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.
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.
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.
A ubiquitin-protein ligase that mediates OXYGEN-dependent polyubiquitination of HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT. It is inactivated in VON HIPPEL-LINDAU SYNDROME.
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.
A cell line derived from cultured tumor cells.
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.
A gene product of the p16 tumor suppressor gene (GENES, P16). It antagonizes the function of MDM2 PROTEIN (which regulates P53 TUMOR SUPPRESSOR PROTEIN by targeting it for degradation). p14ARF is produced from the beta mRNA transcript of the p16 gene. The other gene product, produced from the alternatively spliced alpha transcript, is CYCLIN-DEPENDENT KINASE INHIBITOR P16. Both p16 gene products have tumor suppressor functions.
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.
Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.
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.
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.
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.
Established cell cultures that have the potential to propagate indefinitely.
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.
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.
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.
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.
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.
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.
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.
Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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.
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.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
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.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
A diverse class of enzymes that interact with UBIQUITIN-CONJUGATING ENZYMES and ubiquitination-specific protein substrates. Each member of this enzyme group has its own distinct specificity for a substrate and ubiquitin-conjugating enzyme. Ubiquitin-protein ligases exist as both monomeric proteins multiprotein complexes.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Products of viral oncogenes, most commonly retroviral oncogenes. They usually have transforming and often protein kinase activities.
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.
Proteins transcribed from the E1B region of ADENOVIRUSES which are involved in regulation of the levels of early and late viral gene expression.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
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.
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.
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.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
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.
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.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A family of proteins that are structurally-related to Ubiquitin. Ubiquitins and ubiquitin-like proteins participate in diverse cellular functions, such as protein degradation and HEAT-SHOCK RESPONSE, by conjugation to other proteins.
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.
A membrane protein homologous to the ERM (Ezrin-Radixin-Moesin) family of cytoskeleton-associated proteins which regulate physical properties of membranes. Alterations in neurofibromin 2 are the cause of NEUROFIBROMATOSIS 2.
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).
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.
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.
A negative regulator of beta-catenin signaling which is mutant in ADENOMATOUS POLYPOSIS COLI and GARDNER SYNDROME.
Polyomavirus antigens which cause infection and cellular transformation. The large T antigen is necessary for the initiation of viral DNA synthesis, repression of transcription of the early region and is responsible in conjunction with the middle T antigen for the transformation of primary cells. Small T antigen is necessary for the completion of the productive infection cycle.
A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.
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.
Serologic tests in which a positive reaction manifested by visible CHEMICAL PRECIPITATION occurs when a soluble ANTIGEN reacts with its precipitins, i.e., ANTIBODIES that can form a precipitate.
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.
A large multisubunit complex that plays an important role in the degradation of most of the cytosolic and nuclear proteins in eukaryotic cells. It contains a 700-kDa catalytic sub-complex and two 700-kDa regulatory sub-complexes. The complex digests ubiquitinated proteins and protein activated via ornithine decarboxylase antizyme.
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.
A theoretical representative nucleotide or amino acid sequence in which each nucleotide or amino acid is the one which occurs most frequently at that site in the different sequences which occur in nature. The phrase also refers to an actual sequence which approximates the theoretical consensus. A known CONSERVED SEQUENCE set is represented by a consensus sequence. Commonly observed supersecondary protein structures (AMINO ACID MOTIFS) are often formed by conserved sequences.
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 genus of owlet moths of the family Noctuidae. These insects are used in molecular biology studies during all stages of their life cycle.
Genes that have a suppressor allele or suppressor mutation (SUPPRESSION, GENETIC) which cancels the effect of a previous mutation, enabling the wild-type phenotype to be maintained or partially restored. For example, amber suppressors cancel the effect of an AMBER NONSENSE MUTATION.
Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.
A lipid phosphatase that acts on phosphatidylinositol-3,4,5-trisphosphate to regulate various SIGNAL TRANSDUCTION PATHWAYS. It modulates CELL GROWTH PROCESSES; CELL MIGRATION; and APOPTOSIS. Mutations in PTEN are associated with COWDEN DISEASE and PROTEUS SYNDROME as well as NEOPLASTIC CELL TRANSFORMATION.
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.
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.
Proteins prepared by recombinant DNA technology.
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Formation of an acetyl derivative. (Stedman, 25th ed)
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.
A family of small, non-enveloped DNA viruses infecting birds and most mammals, especially humans. They are grouped into multiple genera, but the viruses are highly host-species specific and tissue-restricted. They are commonly divided into hundreds of papillomavirus "types", each with specific gene function and gene control regions, despite sequence homology. Human papillomaviruses are found in the genera ALPHAPAPILLOMAVIRUS; BETAPAPILLOMAVIRUS; GAMMAPAPILLOMAVIRUS; and MUPAPILLOMAVIRUS.
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.
A family of basic helix-loop-helix transcription factors that control expression of a variety of GENES involved in CELL CYCLE regulation. E2F transcription factors typically form heterodimeric complexes with TRANSCRIPTION FACTOR DP1 or transcription factor DP2, and they have N-terminal DNA binding and dimerization domains. E2F transcription factors can act as mediators of transcriptional repression or transcriptional activation.
A class of enzymes that catalyze the formation of a bond between two substrate molecules, coupled with the hydrolysis of a pyrophosphate bond in ATP or a similar energy donor. (Dorland, 28th ed) EC 6.
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.
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.
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 group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
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.
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.
A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE. It is involved in the biosynthesis of PURINES; PYRIMIDINES; and other amino acids.
Molecular products metabolized and secreted by neoplastic tissue and characterized biochemically in cells or body fluids. They are indicators of tumor stage and grade as well as useful for monitoring responses to treatment and predicting recurrence. Many chemical groups are represented including hormones, antigens, amino and nucleic acids, enzymes, polyamines, and specific cell membrane proteins and lipids.
A negative regulator of the CELL CYCLE that undergoes PHOSPHORYLATION by CYCLIN-DEPENDENT KINASES. It contains a conserved pocket region that binds E2F4 TRANSCRIPTION FACTOR and interacts with viral ONCOPROTEINS such as POLYOMAVIRUS TUMOR ANTIGENS; ADENOVIRUS E1A PROTEINS; and PAPILLOMAVIRUS E7 PROTEINS.
Transport proteins that carry specific substances in the blood or across cell membranes.
An E2F transcription factor that interacts directly with RETINOBLASTOMA PROTEIN and CYCLIN A and activates GENETIC TRANSCRIPTION required for CELL CYCLE entry and DNA synthesis. E2F1 is involved in DNA REPAIR and APOPTOSIS.
Interruption or suppression of the expression of a gene at transcriptional or translational levels.
A negative regulator of the CELL CYCLE that undergoes PHOSPHORYLATION by CYCLIN-DEPENDENT KINASES. RBL2 contains a conserved pocket region that binds E2F4 TRANSCRIPTION FACTOR and E2F5 TRANSCRIPTION FACTOR. RBL2 also interacts with viral ONCOPROTEINS such as POLYOMAVIRUS TUMOR ANTIGENS; ADENOVIRUS E1A PROTEINS; and PAPILLOMAVIRUS E7 PROTEINS.
A transcription factor that possesses DNA-binding and E2F-binding domains but lacks a transcriptional activation domain. It is a binding partner for E2F TRANSCRIPTION FACTORS and enhances the DNA binding and transactivation function of the DP-E2F complex.
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.
A family of structurally related proteins that are induced by CYTOKINES and negatively regulate cytokine-mediated SIGNAL TRANSDUCTION PATHWAYS. SOCS proteins contain a central SH2 DOMAIN and a C-terminal region of homology known as the SOCS box.
Mutation process that restores the wild-type PHENOTYPE in an organism possessing a mutationally altered GENOTYPE. The second "suppressor" mutation may be on a different gene, on the same gene but located at a distance from the site of the primary mutation, or in extrachromosomal genes (EXTRACHROMOSOMAL INHERITANCE).
ONCOGENE PROTEINS from papillomavirus that deregulate the CELL CYCLE of infected cells and lead to NEOPLASTIC CELL TRANSFORMATION. Papillomavirus E7 proteins have been shown to interact with various regulators of the cell cycle including RETINOBLASTOMA PROTEIN and certain cyclin-dependent kinase inhibitors.
A ubiquitously expressed regulatory protein that contains a retinoblastoma protein binding domain and an AT-rich interactive domain. The protein may play a role in recruiting HISTONE DEACETYLASES to the site of RETINOBLASTOMA PROTEIN-containing transcriptional repressor complexes.
Addition of methyl groups to DNA. DNA methyltransferases (DNA methylases) perform this reaction using S-ADENOSYLMETHIONINE as the methyl group donor.
The loss of one allele at a specific locus, caused by a deletion mutation; or loss of a chromosome from a chromosome pair, resulting in abnormal HEMIZYGOSITY. It is detected when heterozygous markers for a locus appear monomorphic because one of the ALLELES was deleted.
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.
Tumors or cancers of the KIDNEY.
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.
Isoforms encoded by the WT1 Wilms tumor suppressor gene (GENES, WILMS TUMOR) and produced by alternative splicings. They are zinc finger-containing transcription factors involved in both transactivation and repression, and are critical for normal development and function of the urogenital tract.
The total amount (cell number, weight, size or volume) of tumor cells or tissue in the body.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
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.
Tumors or cancer of the human BREAST.
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.
A malignant kidney tumor, caused by the uncontrolled multiplication of renal stem (blastemal), stromal (STROMAL CELLS), and epithelial (EPITHELIAL CELLS) elements. However, not all three are present in every case. Several genes or chromosomal areas have been associated with Wilms tumor which is usually found in childhood as a firm lump in a child's side or ABDOMEN.
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.
DNA present in neoplastic tissue.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.
A highly conserved 76-amino acid peptide universally found in eukaryotic cells that functions as a marker for intracellular PROTEIN TRANSPORT and degradation. Ubiquitin becomes activated through a series of complicated steps and forms an isopeptide bond to lysine residues of specific proteins within the cell. These "ubiquitinated" proteins can be recognized and degraded by proteosomes or be transported to specific compartments within the cell.
Human COLORECTAL CARCINOMA cell line.
A sarcoma originating in bone-forming cells, affecting the ends of long bones. It is the most common and most malignant of sarcomas of the bones, and occurs chiefly among 10- to 25-year-old youths. (From Stedman, 25th ed)
Tumor suppressor genes located on human chromosome 13 in the region 13q14 and coding for a family of phosphoproteins with molecular weights ranging from 104 kDa to 115 kDa. One copy of the wild-type Rb gene is necessary for normal retinal development. Loss or inactivation of both alleles at this locus results in retinoblastoma.
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.
Tumor suppressor genes located on the long arm of human chromosome 22. Mutation or loss of these genes causes NEUROFIBROMATOSIS 2.
A group of hydrolases which catalyze the hydrolysis of monophosphoric esters with the production of one mole of orthophosphate. EC 3.1.3.
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.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
A large group of proteins that control APOPTOSIS. This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Proteins transcribed from the E1A genome region of ADENOVIRUSES which are involved in positive regulation of transcription of the early genes of host infection.
A heterogeneous group of sporadic or hereditary carcinoma derived from cells of the KIDNEYS. There are several subtypes including the clear cells, the papillary, the chromophobe, the collecting duct, the spindle cells (sarcomatoid), or mixed cell-type carcinoma.
Genes whose gain-of-function alterations lead to NEOPLASTIC CELL TRANSFORMATION. They include, for example, genes for activators or stimulators of CELL PROLIFERATION such as growth factors, growth factor receptors, protein kinases, signal transducers, nuclear phosphoproteins, and transcription factors. A prefix of "v-" before oncogene symbols indicates oncogenes captured and transmitted by RETROVIRUSES; the prefix "c-" before the gene symbol of an oncogene indicates it is the cellular homolog (PROTO-ONCOGENES) of a v-oncogene.
An autosomal dominant disorder characterized by a high incidence of bilateral acoustic neuromas as well as schwannomas (NEURILEMMOMA) of other cranial and peripheral nerves, and other benign intracranial tumors including meningiomas, ependymomas, spinal neurofibromas, and gliomas. The disease has been linked to mutations of the NF2 gene (GENES, NEUROFIBROMATOSIS 2) on chromosome 22 (22q12) and usually presents clinically in the first or second decade of life.
Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.
Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible.
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 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.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
Transplantation between animals of different species.
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
A malignant epithelial tumor with a glandular organization.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
An autosomal dominant disorder caused by mutations in a tumor suppressor gene. This syndrome is characterized by abnormal growth of small blood vessels leading to a host of neoplasms. They include HEMANGIOBLASTOMA in the RETINA; CEREBELLUM; and SPINAL CORD; PHEOCHROMOCYTOMA; pancreatic tumors; and renal cell carcinoma (see CARCINOMA, RENAL CELL). Common clinical signs include HYPERTENSION and neurological dysfunctions.
A protein found most abundantly in the nervous system. Defects or deficiencies in this protein are associated with NEUROFIBROMATOSIS 1, Watson syndrome, and LEOPARD syndrome. Mutations in the gene (GENE, NEUROFIBROMATOSIS 1) affect two known functions: regulation of ras-GTPase and tumor suppression.
A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.
CELL LINES derived from the CV-1 cell line by transformation with a replication origin defective mutant of SV40 VIRUS, which codes for wild type large T antigen (ANTIGENS, POLYOMAVIRUS TRANSFORMING). They are used for transfection and cloning. (The CV-1 cell line was derived from the kidney of an adult male African green monkey (CERCOPITHECUS AETHIOPS).)
The act of ligating UBIQUITINS to PROTEINS to form ubiquitin-protein ligase complexes to label proteins for transport to the PROTEASOME ENDOPEPTIDASE COMPLEX where proteolysis occurs.
Proteins that originate from insect species belonging to the genus DROSOPHILA. The proteins from the most intensely studied species of Drosophila, DROSOPHILA MELANOGASTER, are the subject of much interest in the area of MORPHOGENESIS and development.
Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.
Genes whose expression is easily detectable and therefore used to study promoter activity at many positions in a target genome. In recombinant DNA technology, these genes may be attached to a promoter region of interest.
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)
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.
Tumors or cancer of the LIVER.
A positive 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.
Elements of limited time intervals, contributing to particular results or situations.
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 insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
Single-stranded complementary DNA synthesized from an RNA template by the action of RNA-dependent DNA polymerase. cDNA (i.e., complementary DNA, not circular DNA, not C-DNA) is used in a variety of molecular cloning experiments as well as serving as a specific hybridization probe.
A continuous cell line of high contact-inhibition established from NIH Swiss mouse embryo cultures. The cells are useful for DNA transfection and transformation studies. (From ATCC [Internet]. Virginia: American Type Culture Collection; c2002 [cited 2002 Sept 26]. Available from http://www.atcc.org/)
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
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.
Enzymes that oxidize certain LUMINESCENT AGENTS to emit light (PHYSICAL LUMINESCENCE). The luciferases from different organisms have evolved differently so have different structures and substrates.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
The part of a cell that contains the CYTOSOL and small structures excluding the CELL NUCLEUS; MITOCHONDRIA; and large VACUOLES. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
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.
Tumor suppressor genes located in the 5q21 region on the long arm of human chromosome 5. The mutation of these genes is associated with familial adenomatous polyposis (ADENOMATOUS POLYPOSIS COLI) and GARDNER SYNDROME, as well as some sporadic colorectal cancers.
A malignant tumor arising from the nuclear layer of the retina that is the most common primary tumor of the eye in children. The tumor tends to occur in early childhood or infancy and may be present at birth. The majority are sporadic, but the condition may be transmitted as an autosomal dominant trait. Histologic features include dense cellularity, small round polygonal cells, and areas of calcification and necrosis. An abnormal pupil reflex (leukokoria); NYSTAGMUS, PATHOLOGIC; STRABISMUS; and visual loss represent common clinical characteristics of this condition. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2104)
Tumors or cancer of the COLON.
A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)
Tumor suppressor genes located on human chromosome 9 in the region 9p21. This gene is either deleted or mutated in a wide range of malignancies. (From Segen, Current Med Talk, 1995) Two alternatively spliced gene products are encoded by p16: CYCLIN-DEPENDENT KINASE INHIBITOR P16 and TUMOR SUPPRESSOR PROTEIN P14ARF.
Proteins, protein complexes, or glycoproteins secreted by suppressor T-cells that inhibit either subsequent T-cells, B-cells, or other immunologic phenomena. Some of these factors have both histocompatibility (I-J) and antigen-specific domains which may be linked by disulfide bridges. They can be elicited by haptens or other antigens and may be mass-produced by hybridomas or monoclones in the laboratory.
Deletion of sequences of nucleic acids from the genetic material of an individual.
Tumors or cancer of the SKIN.
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.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Proteins transcribed from the E4 region of ADENOVIRUSES. The E4 19K protein transactivates transcription of the adenovirus E2F protein and complexes with it.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
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.
Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, Ki-ras, rasK) murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras genes have been detected in human, avian, murine, and non-vertebrate genomes. The closely related N-ras gene has been detected in human neuroblastoma and sarcoma cell lines. All genes of the family have a similar exon-intron structure and each encodes a p21 protein.
RNA present in neoplastic tissue.
Tumors or cancer of the LUNG.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.
Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing.
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.
Proteins coded by oncogenes. They include proteins resulting from the fusion of an oncogene and another gene (ONCOGENE PROTEINS, FUSION).
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
A basic helix-loop-helix transcription factor that plays a role in APOPTOSIS. It is composed of two subunits: ARYL HYDROCARBON RECEPTOR NUCLEAR TRANSLOCATOR and HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT.
Commonly observed structural components of proteins formed by simple combinations of adjacent secondary structures. A commonly observed structure may be composed of a CONSERVED SEQUENCE which can be represented by a CONSENSUS SEQUENCE.
Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
A technique for identifying specific DNA sequences that are bound, in vivo, to proteins of interest. It involves formaldehyde fixation of CHROMATIN to crosslink the DNA-BINDING PROTEINS to the DNA. After shearing the DNA into small fragments, specific DNA-protein complexes are isolated by immunoprecipitation with protein-specific ANTIBODIES. Then, the DNA isolated from the complex can be identified by PCR amplification and sequencing.
A cell line generated from human embryonic kidney cells that were transformed with human adenovirus type 5.
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.
A usually small, slow-growing neoplasm composed of islands of rounded, oxyphilic, or spindle-shaped cells of medium size, with moderately small vesicular nuclei, and covered by intact mucosa with a yellow cut surface. The tumor can occur anywhere in the gastrointestinal tract (and in the lungs and other sites); approximately 90% arise in the appendix. It is now established that these tumors are of neuroendocrine origin and derive from a primitive stem cell. (From Stedman, 25th ed & Holland et al., Cancer Medicine, 3d ed, p1182)
The ability of a protein to retain its structural conformation or its activity when subjected to physical or chemical manipulations.
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.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
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.
Gated transport mechanisms by which proteins or RNA are moved across the NUCLEAR MEMBRANE.
Biochemical identification of mutational changes in a nucleotide sequence.

