's no secret that the regulation of cell cycle is an extremely accurate process and cell cannot afford to make any mistake. (
  • The three of them also shared The Nobel Prize in Physiology or Medicine in 2001 for their pioneering research and discovery in the regulation of cell cycle. (
  • Aziz Sancar, MD, PhD, is a UNC Lineberger Comprehensive Cancer Center member researching DNA repair, DNA damage checkpoints, and regulation of the biological clock. (
  • Errors in the regulation of the cell cycle can cause cancer, which is characterized by uncontrolled cell division. (
  • It is also associated with BRCA1 and is thought to modulate the functions of BRCA1 in transcriptional regulation, DNA repair, and/or cell cycle checkpoint control. (
  • Therefore, we focused on investigation of the impact of hMT-3 up-regulation in N-Myc amplifying neuroblastoma cells. (
  • Most functions in cells are performed by large protein complexes and the regulation of complex formation is critical to cell homeostasis. (
  • Conclusion: The up-regulation of p21 WAF1/CIP1 , which inhibits the cell cycle at G 0 /G 1 and G 2 /M phases, may represent the predominant mechanism for enhancement of MMC-mediated anti-cancer effects by resveratrol. (
  • Understanding the mechanisms that cause cell death is a critical aspect of cell biology, as many diseases involve aberrant regulation of cell death mechanisms. (
  • miR-27a acts as an oncogene in laryngeal squamous cell carcinoma through down-regulation of PLK2 and may provide a novel clue into the potential mechanism of LSCC oncogenesis or serve as a useful biomarker in diagnosis and therapy in laryngeal cancer. (
  • The circadian regulation extends beyond clock genes to involve various clock-controlled genes (CCGs) including various cell cycle genes. (
  • Cell signaling plays a key part in regulation of the immune system. (
  • Studies that address the regulation of heterochromatin on unsynapsed chromosomes and how the PC may inhibit the DNA damage checkpoint will also be undertaken. (
  • A similar benefit would be expected from exercise and diet because that too is a way of establishing healthy energy regulation not only for the whole body, but for tissues and cells in the brain' - See metformin at The Antiaging Store . (
  • A similar non-hierarchical pattern of hematopoiesis could be derived from analysis of published single-cell assay for transposase-accessible chromatin sequencing (scATAC-seq), consistent with a sequential relationship between chromatin dynamics and regulation of gene expression during lineage commitment (first, altered chromatin conformation, then mRNA transcription). (
  • Because the vast majority of work on chromatin regulation has been done during mitotic cell-cycle, we have little idea of how chromatin is regulated during the time cells spend most of their time. (
  • In the long run, these studies will allow us to compare and integrate the principles of chromatin regulation throughout the mitotic cell-cycle and quiescence, such that we can obtain the full picture of chromatin regulation. (
  • The biology, structure and regulation of DUBs have been extensively reviewed elsewhere, so here we focus specifically on roles of DUBs in regulating cell cycle processes in mammalian cells. (
  • However, gaps in the detailed mechanism and regulation of PCNA polyubiquitination still persist in human cells. (
  • Proteomic analysis showed that EZH2 inhibition induced down-regulation of cell cycle regulators in lymphoma cells. (
  • Drawing on their earlier research, the authors found that curcumin specifically binds to and crosslinks to a protein that is involved in cell-cycle regulation. (
  • Cell-cycle development is monitored by checkpoint pathways that pause the cell routine when tension arises to threaten the integrity from the genome. (
  • The checkpoint 2 gene (CHEK2) is an important transducer in DNA damage signaling pathways in response to injury, and therefore, CHEK2 variants may affect susceptibility to kidney disease.MethodsWe used tag-single-nucleotide polymorphisms (tag-SNPs) to evaluate the association of the CHEK2 with kidney function (estimated glomerular filtration rate, eGFR) in 1,549 African-American and 1,423 white Hypertension Genetic Epidemiology Network (HyperGEN) participants. (
  • Cells have thus evolved molecular signalling pathways that sense DNA damage or environmental stress and activate cell cycle checkpoints. (
  • To counteract DNA damage, cells employ genome maintenance pathways that are directed inward, relentlessly to scan and repair the genome. (
  • The DNA damage checkpoints, like other signal transduction pathways, have four components: damage sensors, mediators, signal transducers and effectors. (
  • The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (
  • The differentially up-regulated genes involved in biological pathways related to cellular senescence and cell cycle were identified using electrochemical microarray with consequent bioinformatic processing. (
  • The cell cycle is controlled by a complex series of signaling pathways by which a cell grows, replicates its DNA and divides ( 14 ). (
  • It is indicated that p21-mediated inhibition of cdk2 contributes to the cell cycle arrest imposed by p16 and is a potential point of cooperation between the p16/pRB and p14ARF/p53 tumor suppressor pathways. (
  • Previously, we derived two drug-resistant breast cancer sublines (tamoxifen- and fulvestrant-resistant cell lines) from the MCF7 breast cancer cell line and performed genome-wide mRNA and microRNA profiling to identify differential molecular pathways underlying acquired resistance to these important antiestrogens. (
  • This protein and the closely related kinase ATR are thought to be master controllers of cell cycle checkpoint signaling pathways that are required for cell response to DNA damage and for genome stability. (
  • Here, we describe a genetic strategy that identified four additional checkpoint genes that act in two pathways. (
  • Cells respond to a multitude of signals in the extracellular environment, often by activating intracellular signaling pathways that elicit changes in cell function or behavior. (
  • PPM1G is part of the PP2C family of Ser/Thr protein phosphatases which are known to be negative regulators of cell stress response pathways. (
  • Taken together, brevilin A regulated cell cycle, activated the caspase signaling pathway, and inhibited PI3K/AKT/mTOR and STAT3 signaling pathways in vitro, and exhibited similar efficacy to the common chemotherapeutic cisplatin in vivo, without its associated toxicity. (
  • We are studying which factors in the cell are responsible for recognizing damage in distinct stages of the cell cycle, and how they start the checkpoint pathway by activation of the kinase activity of Mec1/ATR, the initiating protein kinase in this signal transduction pathway. (
  • Chk1, an evolutionarily conserved protein kinase is an necessary element of your DNA harm checkpoint [80]. (
  • Aurora B kinase, the catalytic subunit of the chromosome passenger complex, both destabilizes kinetochore attachments that do not generate tension and simultaneously maintains the spindle checkpoint signal. (
  • that association of type 1 phosphatase (PP1(Dis2)) with both the N terminus of Spc7 and the nonmotor domains of the Klp5-Klp6 (kinesin-8) complex is necessary to counteract Aurora B kinase to efficiently silence the spindle checkpoint. (
  • Rad53 protein, the yeast orthologue of the human checkpoint kinase Chk2, presents two highly conserved phosphorylatable threonine residues (T354 and T358) in the activation domain, whose phosphorylation is critical to allow the activation of the kinase. (
  • Interestingly, we found that the rad53-T358D mutation severely affects the kinase activity and causes accumulation of the S129-phosphorylated isoform of histone H2A, even during an unperturbed cell cycle, thus indicating the accumulation of spontaneous DNA breaks. (
  • Characterization of the activation domain of the Rad53 checkpoint kinase / S. Fiorani, G. Mimun, L. Caleca, D. Piccini, A. Pellicioli. (
  • Immunoblotting demonstrated a dose‑dependent downregulation of cyclin B1, cyclin‑dependent kinase 1, cell division cycle 25c, pro‑caspases ‑3, ‑6, ‑8 and ‑9, and poly (adenosine diphosphate‑ribose) polymerase (PARP) in FCP‑treated A549 cells. (
  • Fascaplysin will prove to be a useful tool in studying the consequence of Cdk4 inhibition, especially in cells containing inactivated p16, and caused G1 arrest and prevented pRb phosphorylation at sites implicated as being specific for Cdk 4 kinase. (
  • Inducible degradation of checkpoint kinase 2 links to cisplatin-induced resistance in ovarian cancer cells. (
  • Polo-like kinase 2 (PLK2) displayed a close relationship with the p53 family in affecting the fate of cells. (
  • The inhibitor of cyclin-dependent kinase 4A ( INK4A ) gene encode the p16 protein, a critical cell cycle regulator that interacts with cyclin dependent kinase (CDK) 4, inhibiting its ability to phosphorylate and inactivate RB [ 12 , 13 ]. (