C-myc overexpression and p53 loss cooperate to promote genomic instability. (1/16353)

p53 monitors genomic integrity at the G1 and G2/M cell cycle checkpoints. Cells lacking p53 may show gene amplification as well as the polyploidy or aneuploidy typical of many tumors. The pathways through which this develops, however, are not well defined. We demonstrate here that the combination of p53 inactivation and c-myc overexpression in diploid cells markedly accelerates the spontaneous development of tetraploidy. This is not seen with either N-myc or L-myc. Tetraploidy is accompanied by significantly higher levels of cyclin B and its associated cdc2 kinase activity. Mitotic spindle poisons accelerate the appearance of tetraploidy in cells either lacking functional p53 or overexpressing c-myc whereas the combination is additive. Restoration of p53 function in cells overexpressing c-myc causing rapid apoptosis, indicating that cells yet to become tetraploid have nonetheless suffered irreversible genomic and/or mitotic spindle damage. In the face of normal p53 function, such damage would either be repaired or trigger apoptotis. We propose that loss of p53 and overexpression of c-myc permits the emergence and survival of cells with increasingly severe damage and the eventual development of tetraploidy.  (+info)

Gadd45, a p53-responsive stress protein, modifies DNA accessibility on damaged chromatin. (2/16353)

This report demonstrates that Gadd45, a p53-responsive stress protein, can facilitate topoisomerase relaxing and cleavage activity in the presence of core histones. A correlation between reduced expression of Gadd45 and increased resistance to topoisomerase I and topoisomerase II inhibitors in a variety of human cell lines was also found. Gadd45 could potentially mediate this effect by destabilizing histone-DNA interactions since it was found to interact directly with the four core histones. To evaluate this possibility, we investigated the effect of Gadd45 on preassembled mononucleosomes. Our data indicate that Gadd45 directly associates with mononucleosomes that have been altered by histone acetylation or UV radiation. This interaction resulted in increased DNase I accessibility on hyperacetylated mononucleosomes and substantial reduction of T4 endonuclease V accessibility to cyclobutane pyrimidine dimers on UV-irradiated mononucleosomes but not on naked DNA. Both histone acetylation and UV radiation are thought to destabilize the nucleosomal structure. Hence, these results imply that Gadd45 can recognize an altered chromatin state and modulate DNA accessibility to cellular proteins.  (+info)

Regulation of p53 function and stability by phosphorylation. (3/16353)

The p53 tumor suppressor protein can be phosphorylated at several sites within the N- and C-terminal domains, and several protein kinases have been shown to phosphorylate p53 in vitro. In this study, we examined the activity of p53 proteins with combined mutations at all of the reported N-terminal phosphorylation sites (p53N-term), all of the C-terminal phosphorylation sites (p53C-term), or all of the phosphorylation sites together (p53N/C-term). Each of these mutant proteins retained transcriptional transactivation functions, indicating that phosphorylation is not essential for this activity of p53, although a subtle contribution of the C-terminal phosphorylation sites to the activation of expression of the endogenous p21(Waf1/Cip1)-encoding gene was detected. Mutation of the phosphorylation sites to alanine did not affect the sensitivity of p53 to binding to or degradation by Mdm2, although alteration of residues 15 and 37 to aspartic acid, which could mimic phosphorylation, resulted in a slight resistance to Mdm2-mediated degradation, consistent with recent reports that phosphorylation at these sites inhibits the p53-Mdm2 interaction. However, expression of the phosphorylation site mutant proteins in both wild-type p53-expressing and p53-null lines showed that all of the mutant proteins retained the ability to be stabilized following DNA damage. This indicates that phosphorylation is not essential for DNA damage-induced stabilization of p53, although phosphorylation could clearly contribute to p53 stabilization under some conditions.  (+info)

Different regulation of the p53 core domain activities 3'-to-5' exonuclease and sequence-specific DNA binding. (4/16353)

In this study we further characterized the 3'-5' exonuclease activity intrinsic to wild-type p53. We showed that this activity, like sequence-specific DNA binding, is mediated by the p53 core domain. Truncation of the C-terminal 30 amino acids of the p53 molecule enhanced the p53 exonuclease activity by at least 10-fold, indicating that this activity, like sequence-specific DNA binding, is negatively regulated by the C-terminal basic regulatory domain of p53. However, treatments which activated sequence-specific DNA binding of p53, like binding of the monoclonal antibody PAb421, which recognizes a C-terminal epitope on p53, or a higher phosphorylation status, strongly inhibited the p53 exonuclease activity. This suggests that at least on full-length p53, sequence-specific DNA binding and exonuclease activities are subject to different and seemingly opposing regulatory mechanisms. Following up the recent discovery in our laboratory that p53 recognizes and binds with high affinity to three-stranded DNA substrates mimicking early recombination intermediates (C. Dudenhoeffer, G. Rohaly, K. Will, W. Deppert, and L. Wiesmueller, Mol. Cell. Biol. 18:5332-5342), we asked whether such substrates might be degraded by the p53 exonuclease. Addition of Mg2+ ions to the binding assay indeed started the p53 exonuclease and promoted rapid degradation of the bound, but not of the unbound, substrate, indicating that specifically recognized targets can be subjected to exonucleolytic degradation by p53 under defined conditions.  (+info)

Analysis of genomic integrity and p53-dependent G1 checkpoint in telomerase-induced extended-life-span human fibroblasts. (5/16353)

Life span determination in normal human cells may be regulated by nucleoprotein structures called telomeres, the physical ends of eukaryotic chromosomes. Telomeres have been shown to be essential for chromosome stability and function and to shorten with each cell division in normal human cells in culture and with age in vivo. Reversal of telomere shortening by the forced expression of telomerase in normal cells has been shown to elongate telomeres and extend the replicative life span (H. Vaziri and S. Benchimol, Curr. Biol. 8:279-282, 1998; A. G. Bodnar et al., Science 279:349-352, 1998). Extension of the life span as a consequence of the functional inactivation of p53 is frequently associated with loss of genomic stability. Analysis of telomerase-induced extended-life-span fibroblast (TIELF) cells by G banding and spectral karyotyping indicated that forced extension of the life span by telomerase led to the transient formation of aberrant structures, which were subsequently resolved in higher passages. However, the p53-dependent G1 checkpoint was intact as assessed by functional activation of p53 protein in response to ionizing radiation and subsequent p53-mediated induction of p21(Waf1/Cip1/Sdi1). TIELF cells were not tumorigenic and had a normal DNA strand break rejoining activity and normal radiosensitivity in response to ionizing radiation.  (+info)

Immunohistochemical expression of mdm2 and p21WAF1 in invasive cervical cancer: correlation with p53 protein and high risk HPV infection. (6/16353)

AIM: To investigate the immunocytochemical staining pattern of mdm2 and p21WAF1 proteins in invasive cervical cancer and to determine its relation with the expression of p53 and with the high risk HPV infection. METHODS: Immunocytochemistry for p53, mdm2, and p21WAF1 was performed in 31 paraffin embedded sections of invasive cervical cancer. The results were assessed by image analysis, evaluating for each protein the optical density of the immunostained area, scored as percentage of the total nuclear area. The presence of high risk human papillomavirus (HPV) infection was detected by using the polymerase chain reaction. RESULTS: Immunostaining for both mdm2 and p21WAF1 was correlated with p53 expression; however, the correlation between p53 and mdm2 (R = 0.49; p < 0.01) was more significant than between p53 and p21WAF1 (R = 0.31; p < 0.05); the less stringent correlation between p53 and p21WAF1 might reflect the p53 independent mechanisms of p21WAF1 induction. Similar average levels of p53, mdm2, and p21WAF1 immunostaining were found in the presence or absence of high risk HPV-DNA, without significant differences between the two groups. CONCLUSIONS: These data suggest that mdm2 and p21WAF1 proteins are expressed in invasive cervical cancer and that their immunocytochemical staining pattern is not abrogated by the presence of high risk HPV genomic sequences.  (+info)

Definition of a major p53 binding site on Ad2E1B58K protein and a possible nuclear localization signal on the Ad12E1B54K protein. (7/16353)

Previous studies have established that adenovirus 2/5 early region 1B (Ad E1B) 58K protein binds p53 strongly and co-localizes with it to cytoplasmic dense bodies whilst the homologous Ad12E1B54K protein binds only weakly and co-localizes primarily to the nucleus in Ad12E1 transformed cells. We have used these properties of the E1B proteins from different viral serotypes to map the p53 binding site on the Ad2/5 protein. A set of chimaeric genes was constructed containing different proportions of the Ad12 and Ad2E1B DNA. These, together with Ad12E1A and E1B19K DNA, were transfected into baby rat kidney cells and transformed lines isolated. From an examination of the properties of these Ad12/Ad2E1B fusion proteins in co-immunoprecipitation and subcellular localization experiments it has been concluded that the p53 binding site on Ad2E1B58K protein lies between amino acids 216 and 235 and that the homologous region on Ad12E1B54K protein also binds p53. In addition, a unique nuclear localization signal is located on Ad12E1B54K between residues 228 and 239. We suggest that primary structure differences in these regions of the Ad2 and Ad12E1B proteins are responsible for the different subcellular localizations in AdE1 transformants.  (+info)

Correlation between the status of the p53 gene and survival in patients with stage I non-small cell lung carcinoma. (8/16353)

The association of p53 abnormalities with the prognosis of patients with non-small cell lung carcinoma (NSCLC) has been extensively investigated to date, however, this association is still controversial. Therefore, we investigated the prognostic significance of p53 mutations through exons 2 to 11 and p53 protein expression in 103 cases of stage I NSCLC. p53 mutations were detected in 49 of 103 (48%) tumors. Two separate mutations were detected in four tumors giving a total of 53 unique mutations in 49 tumors. Ten (19%) of mutations occurred outside exons 5-8. Positive immunohistochemical staining of p53 protein was detected in 41 of 103 (40%) tumors. The concordance rate between mutations and protein overexpression was only 69%. p53 mutations, but not expression, were significantly associated with a shortened survival of patients (P<0.001). Furthermore, we investigated the correlation between the types of p53 mutations and prognosis. p53 missense mutations rather than null mutations were associated with poor prognosis (P < 0.001 in missense mutations and P=0.243 in null mutations). These results indicated that p53 mutations, in particular missense mutations, rather than p53 expression could be a useful molecular marker for the prognosis of patients with surgically resected stage I NSCLC.  (+info)

TPRG1LP1 (tumor protein p63 regulated 1 like pseudogene 1), Authors: Dessen P. Published in: Atlas Genet Cytogenet Oncol Haematol.
The p53 tumor suppressor protein plays a crucial role in tumorigenesis by controlling cell-cycle progression and apoptosis. exacerbate this effect. Cell-cycle studies indicated that TSAP6 could augment Myt1 activity. Overall, KSHV ORF26 antibody these data suggest that TSAP6 may take action downstream to p53 to interface apoptosis and cell-cycle progression. A series of 10 differentially expressed genes designated as either tumor suppressor activated pathway (TSAP) or tumor suppressor inhibited pathway (TSIP) have been described that were either up- or down-regulated, respectively, by p53 activation in LTR6 cells (1). LTR6 cells are derivatives of the murine myeloid M1 cell collection transporting the Val-135 temperature-sensitive p53 mutant (2). After shifting to 32C, LTR6 cells acquire wild-type p53 function and subsequently undergo massive apoptosis (2). Among the isolated genes characterized subsequently are Siah1b (TSAP3) and presenilin-1 (TSIP2) (1). Siah1b is the mammalian homologue of ...
MDM2 is an E3 ubiquitin ligase that binds and ubiquitinates the tumor suppressor protein p53, leading to its proteasomal degradation. Nutlin-3a (Nutlin) is a preclinical drug that binds MDM2 and prevents the interaction between MDM2 and p53, leading to p53 stabilization and activation of p53 signaling events. Previous studies have reported that Nutlin promotes growth arrest and/or apoptosis in cancer cells that express wild-type p53. In the current study, Nutlin treatment caused a cytoskeletal rearrangement in p53 wild-type human cancer cells from multiple etiologies. Specifically, Nutlin decreased actin stress fibers and reduced the size and number of focal adhesions in treated cells. This process was dependent on p53 expression but was independent of p21 expression and growth arrest. Consistent with this, Nutlin-treated cells failed to form filamentous actin-based motility structures (lamellipodia) and displayed significantly decreased directional persistence in response to migratory cues. ...
The p110α and p110β catalytic subunits of phosphoinositide 3-kinase (PI3K) regulate cell cycle events. Marqués et al. found that NIH 3T3 cells overexpressing p110β, but not p110α, divided more rapidly than control cells, whereas cells expressing a catalytically inactive p110β point mutant (Lys805→Arg; K805R) divided more slowly than control cells or cells expressing a catalytically inactive p110α mutant. Specifically, S phase progression was accelerated in cells overexpressing p110β and slowed in cells expressing the K805R mutant, suggesting a role for p110β in DNA elongation. Individual DNA fibers were isolated from synchronously dividing NIH 3T3 cells treated with inhibitors specific for p110α (PIK75) or for p110β (TGX221) and subsequently incubated with bromodeoxyuridine (BrdU). In DNA fibers from TGX221-treated cells, the BrdU-labeled sections were shorter in length and closer together compared with those from PIK75-treated cells, implying that replication fork progression was ...
Tumor protein p53, encoded in humans by the TP53 gene, was originally identified based on its interaction with the large T antigen of simian virus 40 (SV40). p53 is expressed at low levels in most cell types but is upregulated in many transformed (cancer) cell lines. In response to cellular stress, p53 regulates over 100 target genes that control cell cycle arrest, apoptosis, senescence, DNA repair, and metabolic changes. p53 protein has multiple domains that include DNA-binding, transactivation, and oligomerization activities. Mutations in the TP53 gene cause loss of tumor suppression activity and are found in more than 50% of human tumors. Multiple isoforms of p53 are known, with distinct DNA-binding and transcriptional activation properties. p53 is also known as cellular tumor antigen p53, p53 tumor suppressor, transformation-related protein 53, BCC7, LFS1, TRP53, and antigen NY-CO-13.. ...
Tumor Suppressor Proteins: 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.
Treating Cancer by Tinkering with the Clock E. Cancer is the leading cause of death in North Carolina, and death rates from cancer have been escalating since the early 1980s. One of the most significant advances in cancer prevention and treatment in recent years has been recognition of the importance of apoptosis, or programmed cell death, which provides new opportunities for the discovery of cancer therapeutic targets and agents. The protein tumor suppressor p53 plays a critical role in apoptosis induced by anticancer drugs; however, at least 50 percent of human cancers lack functional p53. Lee discovered that disrupting the circadian clock-the major regulatory system that ensures proper adaptation to the constantly changing environment-functionally activates the p73 tumor suppressor protein, which induces cell death in p53-deficient cancer cells. His study indicates that this mechanism provides another way to overcome the resistance to apoptosis of cancer cells selectively.. ...
Knockout Tested Mouse monoclonal p53 antibody [PAb 1801]. Validated in WB, IP, ELISA, RIA, ChIP and tested in Human. Cited in 44 publication(s). Independently reviewed in 10 review(s).
PIG11 protein may play an important role by interaction with other biological molecules in the regulation of apoptosis and provided us a novel angel of view to explore the possible function of PIG11 in vivo ...
The retinoblastoma and p53 pathways represent the major tumor suppressor pathways in mammals and are crucial for the control of cell proliferation and the response to cellular insults (19-21). Rb is frequently mutated or expressed at low levels in several tumors such as retinoblastoma, osteosarcoma, as well as small lung, prostate, bladder, and breast carcinomas (22-26). Thus, miRNAs controlling Rb protein levels are of high clinical interest. Here, we show that miR-335 efficiently controls Rb1 (pRb/p105) protein levels by directly targeting a conserved region in the 3′UTR of Rb1 in placental mammals. Our data show that miR-335-mediated reduction of Rb1 protein results in the activation of the p53 pathway in human and mouse cells, impairing cell proliferation and neoplastic transformation in vitro. In line with this, impairing the p53 pathway is sufficient to drive hyperproliferation and increased transformation in the context of ectopically increased miR-335 levels. We conclude that miR-335 ...
Evaluation of Coupled Nuclear and Cytoplasmic p53 Dynamics: 10.4018/978-1-4666-3604-0.ch061: The tumor suppressor protein p53 predominantly serves as a sequence specific transcription factor that may be activated upon exposure to diverse stimuli. One
TP53 encodes a major tumor suppressor transcription factor, p53, which plays a significant role in regulating cellular responses to DNA damage and other genomic anomalies.
TP53 encodes a major tumor suppressor transcription factor, p53, which plays a significant role in regulating cellular responses to DNA damage and other genomic anomalies.
Dactinomycin;Tumor Necrosis Factor-alpha;Up-Regulation;Tumor Suppressor Protein p53;Papillomaviridae;Oncogene Proteins, Viral;Ceramides;DNA-Binding Proteins;Repressor Proteins;Cell Cycle Checkpoints;Apoptosis;DNA Damage; ...
Dactinomycin;Tumor Necrosis Factor-alpha;Up-Regulation;Tumor Suppressor Protein p53;Papillomaviridae;Oncogene Proteins, Viral;Ceramides;DNA-Binding Proteins;Repressor Proteins;Cell Cycle Checkpoints;Apoptosis;DNA Damage; ...
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p53 antibody [DO-7] (ready-to-use) (tumor protein p53) for IHC-Fr, IHC-P. Anti-p53 mAb (GTX20911) is tested in Human samples. 100% Ab-Assurance.
Two years ago, OShea discovered that E4-ORF3 clears the way for adenovirus to proliferate by deactivating genes that help the cell defend itself against the virus. It literally creates zip files of p53 target genes by compressing them until they can no longer be read, she explains. E4-ORF3 self-assembles inside cells into a disordered, web-like structure that captures and inactivates different tumor suppressor protein complexes. Horng Ou, a postdoctoral researcher in OSheas laboratory, says E4-ORF3 is unusual. It doesnt resemble any known proteins that assemble polymers or that function in cellular tumor suppressor pathways, he says. Most cellular polymers and filaments form uniform, rigid chains. But E4-ORF3 is the viruss Swiss army knife-it assembles into something that is highly versatile. It has the ability to build itself into all sorts of different shapes and sizes that can capture and deactivate the many defenses of a host cell. In collaboration with scientists from the ...
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Nickeleit, I.; Zender, S.; Sasse, E.; Geffers, R.; Brandes, G.; Soerensen, I.; Steinmetz, H.; Kubicka, S.; Carlomagno, T.; Menche, D. et al.; Guetgemann, I.; Buer, J.; Gossler, A.; Manns, M. P.; Kalesse, M.; Frank, R.; Malek, N. P.: Argyrin a reveals a critical role for the tumor suppressor protein p27kip1 in mediating antitumor activities in response to proteasome inhibition. Cancer Cell 14 (1), pp. 23 - 35 (2008 ...
The tumor suppressor protein p53 is often referred to as the guardian of the genome. In the past, controversial findings have been presented for the role of ...
p73 antibody [N1C1] (tumor protein p73) for ICC/IF, IHC-P, WB. Anti-p73 pAb (GTX109045) is tested in Human samples. 100% Ab-Assurance.
TP63 - TP63 (untagged)-Human tumor protein p63 (TP63), transcript variant 1 available for purchase from OriGene - Your Gene Company.
TP73 - TP73 (untagged)-Human tumor protein p73 (TP73), transcript variant 2 available for purchase from OriGene - Your Gene Company.
Complete information for TP53INP1 gene (Protein Coding), Tumor Protein P53 Inducible Nuclear Protein 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
Vernon, E. G.; Malik, K.; Reynolds, P.; Powlesland, R.; Dallosso, A. R.; Jackson, S.; Henthorn, K.; Green, E. D.; Brown, K. W. The parathyroid hormone-responsive B1 gene is interrupted by a t(1;7)(q42;p15) breakpoint associated with Wilms tumour. Oncogene 22: 1371-1380, 2003. PubMed ID : (...). ...
Expression of the tumor suppressor p53 is activated in response to cell stress. The dynamics of p53 activation can vary, depending on the stressor, resulting in either pulsatile or constant p53 levels; however, the functional consequence of these different dynamics is unclear. Purvis et al. developed a method to control p53 dynamics in human cells. Pulsing p53 selectively activated genes involved in cell cycle arrest and DNA repair, allowing recovery from DNA damage. In contrast, sustained p53 promoted induction of terminal genes leading to cellular senescence. Thus, protein dynamics can affect cell fate decisions.. J. E. Purvis, K. W. Karhohs, C. Mock, E. Batchelor, A. Loewer, G. Lahav, p53 dynamics control cell fate. Science 336, 1440-1444 (2012). [Abstract] [Full Text] ...
Cytochromes P450 form a very large superfamily of proteins which metabolize substrates from steroids to fatty acids to drugs and are found in organisms from protists to mammals. P450s all appear to take on a similar structural fold, yet frequently having less than 20% sequence identity and having va …
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Effects of exogenous p62-overexpression. (a) H23 cells were transfected with indicated siRNAs for 3 days. After transfection, cell viability was measured, and
p53小鼠单克隆抗体[DO-1](ab1101)可与人样本反应并经WB, IP, ELISA, IHC, Flow Cyt, ChIP, ICC/IF实验严格验证,被8篇文献引用并得到10个独立的用户反馈。
Aileron is the clinical-stage leader in the field of stapled peptide therapeutics for cancers and other diseases. Our lead product candidate ALRN-6924, which is being evaluated in multiple clinical trials, reactivates p53-mediated tumor suppression by targeting both of the primary p53 suppressor proteins, MDMX and MDM2. The p53 protein is long known for its central role in preventing cancer initiation and progression, and its inactivation is essential for the formation of virtually all cancers. We believe that ALRN-6924 is the first and only product candidate in clinical development that can disrupt the interaction of both MDMX and MDM2 to restore p53 function as the bodys first line of defense against cancer.
Aileron is the clinical-stage leader in the field of stapled peptide therapeutics for cancers and other diseases. Our lead product candidate ALRN-6924, which is being evaluated in multiple clinical trials, reactivates p53-mediated tumor suppression by targeting both of the primary p53 suppressor proteins, MDMX and MDM2. The p53 protein is long known for its central role in preventing cancer initiation and progression, and its inactivation is essential for the formation of virtually all cancers. We believe that ALRN-6924 is the first and only product candidate in clinical development that can disrupt the interaction of both MDMX and MDM2 to restore p53 function as the bodys first line of defense against cancer.
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Tumor protein 53 (p53) is a critical regulator of cell cycle and apoptosis that is frequently disabled in human tumors. In many tumor types, p53 is deleted or mutated, but in others p53 is inactivated by overexpression or amplification of its negative regulator mouse double minute 2 (MDM2). A high-t …
Buy anti-TP53BP1 antibody, Mouse anti-Human Tumor Protein p53 Binding Protein 1 (TP53BP1) Monoclonal Antibody-NP_001135451.1 (MBS2090542) product datasheet at MyBioSource, Primary Antibodies. Application: Western Blot (WB), Immunohistochemistry (IHC), Immunocytochemistry (ICC), Immunoprecipitation (IP)
View Notes - Cancer - Copy from BIO 6 at East Los Angeles College. Tumor-suppressor genes help prevent uncontrolled cell growth Tumor-suppressor Proteins: Repair of damaged DNA, control cell adhesion
Tumor protein p53, also known as p53, cellular tumor antigen p53 (UniProt name), phosphoprotein p53, tumor suppressor p53, antigen NY-CO-13, or transformation-related protein 53 (TRP53), is any isoform of a protein encoded by homologous genes in various organisms, such as TP53 (humans) and Trp53 (mice). This homolog (originally thought to be, and often spoken of as, a single protein) is crucial in multicellular organisms, where it prevents cancer formation, thus, functions as a tumor suppressor. As such, p53 has been described as the guardian of the genome because of its role in conserving stability by preventing genome mutation. Hence TP53 is classified as a tumor suppressor gene. (Italics are used to denote the TP53 gene name and distinguish it from the protein it encodes.) The name p53 was given in 1979 describing the apparent molecular mass; SDS-PAGE analysis indicates that it is a 53-kilodalton (kDa) protein. However, the actual mass of the full-length p53 protein (p53α) based on the sum ...
Marcoux N, Gettinger SN, OKane G, Arbour KC, Neal JW, Husain H, Evans TL, Brahmer JR, Muzikansky A, Bonomi PD, Del Prete S, Wurtz A, Farago AF, Dias-Santagata D, Mino-Kenudson M, Reckamp KL, Yu HA, Wakelee HA, Shepherd FA, Piotrowska Z, Sequist LV. EGFR-Mutant Adenocarcinomas That Transform to Small-Cell Lung Cancer and Other Neuroendocrine Carcinomas: Clinical Outcomes. J Clin Oncol. 2019 02 01; 37(4):278-285 ...
The MDM4 gene encodes a nuclear protein that contains a p53 binding domain at the N-terminus and a RING finger domain at the C-terminus. It is the human homolog of mouse double minute 4 (MDM4) protein and shows structural similarity to p53-binding protein MDM2. MDM4 is also called Mdm4 p53 binding protein homolog (mouse); transformed 3T3 cell double minute 4, p53 binding protein (mouse); MDMX, Mdm2-like p53-binding protein, HDMX, MRP1, MDM4-related protein 1, double minute 4 protein, and p53-binding protein Mdm4. Both MDM4 and MDM2 bind the p53 tumor suppressor protein and inhibit its activity, and have been shown to be overexpressed in a variety of human cancers. However, unlike MDM2 which degrades p53, MDM4 inhibits p53 by binding its transcription activation domain. MDM4 can reverse MDM2-targeted degradation of p53, while maintaining suppression of p53 activity.. ...
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Apoptosis is a normal physiological process which eliminates cells that do not receive adequate extracellular signals. One of the pathways signalling apoptosis is controlled by the small GTPases of the Rho family, also involved in cell proliferation, differentiation and motility. Another major apoptosis signalling pathway involves the p53 tumour suppressor which is activated by a variety of stress and mediates growth arrest or apoptosis in normal cells. We show here that upon detachment from the extracellular matrix, fibroblasts undergo rapid apoptosis that can be rescued by constitutive activation of Rac1 and Cdc42Hs GTPases. Conversely, inhibition of Rac1 and Cdc42Hs efficiently triggers apoptosis in adherent cells. Interestingly, apoptosis is not observed in p53-/- cells either cultured in suspension or inhibited for Rac1 and Cdc42Hs activity. Moreover, Rac1 and Cdc42Hs extinction in normal cells activates endogenous p53. Using specific inhibitors of MAPK pathways, we demonstrate that, in our ...
p53 Tumor Suppressor Protein Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone DO-7 ] validated in WB, IHC-P, IF, FC (AH10778-100), Abgent
Cellular senescence is an irreversible state of terminal growth arrest that requires functional p53. Acting to block tumor formation, induction of senescence has also been demonstrated to contribute to tumor clearance via the immune system following p53 reactivation.1, 2 The Hdm2-antagonist, Nutlin-3a, has been shown to reactivate p53 and induce a quiescent state in various cancer cell lines,3, 4 similar to the G1 arrest observed upon RNAi targeting of Hdm2 in MCF7 breast cancer.5 In the present study we show that HdmX, a negative regulator of p53, impacts the senescence pathway. Specifically, overexpression of HdmX blocks Ras mediated senescence in primary human fibroblasts. The interaction of HdmX with p53 and the re-localization of HdmX to the nucleus through Hdm2 association appear to be required for this activity. Furthermore, inhibiting HdmX in prostate adenocarcinoma cells expressing wild-type p53, mutant Ras and high levels of HdmX induced cellular senescence as measured by an increase in
This gene encodes a member of the ASPP (apoptosis-stimulating protein of p53) family of p53 interacting proteins. The protein contains four ankyrin repeats and an SH3 domain involved in protein-protein interactions. It is localized to the perinuclear region of the cytoplasm, and regulates apoptosis and cell growth through interactions with other regulatory molecules including members of the p53 family. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008 ...
ATP1B2 Antibody (Center), Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab) validated in WB, IHC-P, FC, E (AP9271c), Abgent
KIAA1644 Antibody (N-term), Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab) validated in IHC-P, WB, E (AP10426a), Abcepta
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Cervical cancer is the second leading cause of death from cancer in women worldwide, and recent epidemiological studies have strongly implicated the sexually transmitted human papillomavirus (HPV) as a causative agent. The ability of high-risk HPVs to contribute to malignant progression seems to depend on expression of the viral E6 and E7 oncogenes. The E6 oncoprotein forms a complex with the cellular tumor suppressor protein p53, leading to degradation of p53 via ubiquitin-dependent proteolysis. Thus, E6 expression results in the loss of p53 function in cells, including stimulation of apoptosis and inhibition of the expression of the antiapoptotic protein bcl-2. Recently, we found increased bcl-2 expression in cervical carcinoma cell lines containing mutated or E6-inactivated p53 (X. L. Liang, S. Mungal, A. Ayscue, J. D. Meissner, P. Wodnicki, G. Gordon, S. Lockett, and B. Herman. J. Cell. Biochem., 57: 509-520, 1995). Based on these findings, we examined Papanicolaou smears from 94 women with ...
The oncoprotein MdmX (mouse double minute X) is highly homologous to Mdm2 (mouse double minute 2) in terms of their amino acid sequences and three-dimensional conformations, but Mdm2 inhibitors exhibit very weak affinity for MdmX, providing an excellent model for exploring how protein conformation distinguishes and alters inhibitor binding. The intrinsic conformation flexibility of proteins plays ...
The oncoprotein MdmX (mouse double minute X) is highly homologous to Mdm2 (mouse double minute 2) in terms of their amino acid sequences and three-dimensional conformations, but Mdm2 inhibitors exhibit very weak affinity for MdmX, providing an excellent model for exploring how protein conformation distinguishes and alters inhibitor binding. The intrinsic conformation flexibility of proteins plays ...