  • Perturbations that transiently depolarize the actin cytoskeleton cause delays in bud formation, and a 'morphogenesis checkpoint' detects the actin perturbation and imposes a G2 delay through inhibition of the cyclin-dependent kinase, Cdc28p. (
  • The tyrosine kinase Swe1p, homologous to wee1 in fission yeast, is required for the checkpoint-mediated G2 delay. (
  • Schubert A, Koziol U, Cailliau K, Vanderstraete M, Dissous C, Brehm K (2014) Targeting Echinococcus multilocularis Stem Cells by Inhibition of the Polo-Like Kinase EmPlk1. (
  • The study, published by University of Alberta biologists, identifies an inhibition mechanism of an enzyme called Myt1 kinase, which manages how stem cells develop and differentiate during organ development in fruit flies. (
  • The study, Myt1 kinase couples mitotic cell cycle exit with differentiation in Drosophila , was published in Cell Reports. (
  • The Mre11-Rad50-Nbs1 (MRN) ATPase-nuclease complex is a central player in the cellular response to DSBs and is implicated in the sensing and nucleolytic processing of DSBs, as well as in DSB signaling by activating the cell cycle checkpoint kinase ATM. (
  • Protein kinase CK2 inhibition is associated with the destabilization of HIF-1alpha in human cancer cells. (
  • The mitotic checkpoint monitors the proper assembly of the mitotic spindle and blocks the onset of anaphase unless all of the chromosomes are stably attached to a specialized region known as kinetochore (1) . (
  • DNA can be damaged by agents such as toxic chemicals or radiation, and breaks in DNA strands also occur naturally when chromosomes exchange genetic material in preparation for cell division. (
  • Mistakes in the duplication or distribution of the chromosomes lead to mutations that may be passed forward to every new cell produced from an abnormal cell. (
  • In eukaryotes a cell-cycle control termed a checkpoint causes arrest in the S or G 2 phases when chromosomes are incompletely replicated or damaged. (
  • abstract = "In eukaryotes a cell-cycle control termed a checkpoint causes arrest in the S or G2 phases when chromosomes are incompletely replicated or damaged. (
  • Indeed, the inhibition of the G2/M checkpoint led to a significant increment of normal and aberrant mitotic cells, including those showing tripolar spindles, metaphases with lagging chromosomes and massive chromosomes fragmentation. (
  • However, the most important role of the G 2 checkpoint is to ensure that all of the chromosomes have been replicated and that the replicated DNA is not damaged. (
  • How does UV light damage the DNA when the chromosomes are deep inside the cell? (
  • When UV light falls on the skin it has to go through the cell membrane and the nuclear membrane to reach the chromosomes. (
  • Mitotic defects could lead to excess chromosomes and chromosomal instability (CIN) which was found in most cancer cells[6]. (
  • Chromosomes are pulled to opposite ends of the cell. (
  • The presence of the SAC was initially inferred from observations that cells delay in metaphase when meiotic sex chromosomes fail to pair and align or after the spindle is perturbed by either microtubule poisons or microsurgery. (
  • Prometaphase: chromosomes attach to microtubules and chromosomes move to the equator of the cell. (
  • Metaphase: chromosomes are aligned along the center of the cell in a straight line. (
  • 3. Spindle checkpoint - ensures all chromosomes are attached to the spindle fibers. (
  • However, cell division involving amitosis causes an unequal distribution of chromosomes, or may even lead to abnormalities in reproduction and metabolism. (
  • It is known as a checkpoint protein, she said, because it blocks the onset of anaphase until all chromosomes make proper attachments to the spindle. (
  • Interestingly we found that the proteolysis of the F-box protein Dia2 is definitely regulated from the S-phase checkpoint. (
  • The budding yeast LST8 functions in the delivery of Gap1 protein, and possibly other amino acid permeases, from the Golgi for the cell surface [20]. (
  • Wnt is one protein that animal cells release to control how nearby cells grow and divide. (
  • The cell is stained to reveal DNA (blue), microtubules (red), and the C-terminal portion of the KIF2A protein (green) whi. (
  • Disruption of Microtubules with Nocodazol U2OS human osteosarcoma cells were transduced with 'Cellular Lights' Actin-RFP (Actin-red fluorescent protein) and Cellular Lights MAP4-GFP (MAP4-green fluore. (
  • Laboratorio 5: Reversible phosphorylation processes in cell cycle control: role of Cdc14 protein phosphatases. (
  • In addition, FCP induced caspase‑3 activation and subsequent PARP cleavage, and increased the B‑cell lymphoma (Bcl)‑2‑associated X protein/Bcl‑extra large ratio in A549 cells. (
  • Examination of Chk2 protein revealed a decreased expression of Chk2 protein in cisplatin-resistant ovarian cancer cell lines, suggesting that degradation or decreased expression of Chk2 is partially responsible for chemo-resistance. (
  • Increased levels of Gadd45a transcript and protein are seen after treatment of cells with ionizing radiation as well as many other agents and treatments that damage DNA. (
  • Myriad multicomponent protein complexes and protein phosphoforms, for example, can potentially arise in cell signaling systems and this complexity poses a challenge for other modeling techniques ( 16 , 17 ). (
  • One of the molecular mechanisms driving fidelity of cell division is ubiquitylation (or ubiquitination), which is a covalent, posttranslational modification of substrates by a small protein ubiquitin. (
  • The protein encoded by this gene is a cell cycle checkpoint regulator and putative tumor suppressor. (
  • As at the G 1 checkpoint, cell size and protein reserves are assessed. (
  • Mechanistically, the protein levels of PIK3CA, p-Akt, CCND1, CDK6 are all down-regulated in Lv-KNTC1 SK-HEP-1 cells. (
  • During the two G phases, cell growth, protein synthesis,and enzyme synthesis are occurring, while during the S phase DNA is replicated. (
  • â I would argue that this particular RNA-binding protein is really what makes tumor cells resistant to being killed by chemotherapy when p53 is not around,â explains the studyâ s senior author, Michael Yaffe. (
  • Researchers were able to show that the RNA-binding protein hnRNPA0 controls cell division at two checkpoints in the MK2 pathway. (
  • In lung cancer cells that lack p53, hnRNPA0 stabilizes the coding for a backup protein called Gadd45. (
  • For the other checkpoint, called G1/S, when p53 is missing, hnRNPA0 stabilizes the coding for a backup protein called p27. (
  • â A Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints to Drive Resistance of p53-Defective Tumors to Chemotherapy,â Cancer Cell October 22, 2015, doi:10.1016/j.ccell.2015.09.009. (
  • Furthermore, C-1305 increased phosphorylation of pRb protein and CDK2 at Thr 160 in HL- 60 cells, but not in MCF-7 cells. (
  • Using a high throughput RNA interference screen in Drosophila melanogaster S2 cells, we have identified a new protein (Spindly) that accumulates on unattached kinetochores and is required for silencing the SAC. (
  • In addition, they found that curcumin binds more resolutely to this specific protein when it is phosphorylated, a modification that is generally seen in rapidly proliferating cells, such as in tumors. (
  • 19 ]. Even with such a simple representation, they found that there exists a prominent dynamic gene expression trajectory satisfying the checkpoint conditions, and then it leads back to the G1 stationary state. (
  • Sequence alterations of mitotic checkpoint genes, hBUB1 and hBUBR1 , were examined, and their gene transcripts were quantified using on-line, real-time quantitative reverse transcription-PCR in surgically resected human colorectal cancers and their neighboring normal tissues. (
  • Studies in Eastern European populations reported that people with mutations in one copy of the NBN gene in each cell may be more likely to develop breast cancer, prostate cancer, ovarian cancer, an aggressive form of skin cancer (melanoma), or cancer of blood-forming cells (leukemia) than people who do not carry NBN mutations. (
  • Cells with a mutation in one copy of the NBN gene do not repair DNA as effectively as cells without these mutations. (
  • Daughter cells that inherit these wrong bases carry mutations from which the original DNA sequence is unrecoverable (except in the rare case of a back mutation , for example, through gene conversion ). (
  • 3 Laboratory of Molecular Genetics, Division of Gene Therapy and Hepatology, University of Navarra School of Medicine, Clínica Universitaria and CIMA, Centro de Investigación Biomédica en Red, Pamplona, Spain. (
  • Signal propagation from the cell membrane to a promoter can induce gene expression. (
  • have now examined how the activities of β-catenin and the cyclin D1 gene change in living human cells. (
  • These analyses were initially performed in a population of cells, and confirmed that β-catenin rapidly accumulates after a Wnt signal and that the cyclin D1 gene becomes activated. (