Tumor protein p53, a nuclear protein, plays an essential role in the regulation of cell cycle, specifically in the transition from G0 to G1. It is found in very low levels in normal cells, however, in a variety of transformed cell lines, it is expressed in high amounts, and believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing DNA-binding, oligomerization and transcription activation domains. It is postulated to bind as a tetramer to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome ...
The polymorphism SNP309 (rs2279744) in the promoter region of the MDM2 gene has been shown to alter protein expression and may play a role in the susceptibility to lung cancer. The MDM2 protein is a key inhibitor of p53 and several mechanisms of MDM2/p53 interactions are presently known: modulating DNA-repair, cell-cycle control, cell growth and apoptosis. We used 635 Caucasian patients diagnosed with lung cancer before 51 years of age and 1300 healthy gender and age frequency matched population Caucasian controls to investigate the association between the MDM2 SNP309 and the risk of developing early onset lung cancer. Conditional logistic models were applied to assess the genotype-phenotype association, adjusted for smoking. Compared to the GG genotype, the adjusted ORs for the TG and TT genotype were 0.9 (95% CI: 0.7-1.5) and 1.0 (95% CI: 0.7-1.5), respectively. Also no association was found for histological subtypes of lung cancer. The strength of this study is that within young cases the genetic
Human cancer develops as a result of accumulation of mutations in oncogenes and tumor suppressor genes. Zinc finger protein 668 (ZNF668) has recently been identified and validated as one of the highly mutated genes in breast cancer, but its function is entirely unknown. Here, we report two major functions of ZNF668 in cancer development. (1) ZNF668 functions as a tumor suppressor by regulating p53 protein stability and function. We demonstrate that ZNF668 is a nucleolar protein that physically interacts with both MDM2 and p53. By binding to MDM2, ZNF668 regulates MDM2 autoubiquitination and prevents MDM2-mediated p53 ubiquitination and degradation; ZNF668 deficiency impairs DNA damage-induced p53 stabilization. Notably, ZNF668 effectively suppresses breast cancer cell proliferation and transformation in vitro and tumorigenicity in vivo. Consistently, ZNF668 knockdown readily transforms normal mammary epithelial cells. Together, our studies identify ZNF668 as a novel breast tumor suppressor gene that
The polymorphism SNP309 (rs2279744) in the promoter region of the MDM2 gene has been shown to alter protein expression and may play a role in the susceptibility to lung cancer. The MDM2 protein is a key inhibitor of p53 and several mechanisms of MDM2/p53 interactions are presently known: modulating DNA-repair, cell-cycle control, cell growth and apoptosis. We used 635 Caucasian patients diagnosed with lung cancer before 51 years of age and 1300 healthy gender and age frequency matched population Caucasian controls to investigate the association between the MDM2 SNP309 and the risk of developing early onset lung cancer. Conditional logistic models were applied to assess the genotype-phenotype association, adjusted for smoking. Compared to the GG genotype, the adjusted ORs for the TG and TT genotype were 0.9 (95% CI: 0.7-1.5) and 1.0 ( 95% CI: 0.7-1.5), respectively. Also no association was found for histological subtypes of lung cancer. The strength of this study is that within young cases the ...
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Idea Proposed/Formulated by:Dr L Boominathan Ph.D.. Terms & Conditionsapplyhttp://genomediscovery.org/registration/terms-and-conditions/. Citation:Boominathan, Natural product-based therapy for p53-mutated human cancers: Ursolic acid increases the expression of tumor suppressor p53 homologue TAp63 via down regulation of its target gene, 4/March/2015, 8.31 am,Genome-2-Bio-MedicineDiscovery center(GBMD),http://genomediscovery.org. Significance:This study suggests, for the first time, that Ursolic acid,by decreasing the expression of its target gene,it may increase the expression of TAp63. Thereby, it may inhibit cancer progression.Thus,pharmacological formulationsencompassingUrsolic acid or its analogues can be used to inhibit the progression of human tumors.. Amount: $ 300*. Undisclosed information:How Ursolic acidincreases the expression ofTAp63. Web:http://genomediscovery.org. Courtesy:When you cite drop us a line [email protected] * Research cooperation. ...
The p53 tumor suppressor protein is a transcriptional activator and its transcriptional activity is required for p53 tumor suppression. We show here that p53 markedly activates expression of cyclin DI and the induction of cyclin Dl is at least partially mediated by p21, a target of p53. To further understand features of p53 that contribute to cell cycle arrest and apoptosis several p53-null cell lines were generated that inducibly express wild-type or mutant forms of p53. Our results show that the cellular level of p53 can dictate the response of the cell to undergo either cell cycle arrest or apoptosis and DNA damage can heighten the apoptotic response to p53. We also demonstrate that a full apoptotic response to pS3 requires both its N- and C-termini. In addition, we identify a novel activity within amino acids 43-63 which can activate transcription and mediate apoptosis. Furthermore, we show that the N-terminus of p53 is the target for destabilization mediated by ubiquitin and calpaln and
An essential property of p53 as a tumour suppressor is its ability to induce cell cycle arrest and DNA repair, or apoptotic cell death in response to DNA damage [1]. Whilst it is clear that transcriptional upregulation of specific genes by p53 is crucial in determining cellular outcome, the molecular basis for target gene selectivity remains elusive. To shed light on the considerable amount of data available on this subject, this review summarizes three basic models supported by published literature. Target gene selectivity and cell fate decisions by p53 can be explained, at least in part, by differences in p53 affinity to specific target gene promoters, the effect of post‐translational modifications on p53 and the influence of interacting proteins on target gene selectivity. The underlying mechanisms are perhaps more complicated on the basis of the heterogeneity of p53 responses in vivo, which can be both tissue‐ and stimulus‐specific (reviewed in reference [15]).. Other evidence suggests ...
Aging published Cdkn1a transcript variant 2 is a marker of aging and cellular senescence which reported that cellular senescence is a cell fate response characterized by a permanent cell cycle arrest driven primarily the by cell cycle inhibitor and tumor suppressor proteins p16Ink4a and p21Cip1/Waf1.
In this report, we have demonstrated previously unrealized transcriptional cross talk between the tumor suppressor protein p53 and NF-κB. This regulatory mechanism provides a molecular explanation for how the divergent functional consequences of p53 and NF-κB activation can be integrated by the cell. In these experiments, we show that the ability of p53 or RelA to stimulate transcription is strongly influenced by the relative level of the other protein. Importantly, we have been able to demonstrate that this effect can be observed both with cotransfected expression plasmids (Fig. 1 and 2) and with endogenous levels of these transcription factors (Fig. 4 and 5), indicating its biological relevance and significance. Furthermore, we demonstrate that these results are consistent with competition between p53 and NF-κB for limiting quantities of complexes containing the p300 and CBP coactivator proteins (Fig. 6 and 7). While this report was under review, Ravi et al. similarly reported repression of ...
The tumor suppressor protein p53 binds sequence-specifically to defined DNA targets in the genome. The consensus DNA response element (RE) consists of two decameric half-sites (HS) with the general form RRRCWWGYYY (R=A,G;W=A,T;Y=C,T), separated by a varia
The tumor suppressor protein p53 binds sequence-specifically to defined DNA targets in the genome. The consensus DNA response element (RE) consists of two decameric half-sites (HS) with the general form RRRCWWGYYY (R=A,G;W=A,T;Y=C,T), separated by a varia
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Nutlin-3 is a Mdm2 (mouse double minute 2) antagonist (IC₅₀ = 90 nM for Nutlin-3a and 13.6 µM for Nutlin-3b), p53 pathway activator, and apoptosis inducer.
p63 is a homologue of the tumour suppressor p53. The p53 family of transcription factors consists of three members: p53, p63 and p73 (Mills, 2005). p63 possesses at least two promoters that direct the expression of two fundamentally different classes of protein, namely one which contains an N-terminal transactivation (TA) domain and one which lacks this domain, the N-terminally truncated (ΔN) isoform (Yang et al., 1998). Extensive alternative splicing is seen at the 3′ end of p63 transcripts resulting in three different C termini: α, β andγ . Exogenously expressed p63 can bind to consensus p53 target sequences, and can activate and repress the promoters of several p53 responsive genes. It is generally assumed that ΔNp63 isoforms are repressor molecules against TAp63 and p53. However, the physiological targets, either induced or repressed by p63, are largely unknown (Levrero et al., 2000; Westfall and Pietenpol, 2004).. Despite the high similarity in their transcriptional activities, ...
Rabbit polyclonal antibody raised against synthetic peptide of DUSP19. A synthetic peptide corresponding to amino acids 74-89 of human DUSP19. (PAB14631) - Products - Abnova
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us), National Center for Biotechnology Information (1998-01-01). The p53 tumor suppressor protein. National Center for ... These effects seem to be largely mediated by mutations at guanine in codon 249 of the p53 gene, a tumor suppressing gene, and ... TA transversion at codon 249 of p53, a characteristic mutation seen with this toxin. Prevalence of hepatocellular carcinoma in ... "Aflatoxin genotoxicity is associated with a defective DNA damage response bypassing p53 activation". Liver International. 31 (4 ...
Information (US), National Center for Biotechnology (1998). The p53 tumor suppressor protein. National Center for Biotechnology ... such as caspase proteins and Bcl-2 family regulation proteins. Before such process, the cell cycle withdrawal ensures that ... The CDK detects the presence of these cyclins by binding with these cyclins and produce a type of target protein to move the ... Another type of negative regulator is p53, which halts the cell cycle process upon detection of DNA damage so as to provide to ...
P53 The p53 tumor suppressor protein. National Center for Biotechnology Information (US). 1998. http://www.hsph.harvard.edu/ ... The p53 gene is known as the tumor suppressor gene. Molecular Epidemiology of Hereditary Cancers In his bio on the Harvard T.H ... These investigations have led to the identification and isolation of human cancer genes, the tumor suppressor genes. These ... The diversity of tumor types in this syndrome suggests pathogenetic mechanisms which differ from hereditary cancers arising in ...
... aggregation-prone mutants of the tumor-suppressor protein p53; and semen proteins whose aggregation enhances HIV infection. ... Examples include the proteins involved in Alzheimer's disease - amyloid β-protein (Aβ) and tau; α-synuclein, which is thought ... Amyloid β-protein Assembly: The Effect of Molecular Tweezer CLR01 and CLR03. J. Phys. Chem. B, 2015; 119: 4831-4841. S ... T Schrader, G Bitan, and F-G Klärner, Molecular Tweezers for Lysine and Arginine - Powerful Inhibitors of Pathologic Protein ...
The p53 gene codes for the tumor suppressor p53 proteins. A mutation in this gene can lead to formation of tumors. Five p53 ... In one study, out of 171 workers in a plant manufacturing 4-aminobiphenyl, 11% of them developed bladder tumors. Tumors ... One mechanism by which 4-ABP causes bladder cancer is a mutation in the p53 gene, which are seen in thirty to sixty percent of ... A linear correlation was found between adduct levels and the occurrence of liver tumors in female mice by comparing DNA adducts ...
Tumor suppressor protein 53 (p53) is mutated early in the disease. p53 is the "guardian of the genome", which, during DNA and ... When p53 itself is mutated, other mutations can survive. Phosphatase and tensin homolog (PTEN), another tumor suppressor gene, ... Typically, any tumour presenting as above WHO grade I (i.e. a malignant tumour as opposed to a benign tumour) will have a ... Glioma at the Human Protein Atlas American Brain Tumor Association: Malignant Gliomas Brain and Spinal Tumors: Hope Through ...
This is a consequence of p53, tumor suppressor protein, being inactivated. Wild-type p53 have been shown to suppress cyclin B1 ... A possible treatment option for tumor suppression is to deliver gene or protein to target the degradation of cyclin B1. ... of cyclin B1 as a tumor antigen is a result of its overexpression in human tumors that is caused by non-functional p53". Mol. ... G2/mitotic-specific cyclin-B1 is a protein that in humans is encoded by the CCNB1 gene. Cyclin B1 is a regulatory protein ...
T-antigen also binds and inactivates tumor suppressor proteins (p53, p105-Rb). This causes the cells to leave G1 phase and ... and p53 tumor suppressor proteins. In addition, TAg binds to several other cellular factors, including the transcriptional co- ... Kim HY, Ahn BY, Cho Y (15 January 2001). "Structural basis for the inactivation of retinoblastoma tumor suppressor by SV40 ... Protein-protein interactions between T-antigen and DNA polymerase-alpha directly stimulate replication of the virus genome. ...
"Functional association between Wwox tumor suppressor protein and p73, a p53 homolog". Proc. Natl. Acad. Sci. U.S.A. 101 (13): ... The encoded protein is more than 90% identical to the mouse protein, which is an essential mediator of tumor necrosis factor- ... "An opposing view on WWOX protein function as a tumor suppressor". Cancer Res. 63 (24): 8629-33. PMID 14695174. Chen ST, Chuang ... A candidate tumor suppressor gene involved in multiple tumor types". Proc. Natl. Acad. Sci. U.S.A. 98 (20): 11417-22. doi: ...
"Molecular interactions between telomerase and the tumor suppressor protein p53 in vitro". Oncogene. 18 (48): 6785-94. doi: ... The telomerase-associated proteins are conserved from ciliates to humans. It is also a minor vault protein. GRCh38: Ensembl ... "A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration". Cell. 125 (4): ... Telomerase protein component 1 is an enzyme that in humans is encoded by the TEP1 gene. This gene product is a component of the ...
This transcript negatively regulates tumor suppressor genes such as tumor protein p53. Expression of this locus may be a marker ... "Nuclear retention of the lncRNA SNHG1 by doxorubicin attenuates hnRNPC-p53 protein interactions". EMBO Rep. 18 (4): 536-548. ... Small nucleolar RNA host gene 1 is a non-protein coding RNA that in humans is encoded by the SNHG1 gene. This locus represents ... Yu F, Bracken CP, Pillman KA, Lawrence DM, Goodall GJ, Callen DF, Neilsen PM (2015). "p53 Represses the Oncogenic Sno-MiR-28 ...
... is also a target gene of the tumor suppressor protein p53. TRIM22 possesses E3 ubiquitin ligase activity and is able to ... Tripartite motif-containing 22, also known as TRIM22, is a protein which in humans is encoded by the TRIM22 gene. The protein ... suggesting that function of this protein may be to mediate interferon's antiviral effects. Other proteins that function to ... TRIM22 appears to prevent the movement of the HIV Gag protein to the plasma membrane and hence TRIM22 can block HIV replication ...
DNA damage and/or hyperproliferative signals activate wildtype p53 tumor suppressor protein (TP53; MIM 191170), inducing cell ... Mutations that inactivate p53 occur in 50% of all tumors. Polyak et al. (1997) used serial analysis of gene expression (SAGE) ... 1997) termed these genes 'p53-induced genes,' or PIGs, several of which were predicted to encode redox-controlling proteins. ... Ectoderm-neural cortex protein 1 is a protein that in humans is encoded by the ENC1 gene. ...
This protein has been shown to interact with and dephosphorylates tumor suppressor protein p53, and is thought to regulate the ... "The human Cdc14 phosphatases interact with and dephosphorylate the tumor suppressor protein p53". J. Biol. Chem. 275 (4): 2410- ... "The human Cdc14 phosphatases interact with and dephosphorylate the tumor suppressor protein p53". J. Biol. Chem. 275 (4): 2410- ... The protein encoded by this gene is a member of the dual specificity protein tyrosine phosphatase family. This protein is ...
Inactivation of p53, a tumor suppressor protein that preferentially binds to cruciform structures, is responsible for over 50% ... Stros M, Muselíková-Polanská E, Pospísilová S, Strauss F (June 2004). "High-affinity binding of tumor-suppressor protein p53 ... The BRCA1 protein, a tumor suppressor that functions in DNA repair, binds preferentially to cruciform structures.Mutations in ... Another example of cruciform structure significance is seen in the interaction between p53, a tumor suppressor, and cruciform ...
This protein also interacts with the tumor suppressor P53 after exposure to cell stress. BAK1 is a pro-apoptotic Bcl-2 protein ... Bcl-2 homologous antagonist/killer is a protein that in humans is encoded by the BAK1 gene on chromosome 6. The protein encoded ... binds the BH3 domain of other BCL-2 proteins in its active form. As a member of the BCL2 protein family, BAK1 functions as a ... two proteins of the mitochondrial protein sorting and assembly machinery, are essential for Bak activation during TNF alpha ...
Ordinarily, Aurora A expression levels are kept in check by the tumor suppressor protein p53. Mutations of the chromosome ... Du J, Hannon GJ (December 2002). "The centrosomal kinase Aurora-A/STK15 interacts with a putative tumor suppressor NM23-H1". ... Among these target proteins are TACC, a microtubule-associated protein that stabilizes centrosomal microtubules and Kinesin 5, ... protein with ch-TOG and GAS41/NuBI1 suggests multiple TACC1-containing protein complexes in human cells". Biochem. J. 363 (Pt 1 ...
p53 and p73 are tumor suppressor proteins and their degradation is tightly regulated by ubiquitination. Recently it was shown ... This protein-protein interaction between p53 and NQO1 was non-catalytic. Ornithine decarboxylase (ODC), is a labile protein ... "A mechanism of ubiquitin-independent proteasomal degradation of the tumor suppressors p53 and p73". Genes & Development. 19 (3 ... Altered expression of this protein has been seen in many tumors and is also associated with Alzheimer's disease (AD). Benzene ...
TP53 encodes tumor suppressor p53, a protein that regulates cell proliferation, death, and tumor formation. Mutations in JAK- ... a protein that regulates cell proliferation and the CDKN2B gene which encodes multiple tumor suppressor 2, a protein that ... This gene encodes SET domain containing 2, a protein that acts to reduce the occurrence of gene deletions and tumor formation. ... This gene encodes CREB-binding protein, a protein that activates various transcription factors some of which are implicated in ...
The key target of Mdm2 is the p53 tumor suppressor. Mdm2 has been identified as a p53 interacting protein that represses p53 ... The E3 ubiquitin ligase MDM2 is a negative regulator of the p53 tumor suppressor protein. MDM2 binds and ubiquitinates p53, ... Mdm2 is an important negative regulator of the p53 tumor suppressor. Mdm2 protein functions both as an E3 ubiquitin ligase that ... Momand J, Wu HH, Dasgupta G (January 2000). "MDM2--master regulator of the p53 tumor suppressor protein". Gene. 242 (1-2): 15- ...
"PTEN tumor suppressor regulates p53 protein levels and activity through phosphatase-dependent and -independent mechanisms". ... PTEN also has weak protein phosphatase activity, but this activity is also crucial for its role as a tumor suppressor. PTEN's ... PTEN acts as a tumor suppressor gene through the action of its phosphatase protein product. This phosphatase is involved in the ... When PTEN protein is insufficient, its interaction with p53 triggers deficiencies and defects in other proteins that also have ...