  • It is able to activate some of the p53 target genes, such as p21 (a cell cycle inhibitor) and PUMA (a proapoptosis gene), which regulate cell survival. (
  • By integrating miRNA-related network, gene/miRNA expression and text-mining, the current study provides a computational-based systems biology approach for further investigating the molecular mechanism underlying antiestrogen resistance in breast cancer cells. (
  • Can I assume that it is easier to do targeted gene knock-in in rapidly dividing cells because they should have a short period of G1? (
  • Cellular deconvolution of gene expression profiles was able to discriminate cellular subtypes, highlighting the contribution of plasma cells and NK cells in the course of the disease. (
  • Furthermore, the checkpoint requires the C. elegans homolog of PCH-2, a budding yeast pachytene checkpoint gene, suggesting that the molecular mechanism that detects synaptic failure is widely conserved. (
  • Integration of long noncoding RNA (lncRNA) expression from the same cells demonstrated mRNA transcriptome, lncRNA, and the epigenome were highly homologous in their pattern of gene activation and suppression during hematopoietic cell differentiation. (
  • Particular topics will include cell cycle and checkpoint control, recombination and mating type switching in lower eukaryotes, gene mapping and cloning disease genes in higher eukaryotes and the production of transgenic plants and animals. (
  • In collaboration with the High Throughput Cell-based Screening facility at the IGBMC, we have performed a visual, high-throughput siRNA screen using customized, human 'Ubiquitin Decoders' library and developed multi-parametric control-based gene selection protocols. (
  • Gene Ontology analysis showed that the upregulated genes were associated with visual cycle, phagocytosis, pigment synthesis, cell differentiation, and RPE-related transcription factors. (
  • 2) Compared to low altitude of 2 260 m, the expression level of p21 (cell cycle G1-related gene) in M. baileyi liver tissues under high altitude of 3 300 m was significant increased, while its downstream genes CyclinD1 , CyclinE , CDK6 and CDK2 were significant decreased. (
  • The Cell Cycle Checkpoint Gene, RAD17 rs1045051, Is Associated with Prostate Cancer Risk. (
  • ARCHS4 provides access to gene-function predictions based on RNA-seq co-expression, and gene expression levels across cell and tissues. (
  • P53 is a gene product which takes care of fixing cell damage. (
  • It acts as a backup when a gene called p53, which normally helps healthy cells prevent mutations, is missing. (
  • Differential gene expression and correlation network analyses revealed that EZH2 is the most significantly over-expressed ERG in cancer and is co-regulated with a cell cycle network. (
  • Furthermore, FIR20 cell transcriptome overlapped significantly with canonical radiation response signatures and basal-like breast cancer subtype and exhibited remarkable commonality with endocrine therapy resistance gene signatures. (
  • Predictive and functional enrichment analysis revealed a circRNA-governed, gene-regulatory network that promotes stemness and inflammatory signaling in FIR20 cells. (
  • 10-hour timelapse of the double mutant Clb2dbΔ, Clb5Δ, which has the destruction box region of the CLB2 gene, on the cell cycle control system in budding yeast. (
  • Depletion of Lst8 in budding yeast cells outcomes within a speedy arrest of cell growth [19,20]. (
  • Upon nutrient starvation, the wat1 mutant cells fail to arrest inside the G1 phase and hence are sterile in fission yeast [21,23]. (
  • 2009. E2F4 and ribonucleotide reductase mediate S-phase arrest in colon cancer cells treated with chlorophyllin. . (
  • Fragkos M, Jurvansuu J, Beard P (2009) H2AX is required for cell cycle arrest via the p53/p21 pathway. (
  • EZH2 silencing with RNA interference induces G2/M arrest in human lung cancer cells in vitro. (
  • Previously, we showed in budding yeast that RAD9 and RAD17 are checkpoint genes required for arrest in the G 2 phase after DNA damage. (
  • cdc13 mutants arrested in G 2 and survived at the restrictive temperature, whereas all cdc13 checkpoint double mutants failed to arrest in G 2 and died rapidly at the restrictive temperature. (
  • We conclude that BI 2536 effectively inactivates E. multilocularis germinative cells in parasite larvae in vitro by direct inhibition of EmPlk1, thus inducing mitotic arrest and germinative cell killing. (
  • Hypoxia induces arrest of cell cycles G1 and G2. (
  • After the depletion of Spindly, dynein cannot target to kinetochores, and, as a result, cells arrest in metaphase with high levels of kinetochore-bound Mad2 and RZZ. (
  • Because the APC/C not only ensures that the cell cycle will be halted during spindle disruption but also promotes cell death in response to prolonged mitotic arrest, the authors note, it has become an attractive drug target for cancer therapy. (
  • The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4-20 µg mL −1 [email protected] NR were investigated by comet assay, γ-H2AX assay and micronucleus test. (
  • Our results demonstrated that both Ag + and [email protected] NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells and that the [email protected] NR retained in the nucleus may further release Ag + , aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. (
  • Identification of hub genes and their correlation with infiltration of immune cells in MYCN positive neuroblastoma based on WGCNA and LASSO algorithm. (
  • The phytochemical 3,3'-diindolylmethane decreases expression of AR-controlled DNA damage repair genes through repressive chromatin modifications and is associated with DNA damage in prostate cancer cells. (
  • One of these genes, called cyclin D1 , controls cell division. (
  • The p53 tumor suppressor is a mammalian transcription factor which controls the genes that stop the cell cycle, repair DNA, and even trigger cell death in response to DNA damage ( Kastenhuber and Lowe, 2017 ). (
  • Many cell cycle and DNA repair genes are conserved between vertebrates and plants, yet a p53 ortholog has never been found in any plant genome sequence. (
  • iii ) genes that trigger a cell death program (for when damage is too severe). (
  • A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition. (
  • Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. (
  • For cells, cell lines and tissues in culture till half confluency.Isotype or positive controls by peptides, antibodies and deactivated samples.Guinea pig ELISA kits for plasma and sera samples are used to study human genes through the guinea pig model (Cavia porcellus), also called the cavy rodent model. (
  • At higher levels, Eya1 and Six1 expand the expression of SoxB1 genes (Sox2, Sox3), maintain cells in a proliferative state and block expression of neuronal determination and differentiation genes. (
  • It turned out that the same genes we found in yeast were found in human cells," Hartwell said. (
  • Beginning with nothing much more sophisticated than dishes of yeast cultures, a microscope and toothpicks for sorting, he identified a collection of mutated genes that inhibited different stages of cell division. (
  • Hartwell went on to identify more than 100 genes involved in the cell cycle. (
  • Cells clustered into six distinct groups, which could be assigned to known HSPC subpopulations based on lineage specific genes. (
  • RPE-expressed genes, including RPE65 , RDH5 , and RDH10 , as well as miR-204/211, were greatly increased in the ARPE-19 cells maintained at confluence for 4 months. (
  • The RNA-Seq analysis provided a comprehensive view of the relative abundance and differential expression of the genes in the differentiated ARPE-19 cells. (
  • The results of this study demonstrate that low-passage ARPE-19 cells can express genes specific to native human RPE cells when appropriately cultured and differentiated. (
  • Conclusions The apparent dysregulation of H3K9 trimethylation and KDM4C-associated genes in lymphoblastoid cells supports the hypothesis that the KDM4C variant is causative of the multi-cancer susceptibility in the family. (
  • Evolution and Expression of Liver Cell Cycle-Related Genes in Myospalax baileyi [J]. Sichuan Journal of Zoology, 2020, 39(1): 1-14. (
  • Moreover, no significant differences of the expression levels of cell cycle G2-related genes such as Gadd45α , B99 , 14-3-3-δ and CyclinB1 were detected in M. baileyi and R. norvegicus under different altitudes. (
  • Compared to R. norvegicus , the expression levels of all the tested cell cycle-related genes were significantly higher in M. baileyi . (
  • and the metaphase-to-anaphase transition, also known as the spindle checkpoint. (
  • The spindle checkpoint is the prime cell-cycle control mechanism that ensures sister chromatids are bioriented before anaphase takes place. (
  • Aneuploidy, an abnormal chromosome set, can ensue from failure of the spindle checkpoint, the safeguard mechanism that halts anaphase onset until mitotic spindle assembly. (