It also seems to be important for the regulation of the tumor suppressor protein p53. Cysteine residues from MTs can capture ... This protein functions in primary metal storage, transport, and detoxification. More specifically, Yeast MT stores copper so ... MT was discovered in 1957 by Vallee and Margoshe from purification of a Cd-binding protein from horse (equine) renal cortex. MT ... For the first 40 residues in the protein the polypeptide wraps around the metal by forming two large parallel loops separated ...
Cdk5 phosphorylates and regulates the tumor suppressor protein p53. In apoptotic PC12 cells there is a simultaneous increase in ... The kinase phosphorylates tumor suppressors and transcription factors, which are involved in cell cycle progression. Cdk5 is ... "Per2 - Period circadian protein homolog 2 - Mus musculus (Mouse) - Per2 gene & protein". www.uniprot.org. Retrieved 2020-10-31 ... "CABLES2 protein expression summary - The Human Protein Atlas". www.proteinatlas.org. Retrieved 2020-11-01. "AATK Gene - ...
"Human smooth muscle alpha-actin gene is a transcriptional target of the p53 tumor suppressor protein". Oncogene. 16 (10): 1299- ... ACTA2 (actin alpha 2) is an actin protein with several aliases including alpha-actin, alpha-actin-2, aortic smooth muscle or ... Snásel J, Pichová I (1997). "The cleavage of host cell proteins by HIV-1 protease". Folia Biologica. 42 (5): 227-30. doi: ... Alzheimer amyloid precursor protein and pro-interleukin 1 beta as substrates of the protease from human immunodeficiency virus ...
"Aberrations of the tumor suppressor p53 gene and p53 protein in solar keratosis in human skin". The Journal of Investigative ... Mutation of the p53 tumor suppressor gene, induced by UV radiation, has been identified as a crucial step in AK formation. This ... In particular, mutations in the p53 tumor suppressor gene have been found in 30-50% of AK lesion skin samples. UV radiation has ... tumor suppressor gene, located on chromosome 17p132, allows for cell cycle arrest when DNA or RNA is damaged. Dysregulation of ...
The tumor-suppressor protein p53 accumulates when DNA is damaged due to a chain of biochemical factors. Part of this pathway ... these inhibitory proteins target retinoblastoma tumor-suppressing proteins. These tumor-suppressing proteins regulate the cell ... Finally, adding p53-MDM2 complexes displaces p53 and activates the p53 pathway, leading to cell cycle arrest and apoptosis. ... The adenovirus E1B-55K protein and the hepatitis B virus HBx protein are examples of viral proteins that can perform such a ...
It is also known to form covalent linkage to the p53 tumour suppressor protein. 5.8S rRNA can be used as a reference gene for ... This ribosomal RNA, along with the 28S and 5S rRNA as well as 46 ribosomal proteins, forms the ribosomal large subunit (LSU). ... Fontoura BM, Atienza CA, Sorokina EA, Morimoto T, Carroll RB (June 1997). "Cytoplasmic p53 polypeptide is associated with ... is a non-coding RNA component of the large subunit of the eukaryotic ribosome and so plays an important role in protein ...
One of her areas of interest is the tumour suppressor p53 and related proteins. Her current research is to determine the 3- ... Her contributions to protein structural biology includes the use of NMR and X-ray crystallography to pursue structures of ... Epigenetic protein families: a new frontier for drug discovery. Nature Reviews Drug Discovery 11, 384-400 (2012) "Arrowsmith ... dimensional structures of human proteins of therapeutic relevance by structural proteomics. She has made significant ...
Its major role, however, is to mediate the degradation of p53, a major tumor suppressor protein, reducing the cell's ability to ... The viral oncogenes E6 and E7 promote cell growth by inactivating the tumor suppressor proteins p53 and pRb. Keratinocyte stem ... tumor suppressor genes. Binding at these locations causes transformation of the DLG protein and disruption of its suppressor ... the primary function of the E7 protein is to inactivate members of the pRb family of tumor suppressor proteins. Together with ...
This gene is a transcription factor that regulates the cell cycle and hence functions as a tumor suppressor. By inducing G ( ... There are indications that benzo[a]pyrene diol epoxide specifically targets the protective p53 gene.[25] ... This process increases transcription of certain genes, notably CYP1A1, followed by increased CYP1A1 protein production.[28] ... Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in P53. Science. 1996 October 18;274(5286): ...
Welch C, Chen Y, Stallings RL (2007). "MicroRNA-34a functions as a potential tumor suppressor by inducing apoptosis in ... a role for p53/activator protein 2 transcriptional regulation". Mol. Cancer Ther. 6 (5): 1650-60. doi:10.1158/1535-7163.MCT-06- ... protein C-terminus binding. • protein binding. • four-way junction DNA binding. • identical protein binding. • ... This protein can interact with the ssDNA-binding protein RPA, BRCA2, PALB2[10] and RAD52. ...
In 1988 Ed Harlow demonstrates that cancer-causing and cancer-preventing genes (oncogenes and tumor-suppressor genes) interact; ... A.D. Hershey and Martha Chase, "Independent Functions of Viral Protein and Nucleic Acid in Growth of Bacteriophage," J. General ... Scott Lowe (currently at MSKCC), research on p53, Member of the National Academy of Sciences and investigator of Howard Hughes ... In 2011, Wigler, James Hicks and Nick Navin perform the first genomic profile of single cancer cells from a patient's tumor;[42 ...
... and von Hippel-Lindau tumor suppressor (VHL), as well as a number of proto-oncogenes (Raf, Myc, Myb, Rel, Src, Mos, Abl). The ... The protein degradation processEdit. Ribbon diagram of ubiquitin, the highly conserved protein that serves as a molecular tag ... Ubiquitin-independent mechanisms targeting key cell cycle regulators such as p53 have also been reported, although p53 is also ... Proteasomes are protein complexes which degrade unneeded or damaged proteins by proteolysis, a chemical reaction that breaks ...
Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ... Binding proteins: IGFBP (1, 2, 3, 4, 5, 6, 7). *Cleavage products/derivatives with unknown target: Glypromate (GPE, (1-3)IGF-1) ... a b Proto-Oncogene+Proteins+c-sis at the US National Library of Medicine Medical Subject Headings (MeSH) ... Hannink M, Donoghue DJ (1989). "Structure and function of platelet-derived growth factor (PDGF) and related proteins". Biochim ...
"Genistein mediated histone acetylation and demethylation activates tumor suppressor genes in prostate cancer cells". Int. J. ... In general, proteins fold into discrete units that perform distinct cellular functions, but some proteins are also capable of ... and p53.[38][39] Other food components can reduce DNA damage, such as soy isoflavones[40][41] and bilberry anthocyanins.[42] ... The first way is post translational modification of the amino acids that make up histone proteins. Histone proteins are made up ...
... in the regulation of translation and tumor suppressor activity of aminoacyl-tRNA synthetase-interacting multifunctional protein ... γ) and p53 signalling.[22][23][24][25][26][27][28][29][30] ... For instance, one can start with the gene for a protein that ... McClain WH (November 1993). "Rules that govern tRNA identity in protein synthesis". Journal of Molecular Biology. 234 (2): 257- ... Both classes of aminoacyl-tRNA synthetases are multidomain proteins. In a typical scenario, an aaRS consists of a catalytic ...
... p53 mutations are a late event in the pathology of prostate cancer. Other tumor suppressor genes that are thought to play a ... The protein ZIP1 is responsible for the active transport of zinc into prostate cells. One of the zinc's important roles is to ... Tumor markers. Tissue samples can be stained for the presence of PSA and other tumor markers in order to determine the origin ... ZIP1 is now called a tumor suppressor gene product for the gene SLC39A1. The cause of the epigenetic silencing is unknown. ...
Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ... Notably, El-Deiry et al. identified a protein p21 (WAF1) which was present in cells expressing wild type p53 but not those with ... protein binding. • cyclin-dependent protein serine/threonine kinase inhibitor activity. • ubiquitin protein ligase binding. • ... cyclin-dependent protein serine/threonine kinase activity. • protein kinase inhibitor activity. • protein kinase binding. • ...
"Specific-site methylation of tumour suppressor ANKRD11 in breast cancer". Eur. J. Cancer. 48 (17): 3300-9. doi:10.1016/j.ejca. ... This locus encodes an ankyrin repeat domain-containing protein. The encoded protein inhibits ligand-dependent activation of ... "Identification of ANKRD11 as a p53 coactivator". J. Cell Sci. 121 (Pt 21): 3541-52. doi:10.1242/jcs.026351. PMID 18840648 ... Ankyrin repeat domain 11 is a protein that in humans is encoded by the ANKRD11 gene.[5] ...
The most frequent mutations are a loss of function of p53 protein, a tumor suppressor, or in the p53 pathway, and gain of ... 2002), I.3. Proteins: The Shape and Structure of Proteins *^ Alberts et al. (2002), I.3. Proteins: Protein Function Archived 25 ... like the fibers formed by the protein collagen. Proteins can bind to other proteins and simple molecules, sometimes acting as ... A single nucleotide difference within DNA can cause a change in the amino acid sequence of a protein. Because protein ...
... "microRNAs as oncogenes and tumor suppressors". Developmental Biology. 302 (1): 1-12. doi:10.1016/j.ydbio.2006.08.028. PMID ... In fission yeast this complex contains argonaute, a chromodomain protein Chp1, and a protein called Tas3 of unknown function.[ ... p53 Naked siRNA Kidney injury, acute renal failure I Completed Quark Pharmaceuticals NCT00554359 ... This ancestral RNAi system probably contained at least one dicer-like protein, one argonaute, one PIWI protein, and an RNA- ...
Tumor suppressor genes are genes that inhibit cell division and survival. Malignant transformation can occur through the ... "Negative regulation of BRCA1 gene expression by HMGA1 proteins accounts for the reduced BRCA1 protein levels in sporadic breast ... p53 mutations).[91] Germ line DNA repair mutations are noted on the figure's left side. However, such germline mutations (which ... The dispersed tumors are called metastatic tumors, while the original is called the primary tumor. Almost all cancers can ...
Mutations and deletions of tumor suppressor genes, such as P53, are thought to be the cause of some forms of brain tumor.[23] ... a technique that visualizes the presence or absence of a targeted protein via staining.[30] ... There are two main types of tumors: malignant or cancerous tumors and benign tumors.[2] Cancerous tumors can be divided into ... Often these tumors are associated with clearly outlined tumors in imaging.. *Infiltration is the behavior of the tumor either ...
In these conditions, they regulate the tumor suppressor gene CDON. It has been shown that miR-181 targets the homeobox protein ... analysis revealed that miR-181b expression is strongly associated with mutation status of the tumor suppressor gene p53. miR- ... miRNA are downregulated in many tumors and thus appear to function as tumor suppressor genes. The mature products miR-181a, miR ... Shi L, Cheng Z, Zhang J, Li R, Zhao P, Fu Z, You Y (October 2008). "hsa-mir-181a and hsa-mir-181b function as tumor suppressors ...
Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ... E-cadherin acts as an invasion suppressor and a classical tumor suppressor gene in pre-invasive lobular breast carcinoma.[53] ... protein binding. • ankyrin binding. • gamma-catenin binding. • beta-catenin binding. • GTPase activating protein binding. • ... Shibata T, Gotoh M, Ochiai A, Hirohashi S (August 1994). "Association of plakoglobin with APC, a tumor suppressor gene product ...
The canonical tumor-suppressor function of APC is suppression of β-catenin, but other tumor-suppressor functions of APC may be ... a large multifunction tumour-suppressing protein which acts as a "gatekeeper" to prevent development of tumours. (APC regulates ... Further mutations (e.g., in p53 or kRAS) to APC-mutated cells are much more likely to lead to cancer than they would in non- ... soft tissue tumors, desmoid tumors, and associated cancers". As for FAP but "CHRPE and desmoid tumors are rare" and also ...
... proto-oncogene activation and inhibition of tumour suppressor genes. SCLC may originate from neuroendocrine cells located in ... The DNA contains the information on how the cell function; in practice, it contains the recipes for protein synthesis. If the ... "Acrolein is a major cigarette-related lung cancer agent: Preferential binding at p53 mutational hotspots and inhibition of DNA ... Kuper H, Boffetta P, Adami HO (September 2002). "Tobacco use and cancer causation: association by tumour type". Journal of ...
SMAD protein signal transduction. • transcription, DNA-templated. • positive regulation of transcription initiation from RNA ... a novel PCNA associated factor with increased expression in tumor tissues". Oncogene. 20 (4): 484-9. PMID 11313979. doi:10.1038 ... "Yeast SUB1 is a suppressor of TFIIB mutations and has homology to the human co-activator PC4". The EMBO Journal. 15 (8): 1933- ... "General transcriptional coactivator PC4 activates p53 function". Molecular and Cellular Biology. 24 (5): 2052-62. PMC 350566 ...
... all tumor viruses appear to attack the same cellular control pathways, so-called tumor suppressor pathways.[citation needed] ... inhibits p53 and retinoblastoma protein and suppresses viral genes needed for full virus production and assembly ("lytic ... ORF36 - vPK - viral protein kinase with multiple roles in replication cycle ORF37 - SOX - dual function protein - DNase ... While no other human tumor virus possesses these same genes, other tumor viruses target the same cellular pathways illustrating ...
The p53 protein, produced by the TP53 gene, normally monitors cell division and kills cells if they have Wnt pathway defects. ... The oncogenes and tumor suppressor genes are well studied and are described above under Pathogenesis. ... T stands for tumor stage and ranges from 0, no evidence of primary tumor, to T4 when the tumor penetrates the surface of the ... including both tumor cells and how the tumor invades into healthy tissues and finally if the tumor appears to be completely ...
Boulton SJ (November 2006). "Cellular functions of the BRCA tumour-suppressor proteins". Biochem. Soc. Trans. 34 (Pt 5): 633-45 ... Chai YL, Cui J, Shao N, Shyam E, Reddy P, Rao VN (January 1999). "The second BRCT domain of BRCA1 proteins interacts with p53 ... BRCA1 combines with other tumor suppressors, DNA damage sensors and signal transducers to form a large multi-subunit protein ... a protein that associates with the BRCA1 tumor suppressor". J. Biol. Chem. 275 (24): 18541-9. doi:10.1074/jbc.M909494199. PMID ...
SWI/SNF-associated PRMT5 methylates histone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor ... regulation of signal transduction by p53 class mediator. • peptidyl-arginine methylation, to symmetrical-dimethyl arginine. • ... GO:0001948 protein binding. • protein heterodimerization activity. • ribonucleoprotein complex binding. • histone-arginine N- ... protein-arginine N-methyltransferase activity. • protein-arginine omega-N symmetric methyltransferase activity. • identical ...
Retinoblastoma protein) அல்லது புற்று நோய் வரமால் தடுக்கும் மரபணுவில் (p53) ஏற்படும் பிறழ்வுகளினால் உயிரணு பிரிதல் ... புற்று உயிரணுக்களை கட்டுப்படுத்தும் மரபணுவில் (tumor suppressor genes) ஏற்படும் பிறழ்வுகள். முதல் வகையில், உயிரணு பிரிதலை ... எடுத்துக்காட்டாக, தனிநபர் யார் ஒருவர் மரபுரிமையாக ஒரு மரபுப்பிறழ்ந்த p53 மாற்றுரு (மேலும் அதனால் பிறழ்வுற்ற p53 க்கு ... வீரிய புற்றுகள் (Malignant tumor) கதிரியயக்க படமாக்கத்தில் ...
This enzyme functions in the ubiquitination of the tumor-suppressor protein p53, which is induced by an E3 ubiquitin-protein ... protein complex. • extracellular exosome. Biological process. • ubiquitin-dependent protein catabolic process. • protein ... protein autoubiquitination. • protein ubiquitination. • MyD88-independent toll-like receptor signaling pathway. Sources:Amigo ... ubiquitin-protein transferase activity. • protein binding. • ATP binding. • ubiquitin conjugating enzyme activity. ...
Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ... protein kinase activity. • kinase activity. • protein binding. • protein tyrosine kinase activity. • ATP binding. • Ras guanyl- ... membrane protein proteolysis. • phosphorylation. • transmembrane receptor protein tyrosine kinase signaling pathway. • positive ... Binding proteins: IGFBP (1, 2, 3, 4, 5, 6, 7). *Cleavage products/derivatives with unknown target: Glypromate (GPE, (1-3)IGF-1) ...
... resulting in the incréase of p53 protein level and enhancement of cancer cell-apoptosis. p53 is a tumor suppressor, and is ... and has provided knowledge on the link between p53 and IFN alpha/beta. The p53 response not only contributes to tumor ... "Integration of interferon-alpha/beta signaling to p53 responses in tumor suppression and antiviral defense", ku Akinori Takaoka ... Peran produk apoptotik dina kakebalan tumor[édit , édit sumber]. An interesting case of re-use and feed-back of apoptotic ...
... and the product of PTCH is a tumor suppressor involved in cell signaling. Although the exact role of this protein in NBCCS is ... The protein produced by the TP53 gene, p53, is involved in cell cycle arrest, DNA repair and apoptosis. Defective p53 may not ... Other tumors increased in frequency include; osteomas, adrenal adenomas and carcinomas, thyroid tumors and desmoid tumors. The ... Many of these syndromes are caused by mutations in tumor suppressor genes, genes that are involved in protecting the cell from ...
These studies report that overexpression of the COX-2 enzyme has an adverse effect on the tumor suppressor, p53. p53 is an ... a protein that mediates p53 ligation and tagged destruction, through ubiquitination.[44] The mechanism for this neuroblastoma ... Functional p53 allows DNA damaged neuroblastoma cells to commit suicide through apoptosis, halting tumor growth. ... When cellular DNA is damaged beyond repair, p53 is transported to the nucleus where it promotes p53 mediated apoptosis.[44] Two ...
The p53 gene has been mapped to chromosome 17. In the cell, p53 protein binds DNA, which in turn stimulates another gene to ... is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy of ... mutations in p53 are found in most tumor types, and so contribute to the complex network of molecular events leading to tumor ... Mutant p53 can no longer bind DNA in an effective way, and as a consequence the p21 protein is not made available to act as the ...
Accumulation of p53 tumor suppressor gene protein: An independent marker of prognosis in breast cancers. J Natl Cancer Inst. ... p53 Tumor Suppressor Gene Protein, Immunohistochemical, Paraffin Block. TEST: 481044 Test number copied ... Alterations of the p53 tumor suppressor gene have been shown to serve as an independent prognostic marker in a wide variety of ... Association of p53 protein expression with tumor cell proliferation rate and clinical outcome in node-negative breast cancer. J ...
The p73 protein is a structural and functional homolog of the p53 tumor suppressor protein (12, 13). p73 not only recognizes ... Functional association between Wwox tumor suppressor protein and p73, a p53 homolog. Rami I. Aqeilan, Yuri Pekarsky, Juan J. ... Functional association between Wwox tumor suppressor protein and p73, a p53 homolog ... Functional association between Wwox tumor suppressor protein and p73, a p53 homolog ...
Functional association between Wwox tumor suppressor protein and p73, a p53 homolog.. Aqeilan RI1, Pekarsky Y, Herrero JJ, ... Functional association between Wwox tumor suppressor protein and p73, a p53 homolog ... Functional association between Wwox tumor suppressor protein and p73, a p53 homolog ... Functional association between Wwox tumor suppressor protein and p73, a p53 homolog ...
It has been implicated in transcriptional regulation by modulating protein-protein interactions with p53 tumor suppressor ... Interferon-inducible protein 16: insight into the interaction with tumor suppressor p53.. Liao JC1, Lam R, Brazda V, Duan S, ... Interferon-Inducible Protein 16: Insight into the Interaction with Tumor Suppressor p53 ... Interferon-Inducible Protein 16: Insight into the Interaction with Tumor Suppressor p53 ...
"Tumor Suppressor Protein p53" by people in Harvard Catalyst Profiles by year, and whether "Tumor Suppressor Protein p53" was a ... "Tumor Suppressor Protein p53" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ... Below are the most recent publications written about "Tumor Suppressor Protein p53" by people in Profiles. ... Below are MeSH descriptors whose meaning is more general than "Tumor Suppressor Protein p53". ...