  • Oxidant challenge of checkpoint-arrested cells led to proteolysis of the anaphase inhibitor securin and mitotic cyclins. (
  • The centromere (CEN) is the chromosomal site associated with kinetochore formation, which is the structure responsible for microtubule attachment to the chromosome, and constitutes an essential component of prometaphase congression, mitotic checkpoint control, anaphase poleward segregation, and cytokinesis. (
  • Because the separation of the sister chromatids during anaphase is an irreversible step, the cycle will not proceed until the kinetochores of each pair of sister chromatids are firmly anchored to at least two spindle fibers arising from opposite poles of the cell. (
  • A single misaligned kinetochore is sufficient to generate a wait anaphase signal, thereby ensuring that all sister chromatids segregate to opposite ends of the spindle and are equally distributed to the daughter cells. (
  • Furthermore, a direct inhibition of Rad3-induced phosphorylation of Cds1 or Chk1 in cells exposed to genotoxins has not been demonstrated (Moser (Calvo (Moser deletion on Cdc25 stability in has not been previously reported. (
  • 4) Additionally, these drugs lead to increased T-cell activation by enhancing checkpoint inhibition. (
  • Here, myosin-II inhibition rescues rupture and partially rescues the DNA damage marker γH2AX, but an apparent delay in cell cycle is unaffected. (
  • Mijn scriptie « Nanobody-mediated imaging and inhibition of the immune checkpoint ligand PD-L1 » leert dat het gebruik van nanobodies, gericht tegen het inhibitorisch signaal PD-L1, veelbelovend is voor de diagnose en behandeling van kankerpatiënten. (
  • Bioassay-guided fractionation of the extract yielded the known alkaloids didemnimides A (1) and D (2), the new alkaloid didemnimide E (3), and a new G2 checkpoint inhibitor. (
  • The synthesis revealed that the correct structure for the naturally occurring G2 checkpoint inhibitor is isogranulatimide (5). (
  • Granulatimide (4), the other candidate structure, was also found to be a G2 checkpoint inhibitor, and it was subsequently detected in chromatographic fractions associated with purification of D. granulatum alkaloids. (
  • This greater understanding of Myt1 in fruit flies can be expected to benefit the development of effective cancer therapies with checkpoint inhibitor drugs. (
  • Cyclins and cyclin-dependent kinases (Cdks) are internal molecular signals that regulate cell transitions through the various checkpoints. (
  • Role of cell cycle control and cyclin-dependent kinases in breast cancer. (
  • The cell cycle in mammalian cells is regulated by a series of cyclins and cyclin-dependent kinases (CDKs). (
  • Specific isoforms of cyclin-dependent kinases (CDKs) and polo-like kinases (PLKs), are some of the key regulators of cell cycle checkpoints. (
  • Our current work on excision repair aims to understand the structural and kinetic factors that enable the human excision nuclease to remove virtually infinite types of base lesions and to define the interconnections between DNA excision repair, the DNA damage checkpoints, and the circadian clock. (
  • The SAC effector is the mitotic checkpoint complex (MCC), which binds and inhibits the APC/C. It is incompletely understood how the APC/C switches substrate specificity in a cell cycle-specific manner. (
  • 3,3'-Diindolylmethane, but not indole-3-carbinol, inhibits histone deacetylase activity in prostate cancer cells. (
  • Moreover, overexpression of ANAC044 only inhibits the cell cycle if the DNA is damaged. (
  • We show that 4,4′-biphenol (5) selectively inhibits Rheb signaling and induces cell death suggesting that this compound might be a novel candidate for treatment of tuberous sclerosis-mediated tumor growth. (
  • In plant cells, the kinases ATM and ATR are activated by different types of DNA damage. (
  • Moreover, we show that ubiquitination of PCNA is not regulated by cell cycle checkpoint kinases ATM-Chk2 or ATR-Chk1. (
  • One possibility is that PCNA ubiquitination is regulated by cell cycle checkpoint kinases ATR-Chk1 or ATM-Chk2 given their central role in damage surveillance [ 8 - 11 ]. (
  • Since cell cycle checkpoint kinases are predominantly activated after DNA damage we also sought to determine whether PCNA ubiquitination is regulated by global sensors such as ATR or ATM. (
  • To examine signal transmission through sub-cellular compartments and its effect on transcription levels in individual cells within a population, we used the Wnt/β-catenin signaling pathway as a model system. (
  • this binding then triggers a signaling pathway in the receiving cell that passes information from the surface of the cell to its interior. (
  • Furthermore, a better understanding of Wnt signaling may in future help efforts to develop new drugs that can target the altered pathway in cancer cells. (
  • The 14-3-3 family participates in almost every signaling pathway present in mammalian cells which is why we think of them as the answer to the ultimate question of the life, the universe and everything. (
  • Linking the p53 tumor suppressor pathway to somatic cell reprogramming. (
  • In conclusion, we found that the ATR-CHK1 pathway is involved in the response to Dox-induced DNA damages and we demonstrated that our new in vitro drug schedule that combines Dox followed by ATR/CHK1 inhibitors can increase Dox cytotoxicity against ALL cells, while using lower drug doses. (
  • Because cells deficient in Gadd45a were shown to have a partial defect in the global genomic repair component of the nucleotide excision repair pathway of UV-induced photoproducts, dimethylbenzanthracene (DMBA) carcinogenesis was investigated because this agent produces bulky adducts in DNA that are also repaired by nucleotide excision repair. (
  • Using ductal organoids to model BECs transitioning into hepatocytes, we found that activation of the Wnt/ß-catenin pathway in these cells promoted partial escape from a biliary fate and triggered the acquisition of progenitor cell features. (
  • Therefore, KNTC1 may affect the biological activity of HCC cells through PI3K/Akt signaling pathway. (
  • In the present study we tested the hypothesis that the functional status of p53 in tumour cells might have an impact on the efficiency of C-1305 in experiments with both p53-deficient human HL-60 promyelocytic leukemia cells and human MCF-7 breast cancer cells harboring a functional p53 pathway. (
  • The G1 checkpoint, also known as the restriction point in mammalian cells and the start point in yeast, is the point at which the cell becomes committed to entering the cell cycle. (
  • It was Leland H. Hartwell who discovered the role of checkpoints while experimenting on yeast cells. (
  • In the end, Sir Paul Maxime Nurse discovered the role of CDK's (Cyclin-Dependant Kinase's) while experimenting on yeast cells. (
  • Cell cycle process of budding yeast ( Saccharomyces cerevisiae ) consists of four phases: G1, S, G2 and M. Initiated by stimulation of the G1 phase, cell cycle returns to the G1 stationary phase through a sequence of the S, G2 and M phases. (
  • To our knowledge this is the first work that rigorously examined the timing robustness of the cell cycle process of budding yeast with respect to checkpoint conditions using Boolean models. (
  • The G1 checkpoint, also called the restriction point (in yeast), is a point at which the cell commits to the cell division process. (
  • IBD2 encodes a novel component of the Bub2p-dependent spindle checkpoint in the budding yeast Saccharomyces cerevisiae. (
  • Hartwell credited Roman with demonstrating to him that studying the genetics of yeast could serve as a surrogate for studying the genetics of human cells -- or the cells of any living creatures. (
  • Inspired by Roman, ignoring the critics, Hartwell decided to work with baker's yeast because specific genetic mutations in the yeast produced changes that were visually identifiable as the yeast cells divided and multiplied in number. (
  • The findings in yeast eventually were shown to apply to the cells of nearly all living organisms, including humans. (
  • However, yeast cells in the wild, like other eukaryotic cells, spend most of their time in quiescence. (
  • The G 1 checkpoint, also called the restriction point (in yeast), is a point at which the cell irreversibly commits to the cell division process. (
  • The particulars of PCNA ubiquitination have been elucidated in yeast and to a further extent recently in human cells. (
  • [1] In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA damage, resulting in tens of thousands of individual molecular lesions per cell per day. (
  • DNA damage, due to environmental factors and normal metabolic processes inside the cell, occurs at a rate of 10,000 to 1,000,000 molecular lesions per cell per day. (
  • Upon contact with recipient cells, tumour-derived exosomes alter their phenotypic and functional properties conveying molecular and genetic messages 7 . (
  • When coupled with the cell-cycle checkpoint and pro-apoptotic activities of ATM, these findings provide a molecular explanation for the increase in lymphoid tumours with translocations involving antigen receptor loci associated with ataxia-telangiectasia. (
  • This will include the cancer hallmarks, cell communication, cell cycle and checkpoints, genomics/epigenomics, cancer syndromes and molecular therapies. (
  • The present study was conducted to elucidate the anti‑cancer effect and molecular mechanism of flavonoids from Citrus platymamma (FCP) on A549 cells. (
  • GTPases function as molecular switches in cells and are key players in intracellular signalling. (
  • Most of our studies have focused on the fruit fly Drosophila melanogaster as a model for chromosome function in metazoans, which allows us to address mechanisms in animals by synergistically combining molecular, genetic, cell biological and biochemical approaches. (
  • They integrate approaches from cell biology, molecular biology, genomics, and proteomics to achieve these goals. (
  • Molecular cell. (
  • According to new research published in the journal Cancer Cell , scientists have discovered a molecular mechanism that allows tumors to become resistant to chemotherapy. (
  • Biochimica et Biophysica Acta - Molecular Cell Research. (
  • Seminars in Cell & Developmental Biology. (
  • Over the past three decades, exosomes have surged to the forefront of cell biology research, and recently an increasing body of evidence indicates that this exosomal communication is a deliberate and highly orchestrated process. (
  • Cell biology research seeks to understand all aspects of cell growth, survival, and death in the contexts of both health and disease. (
  • Cell Signaling Technology (CST) provides a diverse and comprehensive catalog of rigorously tested and validated products to generate robust and reliable data and support your research into all aspects of cell biology. (
  • New insights into our understanding of cancer cell biology provide a new opportunity for a fundamental re-ordering of approaches to cancer drug discovery. (
  • Dr. Buchwalter Cool's laboratory is focused on understanding the cell biology of the genome. (
  • Frontiers in Cell and Developmental Biology. (
  • 2-phenylacetylenesulfonamide (PAS) induces p53-independent apoptotic killing of B-chronic lymphocytic leukemia (CLL) cells. (
  • E9 induces apoptotic cell death in various cancer cell lines and upon hypoxia, the compound suppresses CK2-catalyzed HSP90/Cdc37 phosphorylation and induces HIF-1alpha degradation. (
  • Dr. Langhans and her team, along with other groups, have previously shown that curcumin induces cell death in medulloblastoma, the most common pediatric brain tumor, and inhibited tumor growth in in vivo medulloblastoma models. (
  • It much more strongly induces death in these cells, so we can probably use that as a biomarker to predict which patients might respond to curcumin therapy," Dr. Langhans said. (
  • 6] These events lead the cancer cell to escape normal cell growth and control mechanisms, to avoid system control mechanisms (ie, immunologic surveillance), and to establish a nutrient supply. (
  • The timing of events in the cell cycle is controlled by mechanisms that are both internal and external to the cell. (
  • To prevent a compromised cell from continuing to divide, there are internal control mechanisms that operate at three main cell cycle checkpoints. (
  • The first focuses on the mechanisms by which therapy resistance is acquired in colorectal cancer and developing potential therapeutic approaches to re-sensitize tumor cells to therapy with an emphasis on the contribution of iron homeostasis to therapy resistance. (
  • Cell death mechanisms of the anti-cancer drug EPEG on human cardiomyocytes isolated from pluripotent stem cells. (
  • However, cells have developed a number of repair or tolerance mechanisms to counteract the DNA damage caused by UV or any other stressors. (
  • Numerous inherited genetic changes have been shown to predispose to certain or multiple cancer types through, for instance, defective DNA repair or cell-cycle checkpoint mechanisms. (
  • Campbell explained that these checkpoint mechanisms balance cell growth and differentiation as an organism develops, and are required for development of organs and tissues with appropriate size and function. (
  • So in this study we followed up on studying the mechanisms which might explain how it can induce cell death," Dr. Landhans explained. (
  • The major mechanisms for AgNP-induced genetic injuries are considered to be the overproduction of reactive oxidative species, inflammation, and cell cycle disturbance [ 9 , 10 ]. (
  • Tumor cells were treated with a newly designed survivin siRNA, which was modified with 2′-OMe. (
  • PLK2 promotes the survival of human tumor cells, a novel insight into the workings of malignant tumors characterized by TAp73 overexpression, and one that could speed the development of therapies. (
  • Unfortunately, tumor cells often develop resistance to endocrine therapy [ 1 ], representing a major obstacle limiting the success of breast cancer treatment. (
  • An altered vascular network determines irregular blood flow, so that tumor cells spread rapidly beyond the diffusion distance of oxygen in the tissue, with the consequent formation of hypoxic or anoxic areas, where the bulk of glioblastoma stem cells (GSCs) reside. (
  • Curcumin, a potent candidate anticancer agent, is a dietary pigment (phenolic compound) derived from the food flavoring spice turmeric (Curcuma longa), and it has been shown to have inhibitory effects on tumor cells through anti-proliferative and proapoptotic activities. (
  • â It only rescues the bad parts of p53â s function, but it doesn't rescue the part of p53â s function that you would want, which is killing the tumor cells,â explains Yaffe. (
  • So this study may show why curcumin causes death in tumor cells but not in normal cells. (
  • That is the great thing about curcumin because if it only targets tumor cells, then it has very few - if any - side effects. (
  • DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome . (
  • The DNA repair ability of a cell is vital to the integrity of its genome and thus to the normal functionality of that organism. (
  • The purpose of the eukaryotic cell cycle is to accurately duplicate and segregate the genome. (
  • In conclusion, our results indicate that phosphorylation of both T354 and T358 residues strongly influences the catalytic activity of Rad53 also in unperturbed cell cycles, and support the notion that Rad53 is essential to preserve genome integrity, by controlling the level of Sml1 and the functionality of ribonucleotide reductase. (
  • unreadable] DESCRIPTION (provided by applicant): Meiosis generates haploid gametes from a diploid cell such that a diploid genome is restored upon fertilization. (
  • Potential research directions in the post-genome era based on knowledge of repair of radiation-induced DNA double-strand breaks in mammalian somatic cells and the origin of deletions associated with human genomic disorders. (
  • Dr. Narlikar studies how the folding and compartmentalization of our genome is regulated to generate the many cell types that make up our body. (
  • Her current research uses approaches from soft matter physics and polymer physics to study the cell nucleus and its constituents, such as the genome and subnuclear bodies, in particular their dynamics and spatial organization. (
  • The cell-cycle checkpoints are pivotal to genome maintenance and are specifically deregulated in cancer cells and some of them are considered as potential therapeutic targets[5]. (
  • This process of maintaining the standards occur through Cell Cycle Checkpoints and Cell Cycle Regulators. (
  • In fact, the checkpoints depend on the regulators for their functioning. (
  • If checkpoint and regulators failed to their work, then it may lead to uncontrolled cellular growth causing cancer. (
  • So far, SOG1 appears to be the master regulator, delegating downstream responses among various regulators ( Figure 1 ), with ANAC044 and ANAC085 stopping the cell cycle before division. (
  • Displays no effect on the transactivational or cell cycle checkpoint control function of p53. (
  • Control of Swe1p degradation by the morphogenesis checkpoint. (
  • while many of these contribute to various aspects of cell-cycle control, not all are known to be CDK activators [ 2 ]. (
  • Loss of control of the cell cycle lies at the heart of cancer. (
  • Genomic instability, decreased cell cycle checkpoints, and partial loss of normal growth control in cells from Gadd45a-null mice may also contribute to this process. (
  • One of the major challenges the chromatin field is to elucidate how chromatin is globally reprogrammed during processes like cell fate determination, development and cell-cycle control. (
  • A new role for E2F-1 in checkpoint control. (
  • Many checkpoints control this stage. (