Protein p53 is an important checkpoint in the cell cycle, ensuring the integrity of DNA replication. ... Shown here are the DNA-binding regions of the p53 tumor suppressor protein, bound to DNA. ... Shown here are the DNA-binding regions of the p53 tumor suppressor protein, bound to DNA. Protein p53 is an important ...
This thesis presents the first report of the comprehensive and quantitative analysis of the effects of tumor-derived mutations ... on the tetrameric structure of tumor suppressor protein p53, which plays ... and quantitative analysis of the effects of tumor-derived mutations on the tetrameric structure of tumor suppressor protein p53 ... Quantitative Analysis for p53 Tetramerization Domain Mutants Reveals a Low Threshold for Tumor Suppressor Inactivation ...
Earlier work had shown how p53 binds to DNA as a stand-alone entity a...,Structure,determined,for,p53,tumor,suppressor,protein, ... Clearly a detailed view of the p53 protein in direct contact with DNA...Now in a new study featured as a paper of the week and ... on the cover... The bottom line is that we now have a detailed picture of how p53 bin... ... More than half of human cancers involve mutations in the p53 tumor-sup... ...
These functions of p53 are regulated both by protein-protein interactions and phosphorylation. The double-stranded RNA ... The tumor suppressor p53 is a multifunctional protein that plays a critical role in modulating cellular responses upon DNA ... The double-stranded RNA activated protein kinase PKR physically associates with the tumor suppressor p53 protein and ... The tumor suppressor p53 is a multifunctional protein that plays a critical role in modulating cellular responses upon DNA ...
p53 major tumour suppressor protein has presented a challenge for structural biology for two decades. The intact and complete ... The structure of p53 tumour suppressor protein reveals the basis for its funcitonal plasticity ... 5 more authors) (2006) The structure of p53 tumour suppressor protein reveals the basis for its funcitonal plasticity. EMBO ... which enables the protein to bind variably spaced DNA target sequences, essential for p53 transactivation and tumour suppressor ...
p53 Tumor Suppressor Protein Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone BP53-12 ] validated in WB, IHC- ... p53 Tumor Suppressor Protein Antibody - Without BSA and Azide p53 Tumor Suppressor Protein Antibody - Without BSA and Azide. ... Cellular tumor antigen p53, Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53, TP53, P53. ... p53 Tumor Suppressor Protein Antibody - Without BSA and Azide is for research use only and not for use in diagnostic or ...
Stabilization of p53 protein is a result of reduced interaction of p53 and E6. Induction of p53 protein and p21waf-1 mRNA after ... In the present study, we investigated the status and function of p53 tumor suppressor protein in revertant cells. The results ... Stabilization and Reactivation of the p53 Tumor Suppressor Protein in Nontumorigenic Revertants of HeLa Cervical Cancer Cells. ... Analysis of the p53 tumor suppressor gene revealed stabilization and at least partial restoration of wild-type p53 ...
Initiation of autoimmunity to the p53 tumor suppressor protein by complexes of p53 and SV40 large T antigen. X Dong, X Dong ... Initiation of autoimmunity to the p53 tumor suppressor protein by complexes of p53 and SV40 large T antigen.. J Exp Med 1 April ... In this study, high titer ANAs specific for the p53 tumor suppressor protein were induced in mice immunized with purified ... The high levels of autoantibodies to p53 in mice immunized with p53/SVT complexes were transient, but low levels of the ...
One key protein that coordinates DNA repair with cell cycle progression and apoptosis is the tumor suppressor protein p53. P53 ... The tumor suppressor p53 binding protein 1 (53BP1) binds to the DNA-binding domain of p53 and enhances p53-mediated ... Tumor Suppressor P53 Binding Protein 1 (53bp1) Is Involved in DNA Damage-Signaling Pathways Irene Rappold, Irene Rappold ... Irene Rappold, Kuniyoshi Iwabuchi, Takayasu Date, Junjie Chen; Tumor Suppressor P53 Binding Protein 1 (53bp1) Is Involved in ...
For this purpose, the p53 content of 100 human breast biopsies classified as ductal carcinoma (DCIS), was evaluated by ... The focus of this study was to determine if early detection of mutant p53 accumulation may be an early indicator of tumor ... Immunohistochemical Evaluation of Human p53 Tumor Suppressor Protein Content in Ductal Carcinoma in Situ of the Breast ... Aliasgharpour M, Thorne D, Dimitrov N. Immunohistochemical Evaluation of Human p53 Tumor Suppressor Protein Content in Ductal ...
"Tumor Suppressor Protein p53" by people in this website by year, and whether "Tumor Suppressor Protein p53" was a major or ... "Tumor Suppressor Protein p53" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ... Below are the most recent publications written about "Tumor Suppressor Protein p53" by people in Profiles. ... Below are MeSH descriptors whose meaning is more general than "Tumor Suppressor Protein p53". ...
rTP53/1739 is a Recombinant Mouse Monoclonal Antibody to p53 Tumor Suppressor Protein. Validated in WB, IHC-P. Reacts with ... Cellular Tumor Antigen p53, LFS1, TP53, Transformation Related Protein 53 (TRP53), Tumor Protein p53, Tumor Suppressor p53. ... It reacts with the mutant as well as the wild form of p53. It is a tumor suppressor protein expressed in a wide variety of ... p53 Tumor Suppressor Protein. Recombinant Mouse Monoclonal Antibody [Clone rTP53/1739] Printable ...
The p53 tumor suppressor protein plays a crucial role in influencing cell survival in response to cellular stress and while the ... p53 pathway is considered a key determinant of anti-tumor responses in many tumors, its role in cell survival in MB is much ... The inhibition of p53 in the presence of VMY revealed increased late stage apoptosis, increased DNA fragmentation and increased ... Surprisingly, the genetic or chemical silencing of p53 significantly enhanced the cytotoxic effects of both VMY and the DNA ...
Autoantibodies Against The Tumor Suppressor Protein P53. Last Updated on Thu, 16 Apr 2015 , Autoimmune Diseases ... Mutations of this tumor suppressor gene are the most frequently reported gene alteration in human cancers [26, 27]. In 1982, it ... p53 antibody response (in%). 10 Ways To Fight Off Cancer. Learning About 10 Ways Fight Off Cancer Can Have Amazing Benefits For ... As the guardian of the genome, p53 is the main regulator preventing carcinogenic and teratogenic lesions [24, 25]. Therefore ...
p53, a tumor suppressor protein has a prominent role in forestalling tumor development and advancement through its involvement ... abstract = "p53, a tumor suppressor protein has a prominent role in forestalling tumor development and advancement through its ... N2 - p53, a tumor suppressor protein has a prominent role in forestalling tumor development and advancement through its ... AB - p53, a tumor suppressor protein has a prominent role in forestalling tumor development and advancement through its ...
N2 - The tumor suppressor protein p53 exerts its cell cycle-regulatory effects through its ability to function as a sequence- ... AB - The tumor suppressor protein p53 exerts its cell cycle-regulatory effects through its ability to function as a sequence- ... The tumor suppressor protein p53 exerts its cell cycle-regulatory effects through its ability to function as a sequence- ... abstract = "The tumor suppressor protein p53 exerts its cell cycle-regulatory effects through its ability to function as a ...
Molecular interactions between telomerase and the tumor suppressor protein p53 in vitro *He Li ... Rights & permissionsfor article Molecular interactions between telomerase and the tumor suppressor protein p53 ,i,in vitro,/i ... Cathepsin L induced PC-12 cell apoptosis via activation of B-Myb and regulation of cell cycle proteins *Xiao Shen ... permissionsfor article Cathepsin L induced PC-12 cell apoptosis via activation of B-Myb and regulation of cell cycle proteins ...
200µg/ml of Ab Purified from Bioreactor Concentrate by Protein A/G. Prepared in 10mM PBS with 0.05% BSA & 0.05% azide. Also ... Cellular Tumor Antigen p53, LFS1, TP53, Transformation Related Protein 53 (TRP53), Tumor Protein p53, Tumor Suppressor p53. ... Anti-p53 Tumor Suppressor Protein Monoclonal Antibody(Clone: DO-1). Product code: 36-3297. *specify in mg or ml ... Monoclonal antibody PAb1801 does not block the binding of DO-7 MAb to p53 in an ELISA test. p53 is a tumor suppressor gene ...
200µg/ml of Ab Purified from Bioreactor Concentrate by Protein A/G. Prepared in 10mM PBS with 0.05% BSA & 0.05% azide. Also ... Cellular Tumor Antigen p53, LFS1, TP53, Transformation Related Protein 53 (TRP53), Tumor Protein p53, Tumor Suppressor p53. ... Anti-p53 Tumor Suppressor Protein Monoclonal Antibody(Clone: BP53-12). Product code: 36-3289. *specify in mg or ml ... If it occurs in the germ line, such tumors run in families. In most transformed and tumor cells the concentration of p53 is ...
Genetic deficiency of the tumor suppressor protein p53 influences erythrocyte survival Rosi Bissinger, Elisabeth Lang, Irene ...
Restoration of p53 function causes death of tumor cells and is potentially suitable for gene therapy of cancer. In cervical ... Inactivation of tumor suppressor p53 accompanies the majority of human malignancies. ... carcinoma, human papilloma virus (HPV) E6 facilitates proteasomal degradation of p53. Hence … ... Hence, a possible approach to p53 reactivation is the use of small molecules suppressing the function of viral proteins. HeLa ...
Describing the broad roles of tumor suppressors from a perspective based in molecular biology and genetics, the authors detail ... p53 Tumor Suppressor Protein. Ashcroft, Margaret, PhD (et al.). Pages 159-181 ... Tumor Suppressor Genes in Human Cancer illuminates what is currently known of tumor suppressor genes and their regulation, work ... Tumor Suppressor Genes in Human Cancer. Editors. * David E. Fisher Series Title. Cancer Drug Discovery and Development. ...
Tumor Suppressor Protein p53 Upregulation Research. [x] Remove Focus on Tumor Suppressor Protein p53 Upregulation. Filter by ... Pharmacological Actions : Apoptotic, Bcl-2 protein down-regulation, Cell cycle arrest, Tumor Suppressor Protein p53 ... Pharmacological Actions : Apoptotic, Tumor Suppressor Protein p53 Upregulation. Additional Keywords : Natural Substance/Drug ... Pharmacological Actions : Antioxidants, Apoptotic, Tumor Suppressor Protein p53 Upregulation. Additional Keywords : ...
Tumor Suppressor Protein p53 Upregulation Research. [x] Remove Focus on Tumor Suppressor Protein p53 Upregulation. Filter by ... Pharmacological Actions : Cell cycle arrest, Tumor Suppressor Protein p53 Upregulation. Additional Keywords : Location Specific ... Tumor Suppressor Protein p53 Upregulation. 2. 2. Alpha-amylase inhibitor. 1. 1. ...
  • p73 not only recognizes and binds to the p53-responsive elements found in the promoter regions of diverse p53-target genes but can also transactivate the transcription of these target genes to various degrees ( 14 ). (pnas.org)
  • Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. (harvard.edu)
  • Ng SR, Rideout WM, Akama-Garren EH, Bhutkar A, Mercer KL, Schenkel JM, Bronson RT, Jacks T. CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer. (harvard.edu)
  • RB, p130 and p107 differentially repress G1/S and G2/M genes after p53 activation. (harvard.edu)
  • The inhibition of p53 in the presence of VMY revealed increased late stage apoptosis, increased DNA fragmentation and increased expression of genes involved in apoptosis, including CAPN12 and TRPM8, p63, p73, BIK, EndoG, CIDEB, P27 Kip1 and P21 cip1 . (aging-us.com)
  • In Tumor Suppressor Genes in Human Cancer, David Fisher, MD, PhD, and an authoritative panel of academic, cutting-edge researchers review and summarize the current state of the field. (springer.com)
  • Leading-edge and forward-looking, Tumor Suppressor Genes in Human Cancer illuminates what is currently known of tumor suppressor genes and their regulation, work that is already beginning to revolutionize cancer target elucidation, drug discovery, and treatment design. (springer.com)
  • describes he role of tumor suppressor genes in human cancer. (springer.com)
  • It details a current view of these important genes and highlights clinically relevant aspects of the strides made in the field of tumor suppressor biology. (springer.com)
  • A series of 10 differentially expressed genes designated as either tumor suppressor activated pathway (TSAP) or tumor suppressor inhibited pathway (TSIP) have been described that were either up- or down-regulated, respectively, by p53 activation in LTR6 cells (1). (desafioceroaedes.com)
  • The most significant biological function of p53 is to act as a sequence-specific DNA-binding transcription factor, which can induce the expression of a variety of target genes in response to diverse stress stimuli. (elsevier.com)
  • Powerful new tools are now available to discover and understand tumor suppressor genes (TSGs) and the biochemical mechanisms by which they control cancer development and progression. (springer.com)
  • In Tumor Suppressor Genes, Volume 2: Regulation, Function, and Medicinal Applications, leading physician scientists and researchers explore the cell biology and biochemical function of the tumor suppressor genes, as well as their physiological role in vivo. (springer.com)
  • The authors detail the physical methods-NMR, microarray approaches, posttranslational structure analysis, analysis of regulation at the gene expression and protein signaling levels-used to understand the function of tumor suppressor genes. (springer.com)
  • Other aspects reviewed include screening strategies, targeting the blood supply of tumors, and the replacement of defective cancer genes to achieve a therapeutic effect. (springer.com)
  • Comprehensive and authoritative, the two volumes of Tumor Suppressor Genes provide an unparalleled compilation of key data on all known tumor suppressor pathways and a treasury of techniques for their discovery, analysis, and uses in cancer therapeutics. (springer.com)
  • Tumor suppressor genes located in the 5q21 region on the long arm of human chromosome 5. (bioportfolio.com)
  • Tumor suppressor genes and cell proliferation regulatory proteins play a role in the progression of actinic cheilitis to squamous cell carcinoma and in its biological behavior. (scielo.br)
  • Although p53 is one of the most commonly mutated genes in cancer," says co-lead researcher and study author Vincent L. Cryns, who is a professor of medicine, "we still do not have any drugs that specifically target p53. (medicalnewstoday.com)
  • If the decision is to repair the DNA, p53 triggers other genes to start this process. (medicalnewstoday.com)
  • Isolation of a YAC clone covering a cluster of nine S100 genes on human chromosome 1q21: rationale for a new nomenclature of the S100 calcium-binding protein family. (springer.com)
  • Nuclear targets of p53 in zinc deficiency include genes that arrest the cell cycle and induce apoptotic mechanisms leading to cell death (Corniola et al. (nap.edu)
  • The p53 protein regulates the expression of other genes that control the cell cycle, activates the repair of damaged DNA in cells, and, in cases of severe damage, initiates cell death. (nih.gov)
  • To gain an understanding of the mechanism by which E6 protein inhibits the expression of miR-34a during HPV infection, the researchers used a method known as RNA interference, which makes it possible to turn specific genes off and to observe the subsequent effects on cell activity. (nih.gov)
  • Germ-line mutations in the human BRCA1 and BRCA2 breast cancer suppressor genes confer susceptibility to breast and ovarian cancers ( 1 - 4 ). (pnas.org)
  • The STAT proteins are then activated by phosphorylation via members of the JAK family of protein kinases, causing them to dimerise and translocated to the nucleus, where they bind to specific promoter sequences in target genes. (ebi.ac.uk)
  • First, it is known that several genes causing AS/ASD, such as PTEN, CHD8, and CUL3 , are regulators of p53. (aappublications.org)
  • Furthermore, in the absence of both p53 and the autism-associated gene Pten (mouse mutant model lacking both genes), neuronal stem cells have a higher renewal and neuronal differentiation potential. (aappublications.org)
  • However, mutations in p53 are found in most tumor types, and so contribute to the complex network of molecular events leading to tumor formation. (lifeboat.com)
  • This thesis presents the first report of the comprehensive and quantitative analysis of the effects of tumor-derived mutations on the tetrameric structure of tumor suppressor protein p53, which plays a central role in maintaining genomic integrity. (springer.com)
  • More than half of human cancers involve mutations in the p53 tumor-sup. (bio-medicine.org)
  • More than half of human cancers involve mutations in the p53 tumor-suppressor gene, suggesting the critical role played by the normal p53 protein in defending against cancer. (bio-medicine.org)
  • Similarly, roughly 95 percent of cancer-causing mutations in the p53 protein occur in its DNA-binding core domain, pointing to this region of the p53 protein as being pivotal to its anti-cancer activity. (bio-medicine.org)
  • Mutations of this tumor suppressor gene are the most frequently reported gene alteration in human cancers [26, 27]. (clicktocurecancer.info)
  • p53 Localizes in the nucleus, but is detectable at the plasma membrane during mitosis and when certain mutations modulate cytoplasmic/nuclear distribution. (abeomics.com)
  • Mutations arise with an average frequency of 70% but incidence varies from zero in carcinoid lung tumors to 97% in primary melanomas. (abeomics.com)
  • Background: Mutations of the tumor suppressor gene p53 have been identified in breast cancer cell lines, and some breast carcinomas are detectable by immunohistochemical assay because of p53 protein accumulation. (elsevier.com)
  • Kobe, Japan (ots) - Sysmex Corporation has obtained Japanese manufacturing and marketing approval for the OncoBEAM(TM) RAS CRC Kit, used for blood-based circulating tumor DNA (ctDNA) molecular testing of mutations in the RAS gene for advanced colorectal cancer patients. (presseportal.de)
  • DLEC1 was frequently downregulated in ESCC, lung and NPC cell lines and primary tumors, but was readily expressed in normal tissues and immortalized normal epithelial cells, with mutations rarely detected. (thno.org)
  • We have generated short deletions and point mutations within this region and analysed their effect on p53 function and regulation. (elsevier.com)
  • Mutations lead to an abnormally stable but inactive p53 protein that can be detected immunohistochemically by nuclear staining. (thefreelibrary.com)
  • The gene p53 has been described as the "guardian of the genome" due to its prominent role in preventing genetic mutations. (medicalxpress.com)
  • Previous studies had already shown that p53 mutations are more stable than their nonmutant counterparts and can accumulate until they eclipse them in the nucleus. (medicalnewstoday.com)
  • However, the mechanism behind the stability of p53 mutations remained unclear. (medicalnewstoday.com)
  • Over 50% of all human cancers involve p53 mutations, which occur mostly in the sequence−specific DNA−binding central domain (p53c), yielding little/non-detectable affinity to the DNA consensus site. (ias.ac.in)
  • The tumor suppressor p53 functions at the G1/S-phase checkpoint of the cell cycle to direct cells that have accumulated somatic mutations toward apoptosis and away from mitosis. (curehunter.com)
  • abstract = "The p53 tumor suppressor protein is tightly regulated in the cell and is phosphorylated at multiple sites by several different protein kinases. (dundee.ac.uk)
  • abstract = "p53 major tumour suppressor protein has presented a challenge for structural biology for two decades. (utmb.edu)
  • Recombinant human wild type p53 protein expressed in E. coli. (abeomics.com)
  • After shifting to 32C, LTR6 cells acquire wild-type p53 function and subsequently undergo massive apoptosis (2). (desafioceroaedes.com)
  • The stability of wild-type p53 is critical for its apoptotic function. (aacrjournals.org)
  • In some cancers, wild-type p53 is inactivated by interaction with viral and cellular proteins, and restoration of its activity has therapeutic potential. (aacrjournals.org)