  • 3 Telomeres also keep the ends of chromosomal DNA from being perceived as double-stranded DNA breaks during cell cycle damage control checkpoints, preventing loss of chromosomal material. (
  • An image depicting head and neck squamous cell carcinoma in vitro can be seen below. (
  • Head and neck squamous cell carcinoma in vitro (cell culture). (
  • Head and neck squamous cell carcinoma cell lines and osteosarcoma cell lines were used as natural models of the different expression levels of TAp73. (
  • Among the inconsistencies, we noted differences in expression levels of TAp73 between human tumor cell lines such as head and neck squamous cell carcinoma (HNSCC) cell lines originating from epithelial carcinoma and osteosarcoma cell lines originating from mesenchymal sarcoma. (
  • Laryngeal squamous cell carcinoma (LSCC) is one of the most common head and neck cancers in the world. (
  • Genetic polymorphism at codon 546 of the human RAD17 contributes to the risk for esophageal squamous cell carcinoma. (
  • Short-term exposure to 50 Hz ELF-EMF alters the cisplatin-induced oxidative response in AT478 murine squamous cell carcinoma cells med. (
  • Crude methanol ex-tracts of the ascidian Didemum granulatum collected in Brazil showed activity in a new screen for G2 cell cycle checkpoint inhibitors. (
  • Granulatimide (4) and isogranulatimide (5) represent the first examples of a new class of G2 specific cell cycle checkpoint inhibitors and the first ones identified through a rational screening program. (
  • We evaluated the efficacy of a new drug schedule combining Dox and specific ATR (VE-821) or CHK1 (prexasertib, PX) inhibitors in the treatment of human B-/T- cell precursor ALL cell lines and primary ALL leukemic cells. (
  • Abnormal checkpoint response to DNA damage is a universal feature of cancers, and biochemical characterization of the checkpoint response should aid in developing new approaches to cancer chemotherapy. (
  • PPM1G mediates histone dephosphorylation/exchange in response to DNA damage or checkpoint recovery in higher eukaryotes. (
  • In humans, the frequency of cell turnover ranges from a few hours in early embryonic development, to an average of two to five days for epithelial cells, and to an entire human lifetime spent in G0 by specialized cells, such as cortical neurons or cardiac muscle cells. (
  • The RPE, a polarized monolayer of highly differentiated epithelial cells, positioned strategically between the neural retina and the vascular choriocapillaris, performs crucial functions that are necessary to maintain the function and survival of the photoreceptors and other retinal cells. (
  • The effect of calcitriol on growth of HTh74, HTh74R, SW1736 and C643 cell lines was investigated by cell viability assays. (
  • CST offers a variety of assays and reagents designed to enable evaluations of cell viability and cell death. (
  • Obtain precise data by using one of the many high-quality assays that CST has to offer for efficient, convenient, and cost-effective measurements of cell death and viability. (
  • Here, we showed that the differentiation and viability of retinal progenitor cells (RPCs) are severely perturbed in prpf31 knockout zebrafish when compared with other tissues at an early embryonic stage. (
  • Results showed that brevilin A inhibited NPC cell viability in a concentration- and time-dependent manner. (
  • The S Checkpoint is basically a 'surveillance' mechanism. (
  • Here we review current understanding of the mechanism by which cells sense damaged and foreign DNA. (
  • Therefore, these results are the first to indicate a novel mechanism of regulating Chk2 in cisplatin-induced resistance of cancer cells. (
  • Mechanism for switch of embryonic stem cells from 'fast' cell cycle to 'normal' cell cycle? (
  • Here we show that oxidative stress overrides the spindle checkpoint mechanism. (
  • By this mechanism, MIA actively facilitates focal cell detachment from surrounding structures and strongly promotes tumour cell invasion and migration. (
  • Scientists have found a new mechanism responsible for regulating stem cells in fruit flies, with possible implications for cancer therapies. (
  • 1) Differentiate between the G1, G2, and S phases of the eukaryotic cell cycle. (
  • The eukaryotic cell cycle is divided into 5 different phases. (
  • These data demonstrate that at least two distinct pools of PP1, one kinetochore associated and the other motor associated, are needed to silence the spindle checkpoint. (
  • Attachment of each kinetochore to a spindle fiber is assessed at the M checkpoint. (
  • Shown is a fluorescence microscopy image of a HeLa cell at mitotic metaphase. (
  • There are three major checkpoints in the cell cycle: one near the end of G1, a second at the G2/M transition, and the third during metaphase. (
  • These checkpoints occur near the end of G1, at the G2/M transition, and during metaphase (see Figure 10.11). (
  • These checkpoints occur near the end of G 1 , at the G 2 /M transition, and during metaphase (Figure 1). (
  • The M checkpoint occurs near the end of the metaphase stage of karyokinesis. (
  • The equator of the cell is called the metaphase plate. (
  • Cell cycle is a strictly regulated phenomenon that involves duplication and division of cellular material between daughter cells. (
  • This is the multihit theory of tumorigenesis, in which a series of multiple triggering events in the genetic and cellular makeup of a cell ultimately cause cancer. (
  • they are also complex tissues composed of cellular components, such as mesenchymal stem cells (MSCs), cancer-associated fibroblasts (CAFs), endothelial cells, immune cells as well as extracellular matrix (ECM) components, which establish the so-called tumour microenvironment (TME) surrounding the tumour cells. (
  • During this process, not only the genetic material but also the cellular organelles have to be equally distributed to the newborn cells to allow for their proper functioning. (
  • His research focus is on the developed experimental techniques for making highly quantitative measurements in single cells and models for linking those measurements to cellular function. (
  • Advances in cellular immunotherapy that spur genetically modified T cells to attack cancer cells have revolutionized the treatment of certain blood cancers. (
  • To emulate radiotherapy at the cellular level, MCF7 breast cancer cells were exposed to daily radiation doses of 2 Gy up to an accumulated dose of 20 Gy. (
  • ATM-deficient pre-B cells exhibit defects in V(D)J recombination. (
  • This is done to avoid the passing on of altered genetic material to the daughter cells. (
  • Repairing DNA prevents cells from accumulating genetic damage that may cause them to die or to divide uncontrollably. (
  • The MRE11A/RAD50/NBN complex helps maintain the stability of a cell's genetic information through its roles in repairing damaged DNA and regulating cell division. (
  • Genetic disruption of INK4A occurs in approximately 50% of melanomas irrespective of BRAF mutation and has been detected in melanoma cells that developed resistance to BRAFi. (
  • NG2 was frequently co-expressed with nestin and vimentin but rarely with CD133 and the NG2 positive tumour cells harboured genetic aberrations typical for GBM. (
  • however, associations with other myelodysplastic syndromes as well as genetic aberrations in cell-cycle checkpoints have been reported (2). (
  • Centrosomes are the major microtubule nucleating centres within a cell and play a key role in forming the bipolar mitotic spindle required to accurately divide genetic material between daughter cells during cell division. (
  • In turn, as a result of research into the abnormal cancer cell, the basic understanding of the cell has greatly improved. (
  • This, in turn, creates a clonal population of a single abnormal cell. (
  • It is a multifactorial disease contributing towards uncontrolled growth and invasion of the abnormal cells leading to the formation of tumour. (
  • External influences, such as growth factors, play a large role in carrying the cell past the G1 checkpoint. (
  • Checkpoints prevent genomic instability, cancer, and death in multicellular organisms. (
  • It is now known that populations of stem and progenitor cells located in distinct regions of the mature brain ensure the continued neurogenesis process in adults. (
  • There are two identified neurogenic niches in the adult mammalian brain: the subventricular zone (SVZ) of the forebrain lateral ventricles and the subgranular zone (SGZ), in the dentate gyrus of the hippocampus, in which both quiescent stem cells and mitotically active progenitor cells reside [ 35 ]. (
  • We have applied single-cell RNA-sequencing (scRNA-seq) to fresh human bone marrow CD34 + cells and profiled 391 single hematopoietic stem/progenitor cells (HSPCs) from healthy donors to characterize lineage- and stage-specific transcription during hematopoiesis. (