  • Overexpression of homeobox Msx1 induced apoptosis of cancer cells harboring nonfunctional wild-type p53 and suppressed growth of human tumor xenografts in nude mice. (aacrjournals.org)
  • The homeodomain of Msx1 functions as a protein-protein interacting motif rather than a DNA-binding domain and is essential for stabilization, nuclear accumulation, and apoptotic function of wild-type p53. (aacrjournals.org)
  • p53 expression was evaluated in fundic mucosa from different stages of transformation by Western blot analysis and immunohistochemistry using monoclonal antibodies against wild-type p53. (curehunter.com)
  • At the nonpermissive temperature, cessation of large T antigen expression was accompanied by induction of p53, as well as the p53-dependent proteins, wild-type p53-activated fragment-1/Cdk (cyclin-dependent kinase)-interacting protein-1 (p21/Waf1), Bcl (B-cell lymphoma)-associated protein (Bax), and murine double minute 2 (MDM2), that lead to cell cycle-arrest, suicide, and p53 inhibition, respectively. (jneurosci.org)
  • A) An equimolar mixture of His-tagged IFI16 HIN-A or HIN-B domain and a GST fusion protein containing the indicated p53 construct was mixed with glutathione-sepharose ( L ). After washing, protein was eluted with glutathione and visualized by western ( E ) using antibody against His-tag. (nih.gov)
  • SDS-PAGE Analysis Purified p53 Mouse Recombinant Monoclonal Antibody (rTP53/1739). (neobiotechnologies.com)
  • Western Blot Analysis of HeLa cell lysate using p53 Mouse Recombinant Monoclonal Antibody (rTP53/1739). (neobiotechnologies.com)
  • Analysis of Protein Array containing more than 19,000 full-length human proteins using p53 Mouse Monoclonal Antibody (rTP53/1739). (neobiotechnologies.com)
  • Z- and S- Score: The Z-score represents the strength of a signal that a monoclonal antibody (MAb) (in combination with a fluorescently-tagged anti-IgG secondary antibody) produces when binding to a particular protein on the HuProtTM array. (neobiotechnologies.com)
  • The specificity of this monoclonal antibody to its intended target was validated by HuProtTM Array, containing more than 19,000, full-length human proteins. (neobiotechnologies.com)
  • Positive nuclear staining with p53 antibody has been reported to be a negative prognostic factor in breast, lung, colorectal, and urothelial carcinoma. (neobiotechnologies.com)
  • Fig. 1: Formalin-fixed, paraffin-embedded human Colon Carcinoma stained with p53 Mouse Monoclonal Antibody (DO-1). (abeomics.com)
  • Monoclonal antibody PAb1801 does not block the binding of DO-7 MAb to p53 in an ELISA test. (abeomics.com)
  • 3) In fibroblasts infected with p53-expressing adenovirus, wild-p53 protein was co-immunoprecipitated with anti-E6AP antibody. (fujita-hu.ac.jp)
  • Methods: IgGl monoclonal antibody to human p53 protein (PAb 1801) and immunohistochemical methods were used to detect p53 protein accumulation in archival formalin-fixed, paraffin-embedded, randomly selected carcinomas. (elsevier.com)
  • Overall, KSHV ORF26 antibody these data suggest that TSAP6 may take action downstream to p53 to interface apoptosis and cell-cycle progression. (desafioceroaedes.com)
  • 53BP1 contains two breast cancer susceptibility gene 1 COOH terminus (BRCT) motifs, which are present in several proteins involved in DNA repair and/or DNA damage-signaling pathways. (rupress.org)
  • The effect of the two most active compounds was studied with cell lines differing in the state of p53-dependent signaling pathways. (nih.gov)
  • The compounds each specifically activated p53 in cells expressing HPV-18 and, to a lesser extent, HPV-16 and exerted no effect on control p53-negative cells or cells with the intact p53-dependent pathways. (nih.gov)
  • Describing the broad roles of tumor suppressors from a perspective based in molecular biology and genetics, the authors detail the major suppressors and the pathways they regulate, including cell cycle progression, stress responses, apoptosis, and responses to DNA damage. (springer.com)
  • contamination results in circumstances of cellular tension because the bacterias induce DNA harm and disturb regular mobile homeostasis (including aberrant activation of multiple oncogenic pathways), which are circumstances that typically activate p53 [27,28]. (uberbrain.net)
  • Molecular signatures associated with tumor aggressiveness as well as with disease progression and their relation to differences in signaling pathways implicated in gliomagenesis have recently been described. (mdpi.com)
  • Taken together, these findings indicate that xanthohumol-induced cell death might involve intrinsic and extrinsic apoptotic pathways, as well as downregulation of XIAP, upregulation of p53 proteins, and S phase cell cycle arrest in Ca Ski cervical cancer cells. (hindawi.com)
  • Repression of HPV oncoproteins would therefore result in reactivation of tumor suppressor pathways and cause apoptosis in cancer cells. (healthymuslim.com)
  • Resveratrol suppresses IGF-1 induced human colon cancer cell proliferation and elevates apoptosis via suppression of IGF-1R/Wnt and activation of p53 signaling pathways. (biomedsearch.com)
  • Treatment with resveratrol suppressed IGF-1R protein levels and concurrently attenuated the downstream Akt/Wnt signaling pathways that play a critical role in cell proliferation. (biomedsearch.com)
  • Our data suggests that resveratrol not only suppresses cell proliferation by inhibiting IGF-1R and its downstream signaling pathways similar to that of IGF-1R siRNA but also enhances apoptosis via activation of the p53 pathway. (biomedsearch.com)
  • CONCLUSIONS: For the first time, we report that resveratrol suppresses colon cancer cell proliferation and elevates apoptosis even in the presence of IGF-1 via suppression of IGF-1R/Akt/Wnt signaling pathways and activation of p53, suggesting its potential role as a chemotherapeutic agent. (biomedsearch.com)
  • 10 - 13 However, given that each of these proteins has multiple functions, the implication of p53 directly might help us focus on a subset of their activities with regard to AS-relevant pathways. (aappublications.org)
  • In the case of DNA damage, the p53-mediated pathways are activated leading to cell cycle arrest and repair of the DNA. (ias.ac.in)
  • In this paper, we give an overview of our studies on the p53-MDM2 module and the associated pathways from a systems biology perspective. (ias.ac.in)
  • Since the p53 tumor-suppressor protein (TP53) is thought to play a novel role in cellular responses of a variety of non-genotoxic metabolic stresses, we characterized the involvement of TP53 in the response of breast cancer cells to FAS inhibition. (ingentaconnect.com)
  • Treatment with either cerulenin or C75 induced TP53 protein accumulation at 24 h in MCF-7 cells. (ingentaconnect.com)
  • In these conditions, TP53 protein levels were unchanged during the period of FAS-inhibitor exposure. (ingentaconnect.com)
  • To investigate the association and interaction of heat shock proteins B1(HSPB1)gene rs2868371 and tumor-suppressor protein p53(TP53)gene rs1042522 polymorphisms with chromosome damage levels among coke oven workers. (cdc.gov)
  • Symbolic non-synonymous single nucleotide variants (SNVs) of both the TP53 gene (P33R) in each single aneuploid CTCs, and the cyclin-dependent kinase inhibitor 2A ( CDKN2A ) tumor suppressor gene in each examined aneuploid CECs, were identified for the first time across patients with diverse carcinomas. (mdpi.com)
  • In addition, a recent report showed that ectopic expression of Wwox in breast cancer cells inhibits tumor growth in vivo ( 9 ). (pnas.org)
  • These novel findings raise the possibility of a functional interaction between PKR and p53 in vivo, which may account, at least in part, for the ability of each protein to regulate gene expression at both the transcriptional and the translational levels. (nih.gov)
  • These results suggest that SRC-1 and its family members may differentially modulate the p53 transactivation in vivo. (elsevier.com)
  • 1) Using proteasome inhibitors, p53 protein was significantly accumulated in primary nbroblasts as well as HeLa cells in vivo. (fujita-hu.ac.jp)
  • The kinetics of p53 in contaminated cells in vivo is apparently complex. (uberbrain.net)
  • Tryptic phosphopeptides of recombinant p53 phosphorylated in vitro by MAP kinase comigrated on two-dimensional maps with p53 from SV3T3 cells labeled in vivo with [32P]orthophosphate, suggesting that MAP kinase targets a site in p53 that is phosphorylated in the cell. (dundee.ac.uk)
  • ORF73, the HVS homologue of LANA, is shown to bind both p53 and pRb in vitro and in vivo, to colocalize with p53 in human T cells infected with HVS, and in cells overexpressing both ORF73 and p53, as well as to adversely influence pRB/E2F and p53 transcriptional regulation. (unr.edu)
  • In vivo, WA resulted in reduction of nearly 70% of the tumor volume in athymic nude mice with essentially similar trend in the modulation of molecular markers as in vitro. (healthymuslim.com)
  • Here we show that Msx1 interacts with p53 and inhibits tumor growth by inducing apoptosis in vitro and in vivo . (aacrjournals.org)
  • They provide evidence that the protein Mdm2 is a target for phosphorylation by Akt in vitro and in vivo. (sciencemag.org)
  • Here we show that the BRCA2 gene product is a 460-kDa nuclear phosphoprotein, which forms in vivo complexes with both p53 and RAD51. (pnas.org)
  • Our data suggest i) that neither Raf-l kinase nor PKC phosphorylate p53 directly in vivo, ii) that the reduced phosphorylation observed upon PMA treatment is independent of Raf, and perhaps mediated by indirect activation of phosphatases, iii) that the effects of PMA on p53-dependent transcription are not mediated by changes in the phosphorylation state of p53 itself. (spandidos-publications.com)
  • p53, a tumor suppressor protein has a prominent role in forestalling tumor development and advancement through its involvement in cell division control and initiation of apoptosis. (elsevier.com)
  • In the cell, p53 protein binds DNA, which in turn stimulates another gene to produce a protein called p21 that interacts with a cell division-stimulating protein (cdk2). (lifeboat.com)
  • HIN-A domain binds to the basic C terminus of p53, whereas the HIN-B domain binds to the core DNA-binding region of p53. (nih.gov)
  • Earlier work had shown how p53 binds to DNA as a stand-alone entity a. (bio-medicine.org)
  • This naturally occurring form contains a pairing of two p53 proteins, called a dimer, that then binds to a second p53 dimer in a similar way to create the precisely oriented four-protein complex, called a tetramer, that binds DNA. (bio-medicine.org)
  • The bottom line is that we now have a detailed picture of how p53 binds DNA," says Ronen Marmorstein, Ph.D., a professor in the Gene Expression and Regulation Program at Wistar and senior author on the study. (bio-medicine.org)
  • Earlier work had shown how p53 binds to DNA as a stand-alone entity, a form that does not represent the natural state of p53 binding to DNA. (bio-medicine.org)
  • The tumor suppressor p53 binding protein 1 (53BP1) binds to the DNA-binding domain of p53 and enhances p53-mediated transcriptional activation. (rupress.org)
  • For example, if a MAb binds to protein X with a Z-score of 43 and to protein Y with a Z-score of 14, then the S-score for the binding of that MAb to protein X is equal to 29. (neobiotechnologies.com)
  • It binds to MDM2, SV40 T antigen and human papilloma virus E6 protein. (neobiotechnologies.com)
  • PIP2 also binds strongly to p53 and causes the protein to associate with "small heat shock proteins. (medicalnewstoday.com)
  • Mdm2 binds to p53 in the nucleus and inhibits transcriptional activation by p53, and also carries p53 out of the nucleus, where the E3 ubiquitin ligase activity of Mdm2 modifies p53 and targets it for degradation. (sciencemag.org)
  • The amount of information that exists on all aspects of p53 normal function and mutant expression in human cancers is now vast, reflecting its key role in the pathogenesis of human cancers. (lifeboat.com)
  • Accumulation of p53 tumor suppressor gene protein: An independent marker of prognosis in breast cancers. (labcorp.com)
  • Defects of p53 are implicated in 50% of all cancers. (sciencephoto.com)
  • Structure determined for p53 tumor suppressor protein as bound to DNA for anti-cancer activity ( More than half of human cancers involve. (bio-medicine.org)
  • Clearly, a detailed view of the p53 protein in direct contact with DNA could provide important insights into preventing and treating an array of human cancers. (bio-medicine.org)
  • Given the fact that p53 is an important tumor suppressor that is mutated in the majority of human cancers, this will undoubtedly be useful information. (bio-medicine.org)
  • One new insight from the current study, for example, is that the point of contact between the two core domains of a pair of p53 proteins forming a dimer tracks to a part of the protein often mutated in cancers. (bio-medicine.org)
  • Combination therapy with sulindac and vitamin C could be a novel anti-cancer therapeutic strategy for p53 wild type colon cancers. (greenmedinfo.com)
  • Purpose: This study was designed to determine whether p53 protein accumulation in breast cancers correlates with p53 gene mutation, with survival, and with five pathobiologic factors associated with prognosis. (elsevier.com)
  • The authors also discuss how one ultimately derives a "tumor progression model," the drug discovery process, and the weaknesses of cancers that allow drugs to selectively kill them. (springer.com)
  • The team suggests that getting rid of mutant p53 could be a powerful way to fight cancers in which it is the key driver. (medicalnewstoday.com)
  • I am interested in the secreted frizzled-related proteins (SFRPs) because they are a family of proteins that antagonize Wnt signaling and loss of SFRP expression is found in a multitude of cancers, including breast cancer. (umass.edu)
  • Our data imply that, in addition to HPV, other tumor viruses may also contribute to the abnormal expression of cellular microRNAs in virus-associated cancers. (nih.gov)
  • Scientists have uncovered a survival mechanism that occurs in breast cells that have just turned premalignant-cells on the cusp between normalcy and cancers-which may lead to new methods of stopping tumors. (labspaces.net)
  • The p53 gene is commonly mutated in human cancers , but the molecular mechanisms regulating this event are not clear. (curehunter.com)
  • Targeting this nerve-tumor crosstalk could lead to more effective treatments for people with head and neck cancers. (nih.gov)
  • Past studies showed that these signals can also promote tumor progression in other cancers. (nih.gov)
  • Mutant p53 can no longer bind DNA in an effective way, and as a consequence the p21 protein is not made available to act as the 'stop signal' for cell division. (lifeboat.com)
  • B) Agarose EMSA of p53 (82-393) with wild-type or mutant IFI16 HIN-A (left). (nih.gov)
  • Furthermore, functional control of p53 via tetramer formation was demonstrated, based on the structure-function analysis of mutant p53. (springer.com)
  • The focus of this study was to determine if early detection of mutant p53 accumulation may be an early indicator of tumor aggressiveness and transformation to invasive breast cancer. (ac.ir)
  • It reacts with the mutant as well as the wild form of p53. (neobiotechnologies.com)
  • 2) Recombinant p53 proteins destined for wild- or mutant(273His)-type were analysed in an appropriate buffer and rabbit reticulpcyte lysates in vitro. (fujita-hu.ac.jp)
  • Much slower degradation of mutant-p53 was found compared with the case of wild-p53. (fujita-hu.ac.jp)
  • Uoiguitinated mutant-p53 becomes resistant to degradation, suggesting that mutant-p53 is hardly recognized and/or degraded by proteasome due to unknown mechanism. (fujita-hu.ac.jp)
  • LTR6 cells are derivatives of the murine myeloid M1 cell collection transporting the Val-135 temperature-sensitive p53 mutant (2). (desafioceroaedes.com)
  • p53 mutant oncoprotein has also been implicated in various tumours. (bvsalud.org)
  • Immunohistochemical analysis was employed to detect the co-expression of HPV and p53 mutant protein in biopsy specimens of patients of cancer oesophagus as well as controls. (bvsalud.org)
  • Seventy-seven percent of cases of oesophageal carcinoma showed strong immuno- staining for mutant p53 protein . (bvsalud.org)
  • A higher percentage (89%) of tissues showed immunoexpression of mutant p53 protein in conjunction with E6 oncoprotein of HPV 16 /18 indicating a selective degradation of key cellular protein of p53 having regulatory properties which in turn leads to uncontrolled cellular proliferation . (bvsalud.org)
  • Therefore, coexpression of oncoprotein E6 of HPV 16 /18 and mutant p53 protein may be considered as a "high risk " factor for progression to oesophageal malignancy . (bvsalud.org)
  • In support of this, the deletion was found to induce second-site reversion of the Val135 temperature-sensitive mutant of murine p53. (elsevier.com)
  • However, many mutant forms of p53 involve a change to a single building block, or amino acid, in the protein molecule, which prevents it from stopping the replication of cells with damaged DNA. (medicalnewstoday.com)
  • It is this association with heat shock proteins that stabilizes mutant p53 and allows it to promote cancer. (medicalnewstoday.com)
  • In our case, their binding to mutant p53 likely facilitates its cancer-promoting actions, something we are actively exploring," he adds. (medicalnewstoday.com)
  • They also found that disrupting the PIP2 pathway prevented the accumulation of mutant p53, effectively stopping it from promoting tumor development. (medicalnewstoday.com)
  • The researchers are already trawling for compounds that block PIPK1-alpha and could become candidate drugs for the treatment of tumors with mutant p53. (medicalnewstoday.com)
  • It has been implicated in transcriptional regulation by modulating protein-protein interactions with p53 tumor suppressor protein and other transcription factors. (nih.gov)
  • p53 plays an important role in cell cycle regulation. (elsevier.com)
  • Vitamin C enhanced cisplatin sensitivity and apoptosis via up-regulation of p53. (greenmedinfo.com)
  • The tumor suppressor p53 protein is most important for cell regulation such as cell cycle and apoptosis. (fujita-hu.ac.jp)
  • Down-regulation of DL-cycloserine manufacture p53 was discovered to facilitate autophagy in contaminated cells [35]. (uberbrain.net)
  • In contaminated Mongolian gerbils, which are generally used for research of infection, manifestation of p53 was transformed inside a bimodal style, with a build up after initial contamination that was accompanied DL-cycloserine manufacture by an instant down-regulation of p53 proteins in gastric epithelial cells. (uberbrain.net)
  • Since p53 is targeted by Mdm2 for ubiquitin-mediated proteasome-dependent degradation, this region is also essential for the regulation of p53's stability in response to stress signals. (elsevier.com)
  • As these cells with limited functions are inefficient in performing body activities, they are programmed to self demolition under the presence of apoptotic signals, such as caspase proteins and Bcl-2 family regulation proteins. (wikipedia.org)
  • Therefore, decreased functional p53 and p21 tumor suppression may allow for tumor progression and loss of BCL2 suggests improper regulation of apoptosis. (thefreelibrary.com)
  • One of the most effective mechanisms is regulation of p53 protein stability. (aacrjournals.org)
  • This modification of p53 has far-reaching implications for the regulation of biochemical and cellular functions of p53. (eurekalert.org)
  • This study is the first compelling evidence to show tumor viruses are involved in the regulation of microRNA expression," said Zheng. (nih.gov)
  • The following experiments examined the role of the gonadal hormone estrogen in comparison to the neurotrophins, in the regulation of p53-dependent cortical cell fate. (jneurosci.org)
  • 2014). The tumor suppressor secreted frizzled related protein 1 regulates p53-mediated apoptosis. (umass.edu)
  • 19 - 21 At the same time, p53 negatively regulates the proliferation and survival of adult neuronal stem cells, without affecting their differentiation potential. (aappublications.org)
  • MDM2 negatively regulates the activity of p53. (ias.ac.in)
  • Remarkably, tumor-associated FAS hyperactivity represents a novel target for anti-metabolic therapy because pharmacological inhibitors of FAS are selectively cytotoxic for tumor cells, triggering their apoptotic cell death. (ingentaconnect.com)