  • Even in organisms as diverse as humans and fruit flies, adult stem cells produce progenitor cells that differentiate into specialized types to regenerate intestinal cell walls, balancing cell loss by injury, infection and aging with new growth. (
  • Using fruit flies as a model, graduate student Reegan Willms discovered that loss of Myt1 caused hyperproliferation of intestinal stem cells and progenitor cells," said Campbell. (
  • When fast-dividing mammalian cells are grown in culture (outside the body under optimal growing conditions), the length of the cycle is about 24 hours. (
  • Then, Sir Richard Timothy Hunt went on to discover the role of cyclins while experimenting on sea urchin egg cells. (
  • Cyclins decide whether a cell should divide or not. (
  • Microtubule-stabilizing properties of the avocado-derived toxins (+)-(R)-persin and (+)-(R)-tetrahydropersin in cancer cells and activity of related synthetic analogs. (
  • Cancer stem cells (CSCs), a very small fraction of cancer cells, are widely believed to be responsible for cancer initiation, relapse and metastasis. (
  • Calcitriol inhibited the growth of CSCs derived from anaplastic thyroid cancer cells. (
  • HDAC6 activity is not required for basal autophagic flux in metastatic prostate cancer cells. (
  • 2013. HDAC turnover, CtIP acetylation and dysregulated DNA damage signaling in colon cancer cells treated with sulforaphane and related dietary isothiocyanates. . (
  • Analysis of autophagic flux in response to sulforaphane in metastatic prostate cancer cells. (
  • CtIP suppresses primary microRNA maturation and promotes metastasis of colon cancer cells in a xenograft mouse model. (
  • It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death. (
  • However, cancer cells with an immature stem-like phenotype are hypothesised to play a role in radioresistance. (
  • However, the use of cancer cells may result in a distortion of the physiological damage response. (
  • Gadd45 and p27 help cancer cells pause cell division, allowing DNA to be repaired. (
  • Measurements of DNA concentrations in single cells revealed that C-1305 arrested the tested cancer cells at the G 2 /M transition. (
  • Many cancer cells show distorted epigenetic landscapes. (
  • In conclusion we established for the first time a comprehensive, high confidence ceRNA network that governs the radioadaptive response of radioresistant MCF7 breast cancer cells. (
  • but telomerase, the RNA transcriptase responsible for adding nucleotides back on to telomeres, is also highly active in cancer cells and contributes to cancer cell immortality. (
  • All living organisms are the products of repeated rounds of cell growth and division. (
  • Growth Factors: The cell checks if it is receiving external growth promoting signals to divide. (
  • Cancer is characterized by uncontrolled growth and division of a cell, with extension beyond the normally limiting basement membrane and through the boundaries of normal cells. (
  • Because of its mutated aggressive genetics, this cell has a selective growth advantage over its neighbors. (
  • An event may be as simple as the death of a nearby cell or as sweeping as the release of growth-promoting hormones, such as human growth hormone (HGH). (
  • This model was chosen in part because of the extensive knowledge of how each substance affects tumor cell growth in other systems, as well as the relative availability of human colorectal cancer tissues. (
  • Crucial to AE pathology is continuous infiltrative growth of the parasite's metacestode stage, which is driven by a population of somatic stem cells, called germinative cells. (
  • Current anti-AE chemotherapy using benzimidazoles is ineffective in eliminating the germinative cell population, thus leading to remission of parasite growth upon therapy discontinuation. (
  • Furthermore, low doses of BI 2536 eliminated germinative cells from Echinococcus larvae in vitro and prevented parasite growth and development. (
  • Working with post-doctoral researcher Jie Zeng, Willms demonstrated that Myt1 is critical to inhibiting this process during normal cell growth. (
  • External influences, such as growth factors, play a large role in carrying the cell past the G 1 checkpoint. (
  • The g1 phase, Gap 1 phase, or Growth 1 phase, is the first of four phases of the cell cycle that takes place in eukaryotic cell division. (
  • One significant difference between growth phases is that the first growth phase is about cell growth while G2 is about cell division. (
  • Lack of nutrition, lack of growth factors, and the inability of the cells to undergo metabolic changes are few of the reasons for cells to get arrested in G1 phase. (
  • External insults (eg, infections, radiation, drugs) may disrupt stem cell homeostasis in marrow environment, leading to altered growth. (
  • In stem-enriched cells derived from thyro-spheres cell cycle analysis and apoptotic assays were performed. (
  • For instance, melanoma cells are mesenchymal in nature ensuring that a larger percentage of cells can act as stem cells with self-renewal capacity. (
  • Senoo M . Epidermal Stem Cells in Homeostasis and Wound Repair of the Skin. (
  • Prospective analysis of antigen-specific immunity, stem cell antigens and immune checkpoints in monoclonal gammopathy. (
  • It is well-known that embryonic stem cells have a fast cell cycle (very roughly about 12 hours), while typically normal cells have a much longer cell cycle (very roughly about 24 hours). (
  • Potentially increases reprogramming efficiency of human somatic cells to induced pluripotent stem cells (iPSCs) by silencing p53. (
  • Cancer stem cells (CSCs) were first isolated in acute myeloid leukemia (AML) patients proving that CSCs are able to reproduce many features of human AML in immunodeficient mice [ 1 ]. (
  • The brain has been for a long time defined as an organ with limited regeneration ability, until the discovery of neural stem cells in adult brain [ 8 - 10 ]. (
  • thus, they may potentially give rise to cell transformation into tumor stem cells [ 11 ]. (
  • The presence of cells with stem-like properties in human brain tumors was firstly demonstrated by Ignatova et al. (
  • In vitro , stem-like cells derived from brain tumors have high regenerative capacity and the ability to differentiate into neuronal or glial cells as they can express specific neural markers. (
  • Brain tumor stem cells in vitro showed many stem-cell features such as extensive self-renewal, multipotency, and generation of many progenies. (
  • The tumors developed in mice model injected with glioblastoma stem cells (GSCs) display high extensive migratory and infiltrative capacity, indicating that isolated brain tumor stem cells in vivo may induce tumor to the brain similar to those observed in glioblastoma multiforme [ 7 , 14 , 15 ]. (
  • Many scientific reports still debate on the origin of brain tumors, particularly whether they may derive from the dedifferentiation of a brain cell or from the transformation of a neural stem cell (NSC) or progenitor cell [ 20 ]. (
  • Allogenic haematopoietic stem cell transplantation (allo-HSCT) is currently not considered. (
  • Comparison of the ARPE-19 RNA-Seq data set with that of primary human fetal RPE, embryonic stem cell-derived RPE, and native RPE revealed an important overall similar expression ratio among all the models and native tissue. (
  • Telomerase is present in germ cells, stem cells, and hematopoietic cells, but is inactive in most somatic cells. (
  • The theoretical basis for marrow failure includes primary defects in or damage to the stem cell or the marrow microenvironment. (
  • Another central question is how human cells regulate mono and polyubiquitination of PCNA and hence how they induce or limit the deployment of DNA repair machinery in the presence or absence of damage. (
  • ARPE-19 cells grown for 4 months developed the classic native RPE phenotype with heavy pigmentation. (
  • High levels of telomerase activity correlate with longer telomeres and prevention or postponement of cell senescence, theoretically resulting in cells and tissues with more youthful behavior in terms of health and phenotype. (
  • We propose a model where Dia2 mediates Mrc1 degradation to greatly help cells job application the cell routine during recovery from MMS-induced DNA harm in S-phase. (
  • The checkpoint mediator Mrc1 has recently been identified as a ubiquitin-mediated degradation substrate of SCFDia2 (Mimura 2009). (
  • Several different perturbations of actin organization all prevent Swe1p degradation, leading to the persistence or further accumulation of Swe1p, and cell cycle delay in G2. (
  • We have already established an in vitro system that recapitulates some of the key features of the human DNA damage checkpoint response to base damage. (
  • Pifithrin- μ reduces cell death induced by γ-radiation in vitro and protects mice from doses of radiation that cause lethal hematopoietic syndrome. (
  • However, there is no report showing curcumin-induced apoptotic cell death in human nasopharyngeal carcinoma cells in vitro. (
  • In vitro, cabazitaxel showed similar antiproliferative activity to docetaxel in taxane-sensitive cell lines and markedly greater activity in cell lines resistant to taxanes. (
  • Cross resistance of FIR20 cells to tamoxifen was confirmed in vitro. (
  • Dr. Hartwell's extraordinary creativity and imagination led to ground-breaking advances in understanding the cell cycle," said Dr. Marvin Cassman , director of general medical sciences at the National Institutes of Health in Bethesda, Md. "His research proved that it was possible to use the tools of genetics to understand the cell cycle and the way defects in this cycle can result in disease. (
  • Further, flow cytometry revealed that FCP significantly increased the sub‑G1 (apoptotic cell population) and G2/M phase population, and the total number of apoptotic cells, in a dose‑dependent manner. (
  • Doxorubicin (Dox) is one of the most commonly used anthracyclines for the treatment of solid and hematological tumors such as B-/T-cell acute lymphoblastic leukemia (ALL). (
  • Several reports indicate that brain tumors might rise from the transformation of undifferentiated precursor cells, which are located not only in germinal regions of the developing and early-postnatal CNS, but also in regions of mature brain in which neurogenesis persists throughout adulthood [ 11 ]. (
  • The cell will instead repair itself and then move to the next phase. (
  • If the student does not pass the exam, he/she has to give a re-exam and the same goes for a cell too, which, if doesn't pass, has to repair itself. (
  • The rate of DNA repair is dependent on many factors, including the cell type, the age of the cell, and the extracellular environment. (
  • In addition, we are investigating the connection between the circadian cycle and DNA repair and how disruption of the circadian cycle might affect the susceptibility of mice and humans to cancers. (
  • Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. (
  • Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. (
  • Instead, plants use SOG1 (short for suppressor of gamma-response 1), a plant-specific transcription factor that also arrests the cell cycle, coordinates DNA repair and promotes cell death. (
  • It allows damaged DNA cells to repair their DNA but does not trigger cell death if the damaged DNA is unrepairable. (
  • For healthy cells, p53 shuts down cell division to repair damaged DNA. (
  • This system acts like a timer, or a clock, which sets a fixed amount of time for the cell to spend in each phase of the cell cycle, while at the same time it also responds to information received from the processes it controls. (
  • The decision to commit to a new round of cell division occurs when the cell activates cyclin-CDK-dependent transcription which promotes entry into S phase. (
  • These findings suggest that Dia2 plays a role in the S-phase checkpoint. (
  • While moving through the cell cycle, the cells don't transition from one phase to another just simply. (
  • If any of the above issues are encountered, the cell will not move to the next phase of the cycle. (
  • Just like how a student has to pass an exam to get promoted to the next semester, a cell has to pass the checkpoint to get promoted to the next phase. (
  • G1 Checkpoint (at the end of G1 Phase, before entering S Phase). (
  • S Checkpoint (partway through S Phase). (
  • G2 Checkpoint (at the end of G2 Phase, before entering M Phase). (
  • If any of the above requirements are not met, the cell will immediately stop the process of division and will not transition to the S Phase. (
  • Towards the end of the G2 Phase comes the G2 Checkpoint to check if the cell is ready to transition to the M Phase. (
  • During the cell cycle, a cell verifies whether necessary conditions are satisfied at the end of each phase (i.e., checkpoint) since damages of any phase can cause severe cell cycle defect. (
  • The cell cycle can proceed to the next phase properly only if checkpoint conditions are met. (
  • It is important to reach the final phase after completing each phase properly since any mistakes can cause significant defect to the cell cycle process. (
  • Before entering S phase, the cell must be large enough and have undamaged DNA (G1 phase checkpoint). (
  • Before entering M phase, DNA synthesis should be completed (S and G2 phase checkpoint). (
  • There is also variation in the time that a cell spends in each phase of the cell cycle. (
  • In rapidly dividing human cells with a 24-hour cell cycle, the G1 phase lasts approximately nine hours, the S phase lasts 10 hours, the G2 phase lasts about four and one-half hours, and the M phase lasts approximately one-half hour. (
  • Moving forward from this initiation point, every parameter required during each cell cycle phase must be met or the cycle cannot progress. (
  • A cell that does not meet all the requirements will not be allowed to progress into the S phase. (
  • Agarwal ML, Agarwal A, Taylor WR et al (1998) A p53-dependent S-phase checkpoint helps to protect cells from DNA damage in response to starvation for pyrimidine nucleotides. (
  • Giaccone G, Herbst RS, Manegold C et al (2004) Gefitinib in combination with gemcitabine and cisplatin in advanced non-small-cell lung cancer: a phase III trial-INTACT 1. (
  • M to G1 phase transition checkpoint? (
  • I know that G0 phase occurs when certain cells exit the cell cycle during G1 phase but that means it goes to G0 phase after M phase right? (
  • Required for the entry in S phase and for cell division. (
  • In rapidly dividing human cells with a 24-hour cell cycle, the G 1 phase lasts approximately nine hours, the S phase lasts 10 hours, the G 2 phase lasts about four and one-half hours, and the M phase lasts approximately one-half hour. (
  • The G 2 checkpoint bars entry into the mitotic phase if certain conditions are not met. (
  • What is g1 phase in cell cycle? (
  • What is the longest phase in the life of a cell? (
  • The shortest phase of the cell cycle is cytokinesis because all the previous stages help prepare the cell to divide, so all the cell has to do is divide and nothing else. (
  • What phase do cells spend the least time in? (
  • G1 is typically the longest phase of the cell cycle. (
  • In the G1 phase, a cell grows rapidly and carries out its routine functions. (
  • Here the daughter cells of the previous M phase begin G1 phase. (
  • Normal cell metabolism takes the center stage in this phase. (
  • G1 phase duration is different for different cells. (
  • A checkpoint called, Restriction point determines whether a cell continues its journey of cell cycle, dies or enters into G0 phase. (
  • Terminally differentiated cells or end cells which do not have the capacity to divide any further like neurons and striated muscle cells or voluntary muscle cells are arrested in this G1 phase. (
  • iii) alteration of the sEV-mediated communication of tumour cells might be a therapy-induced host response, with a potential influence on treatment efficacy. (
  • Since malignant melanoma is one of the most aggressive cancers, the B16F1 mouse melanoma cell line was chosen as a tumour cell model for this study. (
  • Quantification of NG2 expression in 74 GBM biopsies from newly diagnosed and untreated patients revealed that 50% express high NG2 levels on tumour cells and associated vessels, being associated with significantly shorter survival. (
  • BPDCN is an exceedingly rare and aggressive tumour, derived from precursors of plasmacytoid dendritic cells, usually affecting elderly males. (
  • Boraginaceae) aerial parts against four tumour cell lines (MCF-7, MDA-MB-231, RKO, and R₂C). (
  • Gama A , Alves A, Gartner F, Schmitt F. p63: A Novel Myoepithelial Cell Marker in Canine Mammary Tissues. (
  • The relative lack of specificity of the majority of chemotherapeutic drugs for malignant cells is largely responsible for the toxicity to normal tissues experienced by patients ( 1 ). (
  • Because of the dual problem of limited effectiveness against malignant cells and significant toxicity to normal tissues, numerous approaches to enhance the clinical effectiveness of chemotherapy without increasing its toxicity have been tested. (
  • Similar cells with the capacity of self-renewal are identified in other tissues. (
  • For cells, cell lines and tissues in culture till half confluency.Isotype or positive controls by peptides, antibodies and deactivated samples. (
  • This phosphorylation occurs in cancer cell lines, as well as in primary breast tissues and lymphocytes. (
  • The M checkpoint is also known as the spindle checkpoint, because it determines whether all the sister chromatids are correctly attached to the spindle microtubules. (
  • It forms during the cell cycle so that the sister chromatids (it is a chromosome that is newly copied where two of them are still attached to each other) can be separated to form daughter cells. (
  • We discovered that checkpoint-defective alleles suppress the MMS awareness as well as the checkpoint recovery defect of cells. (
  • But if there is a defect in the checkpoint, this process is disrupted," Dr. Langhans added. (