  • When the HCT116 ( $p53^{+/+}$ ) and HCT116 ( $p53^{-/-}$ ) cells were treated with $2.5{\sim}10{\mu}M$ $17{\alpha}-E_2$ for 48 h or with $10{\mu}M$ for various time periods, cytotoxicity and an apoptotic sub- $G_1$ peak were induced in the HCT116 ( $p53^{+/+}$ ) cells in a dose- and time-dependent manner. (koreascience.or.kr)
  • However, the HCT116 ( $p53^{-/-}$ ) cells were much less sensitive to the apoptotic effect of $17{\alpha}-E_2$ . (koreascience.or.kr)
  • Together, these results show that among the components of the $17{\alpha}-E_2$ -induced apoptotic-signaling pathway, which proceeds through mitotic spindle defects causing mitotic arrest, subsequent activation of Bak and Bax and the mitochondria-dependent caspase cascade, leading to PARP degradation, $17{\alpha}-E_2$ -induced activation of Bak and Bax is the upstream target of proapoptotic action of p53. (koreascience.or.kr)
  • Identifying a key role for the apoptotic protein, Bax, in p53-mediated cell death signaling. (washington.edu)
  • If repair is not possible due to excessive damage, the p53-mediated apoptotic pathway is activated bringing about cell death. (ias.ac.in)
  • Thus cells divide uncontrollably, and form tumors. (lifeboat.com)
  • C ) p53 and Myc-Wwox were coexpressed in 293 cells and immunoprecipitated by anti-p53, anti-IgG, or anti-Myc antibodies, followed by immunoblotting with anti-p53 ( Upper ) or anti-Myc ( Lower ). (nih.gov)
  • Abgent has over fifteen years of experience producing recombinant proteins in E. coli and mammalian cells (CHO and HEK293, etc), and we have added a powerful yeast expression platform to our menu of services. (abgent.com)
  • Stabilization and Reactivation of the p53 Tumor Suppressor Protein in Nontumorigenic Revertants of HeLa Cervical Cancer Cells -- Athanassiou et al. (aacrjournals.org)
  • First, altered antigen processing resulting from the formation of p53/SVT complexes might activate autoreactive T helper cells specific for cryptic epitopes of murine p53, driving anti-p53 autoantibody production. (rupress.org)
  • Alternatively, SVT-responsive T cells may provide intermolecular-intrastructural help to B cells specific for murine p53. (rupress.org)
  • In a second stage, these activated B cells might themselves process self p53, generating p53-responsive autoreactive T cells. (rupress.org)
  • The histone demethylase JMJD2B is critical for p53-mediated autophagy and survival in Nutlin-treated cancer cells. (rush.edu)
  • Modeling the Etiology of p53-mutated Cancer Cells. (rush.edu)
  • Novel roles for p53 in the genesis and targeting of tetraploid cancer cells. (rush.edu)
  • Interestingly, cotransfection of HeLa cells with SRC-1- or p/ClP expression vector potentiated the p53-mediated transactivation, whereas AIB1 and xSRC-3 were repressive. (elsevier.com)
  • In most transformed and tumor cells the concentration of p53 is increased 51000 fold over the minute concentrations (1000 molecules cell) in normal cells, principally due to the increased half-life (4 h) compared to that of the wild-type (20 min). (abeomics.com)
  • Restoration of p53 function causes death of tumor cells and is potentially suitable for gene therapy of cancer. (nih.gov)
  • HeLa cervical carcinoma cells (HPV-18) with a reporter construct containing the b -galactosidase gene under the control of a p53-responsive promoter were used as a test system to screen a library of small molecules for restoration of the transcriptional activity of p53. (nih.gov)
  • Activation of p53 in cervical carcinoma cells was accompanied by induction of p53-dependent CDKN1 (p21), inhibition of cell proliferation, and induction of apoptosis. (nih.gov)
  • In HPV-infected cells including HeLa cells, a viral oncpprptein E6 and a cellular E6-associated protein (E6AP) function together as a ubiquitin ligase targetting for p53. (fujita-hu.ac.jp)
  • However, the mechanism of p53 degradation in normal cells remains unclear. (fujita-hu.ac.jp)
  • In summary, E6AP may also work in the p53 ubiquitination in normal cells adding to E6-dependent case. (fujita-hu.ac.jp)
  • disease is known as to end up being the most powerful known risk aspect for gastric tumor, and epidemiological research have approximated that, in the lack of infection depends upon connections between bacterial elements and web host cells. (uberbrain.net)
  • One of the most well characterized bacterial virulence determinants will be the vacuolating cytotoxin A (pathogenicity isle (can be a 40 kb area of DNA that encodes a sort IV secretion program (T4SS) that forms a syringe-like pilus framework useful for the shot of the bacterial proteins CagA (cytotoxin-associated gene A) into gastric cells. (uberbrain.net)
  • Open up in another home window Fig 2 Discussion between and gastric epithelial cells leads to cellular tension.After adherence, translocates CagA protein into host cells using the T4SS. (uberbrain.net)
  • Following serum stimulation of quiescent C57MG cells, two p53 kinases, which were resolved by chromatography on Mono Q, were stimulated 15-20-fold within 5 min. (dundee.ac.uk)
  • These protein kinase activities were also stimulated following exposure of the cells to ultraviolet radiation, but with slightly delayed kinetics. (dundee.ac.uk)
  • Their gene products are known to activate telomerase, prevent death of human primary epithelial cells, and inactivate major tumor suppressors (p53 and pRB proteins) [ 2 ]. (hindawi.com)
  • p53 also blocks cells at the G2/M checkpoint by inhibiting the function of p34cdc2, the cyclin-dependent kinase required for access into mitosis. (desafioceroaedes.com)
  • The regulatory effect of the tumor-suppressor protein p53 on the apoptogenic activity of $17{\alpha}$ -estradiol ( $17{\alpha}-E_2$ ) was compared between HCT116 ( $p53^{+/+}$ ) and HCT116 ( $p53^{-/-}$ ) cells. (koreascience.or.kr)
  • In addition, $17{\alpha}-E_2$ -induced activation of Bak and Bax, ${\Delta}{\Psi}m$ loss, and PARP degradation were more dominant in the HCT116 ( $p53^{+/+}$ ) than in the HCT116 ( $p53^{-/-}$ ) cells. (koreascience.or.kr)
  • In accordance with enhancement of p53 phosphorylation (Ser-15) and p53 levels, p21 and Bax levels were elevated in the HCT116 ( $p53^{+/+}$ ) cells treated with $17{\alpha}-E_2$ . (koreascience.or.kr)
  • The HCT116 ( $p53^{-/-}$ ) cells exhibited barely or undetectable levels of p21 and Bax, regardless of $17{\alpha}-E_2$ treatment. (koreascience.or.kr)
  • On the other hand, although the level of Bcl-2 was slightly lower in the HCT116 ( $p53^{+/+}$ ) than in the HCT116 ( $p53^{-/-}$ ) cells, it remained relatively constant after the $17{\alpha}-E_2$ treatment. (koreascience.or.kr)
  • This is the first demonstration indicating that WA significantly downregulates expression of HPV E6/E7 oncogenes and restores the p53 pathway, resulting in apoptosis of cervical cancer cells. (healthymuslim.com)
  • The p53 tumour suppressor protein plays a central role in maintaining genomic integrity in eukaryotic cells. (elsevier.com)
  • The mechanisms involve the proteins and DNA sequences inside cells. (wikipedia.org)
  • RATIONALE: Sorafenib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. (bioportfolio.com)
  • The p53 protein functions to selectively destroy stressed or abnormal cells to prevent the progression to cancer (3) . (aacrjournals.org)
  • Protein stability is regulated, in normal as well as malignant cells, by ubiquitin-dependent proteolysis. (aacrjournals.org)
  • A complete switch from Mdm2 to E6-dependent degradation of p53 has been shown to occur in HPV-positive cervical cancer cells (9) . (aacrjournals.org)
  • Consistent with this, the expression of peptides that specifically bind to E6 results in p53 accumulation and apoptosis in HPV-positive cancer cells (10) . (aacrjournals.org)
  • Roles of DNA-dependent protein kinase and ATM in cell-cycle-dependent radiation sensitivity in human cells. (biomedsearch.com)
  • PURPOSE: The roles of DNA-dependent protein kinase (DNA-PK) and ATM in the cell-cycle-dependent radiosensitivity in human cells were investigated. (biomedsearch.com)
  • Scientists at EPFL have found a way to starve liver cancer cells by blocking a protein that is required for glutamine breakdown-while leaving normal cells intact. (medicalxpress.com)
  • In this way, nonmutant p53 prevents cells with damaged DNA from dividing and potentially growing into cancerous tumors. (medicalnewstoday.com)
  • Using a range of cell cultures, the team behind the new study discovered that the PIPK1-alpha enzyme links up with p53 to make PIP2 when cells become stressed due to DNA damage or another cause. (medicalnewstoday.com)
  • white blood cells (WBCs)), or those unique carcinoma cells with double positive expression of surface epithelial cell adhesion molecule (EpCAM) for isolation, and intracellular structural protein cytokeratins (CKs) for identification. (mdpi.com)
  • With respect to detecting the full spectrum of highly heterogeneous circulating rare cells (CRCs), including CTCs and circulating endothelial cells (CECs), it is imperative to develop a strategy systematically coordinating all tri-elements of nucleic acids, biomarker proteins, and cellular morphology, to effectively enrich and comprehensively identify CRCs. (mdpi.com)
  • Circulating tumor cells (CTCs) are cancer cells shed from primary or metastatic solid tumors into peripheral blood, whereas circulating endothelial cells (CECs) are derived from endothelial cells (ECs) of blood vessels into circulation. (mdpi.com)
  • In addition to aneuploid cancer cells and aneuploid endothelial cells localized in tumor tissues, existence of aneuploid CTCs and CECs in peripheral blood has been recently reported [ 8 ]. (mdpi.com)
  • Nonetheless, how those diverse types of aneuploid malignant cells cross-talk and inter-play in tumor formation and metastasis remains to be further investigated. (mdpi.com)
  • Detection of circulating rare cells (CRCs), including both CTCs and CECs, is the most representative of liquid biopsy due to its unique availability of frequent and non-invasive detecting tumor cells in carcinoma patients. (mdpi.com)
  • Distinguished contributions to understanding p53 tumor suppression in stem cells and breakthrough advances in treating breast cancer have earned two scientists at The University of Texas MD Anderson Cancer Center membership in a notable association of scholars. (mdanderson.org)
  • The team found that interfering with the expression of E6 in HPV-infected cervical cancer cells grown in the laboratory led to increased expression of both p53 protein and miR-34a. (nih.gov)
  • The Zheng team is working to identify miR-34a targets in HPV-infected cells in order to understand the mechanism by which decreased expression of a microRNA favors tumor formation. (nih.gov)
  • But some will become tumors and, at this point, there is no way to predict which of these cells are a risk. (labspaces.net)
  • Scientists also recognized that cancer cells that "want" to spread learn how to use TGF-β wound-healing function to break from a tumor, he says. (labspaces.net)
  • The p53 pathway must be sabotaged for cells to become cancerous," Lopez-Diaz says. (labspaces.net)
  • The team examined premalignant as well as cancer cells from breast and lung tumors and matched normal and premalignant breast cells from healthy women provided by scientists at the University of California San Francisco. (labspaces.net)
  • The STAT protein (Signal Transducers and Activators of Transcription) family contains transcription factors that are specifically activated to regulate gene transcription when cells encounter cytokines and growth factors, hence they act as signal transducers in the cytoplasm and transcription activators in the nucleus [ PMID: 12039028 ]. (ebi.ac.uk)
  • In normal cells, the level of p53 proteins is kept low by MDM2, i.e. (ias.ac.in)
  • The phosphorylation pattern of p53 was analysed in normal or v-raf-transformed rat cells or in insect cells which were co-infected with recombinant baculoviruses encoding p53, protein kinase C and c-Raf. (spandidos-publications.com)
  • The presence of activated v-raf kinase or treatment of cells with PMA, which resulted in activation of both v-raf and c-Raf kinases, did not reveal any additional phosphorylation sites in p53 nor did any of the known sites show enhanced phosphorylation, neither in rat nor in baculovirus-infected insect cells. (spandidos-publications.com)
  • Gastrin-regulated expression of p53 in transformed enterochromaffin-like cells in the African rodent mastomys. (curehunter.com)
  • RT-PCR and molecular sequence analysis of p53 were undertaken with mRNA isolated from purified ECL cells. (curehunter.com)
  • Overproduction of the wild type of p53 was evident in ECL cells during hypergastrinemia, and the molecular characteristics of p53 were determined in naive and transformed ECL cells. (curehunter.com)
  • Cells that were dosed with the pollutants showed all three stress markers at higher levels than control cells that were not exposed to them: The pollutants from the organic solvent, for instance, increased p53 production about sixfold. (popularmechanics.com)
  • Scientists discovered a new role for nerves in oral cancer progression, in which tumor cells send genetic messages that transform nerves into cancer-promoting agents. (nih.gov)
  • Effective therapies must target both the tumor and its microenvironment-the supportive network of connective tissue, blood vessels, cells, and molecules that surround the tumor. (nih.gov)
  • Sensory neurons (a type of nerve cell) in culture that were exposed to p53-deficient oral cancer cells sprouted projections called neurites. (nih.gov)
  • The scientists found that spherical delivery vehicles called extracellular vesicles were transferring the microRNAs from tumors to nerve cells in the microenvironment. (nih.gov)
  • 5. Visakorpi T, Kallioniemi OP, Heikkinen A, Koivula T, Isola J. Small subgroup of aggressive, highly proliferative prostatic carcinomas defined by p53 accumulation. (labcorp.com)
  • There was complete concordance between p53 gene mutation and p53 protein accumulation in the 15 snap-frozen carcinomas and in both breast carcinoma cell lines. (elsevier.com)
  • Statistically significant associations of p53 protein accumulation with estrogen receptor negativity and with high nuclear grade were found. (elsevier.com)
  • There were statistically significant associations, independent of other prognostic factors, between p53 protein accumulation and metastasis-free and overall survival, for randomly accrued and for both sporadic and familial tumors. (elsevier.com)
  • Conclusions: Immu-nohistochemically detected p53 protein accumulation was an independent marker of shortened survival and was seen more often in familial than in sporadic carcinomas. (elsevier.com)
  • Our findings also suggest a correlation between p53 protein accumulation was an independent marker of shortened survival and was seen more often in familial than in sporadic carcinomas. (elsevier.com)
  • Our findings also suggest a correlation between p53 protein accumulation and p53 gene mutation. (elsevier.com)
  • Analysis of binding affinities of TTD toward methylated p53 and histones reveals strong preference of 53BP1 for p53K382me2, H4K20me2, and H3K36me2 and suggests a possible role of multivalent contacts of 53BP1 in p53 targeting to and accumulation at the sites of DNA damage. (rcsb.org)
  • This structure revolutionises existing concepts of p53's molecular organisation and resolves conflicting data relating to its biochemical properties. (whiterose.ac.uk)
  • With state-of-the art molecular biology and protein biochemistry labs, we work with our clients to rapidly evaluate in parallel to identify the optimal expression system for candidate proteins. (abgent.com)
  • The identification of a novel function of Msx1 as a p53 regulator may open new avenues for developing improved molecular therapies for tumors with a nonmutational p53 inactivation mechanism. (aacrjournals.org)
  • The discovery concerns the molecular activity of the tumor suppressor protein p53. (medicalnewstoday.com)
  • Our discovery of this new molecular complex points to several different ways to target p53 for destruction, including blocking [PIPK1-alpha] or other molecules that bind to p53. (medicalnewstoday.com)
  • Comprehensive co-detecting observable aneuploid CTCs and CECs by SE-iFISH, along with applicable genomic and/or proteomic single cell molecular profiling, are anticipated to facilitate elucidating how those disparate categories of aneuploid CTCs and CECs cross-talk and functionally interplay with tumor angiogenesis, therapeutic drug resistance, tumor progression, and cancer metastasis. (mdpi.com)
  • p53 triggers several molecular processes that bring cell division to a stop ("cell cycle arrest") and improve the accuracy of DNA repair. (eurekalert.org)
  • The scientists from Konstanz have now deciphered the molecular mechanism how the biochemical and cellular functions of p53 in interaction with the enzyme PARP-1 are controlled. (eurekalert.org)
  • Metallothionein (MT) is a family of cysteine-rich, low molecular weight (MW ranging from 500 to 14000 Da) proteins. (wikipedia.org)
  • In their Molecular Cell study, the Salk Institute researchers report that a protein known as transforming growth factor beta (TGF-β), considered a tumor suppressor in early cancer development, can actually promote cancer once a cell drifts into a pre-cancerous state. (labspaces.net)
  • Nevertheless, initial research from the p53 tension response revealed that's in a position to dampen activity of p53 proteins by inducing its quick degradation [20]. (uberbrain.net)
  • The transactivation activity of p53 was assayed under the same conditions, using an mdm2-promoter luciferase reporter gene construct. (spandidos-publications.com)
  • Thus, PMA seemed to have separable effects on phosphorylation and transactivation activity of p53. (spandidos-publications.com)
  • Recombinant wild-type mouse p53 was phosphorylated in vitro by activated recombinant p42-MAP kinase but not by inactive MAP kinase or by the activating protein, MAP kinase kinase. (dundee.ac.uk)
  • The two kinase activities from the lysates targeted the same phosphorylation sites on p53 as the purified recombinant MAP kinase. (dundee.ac.uk)
  • Expression of p53 protein in colorectal cancer and its relationship to short-term prognosis. (labcorp.com)
  • Preliminary data indicated that the presence of immunopositive p53 may be a valid predictive indicator of the prognosis of individuals with DCIS and transformation to invasive breast cancer. (ac.ir)
  • Another protein, P53 is a known tumor suppressor. (labspaces.net)
  • PKR/p53 complex formation in vitro requires the N-terminal regulatory domain of PKR and the last 30 amino acids of the C-terminus of human p53. (nih.gov)
  • In addition, p53 may function as a substrate of PKR since phosphorylation of human p53 on serine392 is induced by activated PKR in vitro. (nih.gov)
  • Efforts to elucidate its function have revealed a putative transcriptional activation domain and in vitro interaction with the DNA repair protein RAD51. (pnas.org)
  • Moreover, yeast two-hybrid and glutathione S -transferase (GST) pull-down analysis revealed that BRCA2 interacts in vitro with RAD51, a protein involved in DNA double-strand break repair and homologous recombination ( 27 , 35 , 36 ). (pnas.org)
  • Elevation of TSAP6 expression augments cell-cycle delay and apoptosis, suggesting that TSAP6 might play a pivotal role in tumor suppression. (desafioceroaedes.com)
  • HPV inhibits natural tumor suppression by inactivating a cellular tumor suppressor protein called p53. (nih.gov)
  • The researchers also observed that induced expression of miR-34a suppressed cell growth and promoted cell death, which suggests that this microRNA also plays a role in tumor suppression. (nih.gov)
  • PKR is an interferon (IFN)-inducible protein that is thought to mediate the anti-viral and anti-proliferative effects of IFN via its capacity to inhibit protein synthesis. (nih.gov)
  • In particular, our results imply that autoimmunity can be initiated by a "hit and run" mechanism in which the binding of a viral antigen to a self protein triggers an immune response that subsequently can be perpetuated by self antigen. (rupress.org)
  • Hence, a possible approach to p53 reactivation is the use of small molecules suppressing the function of viral proteins. (nih.gov)
  • Viral proteins, in complexes termed "capsomers," form the surface of the icosahedron. (encyclopedia.com)
  • These functions of p53 are regulated both by protein-protein interactions and phosphorylation. (nih.gov)
  • The aim of this study was to characterise this conserved region and investigate its role in the biological functions of p53. (elsevier.com)
  • Nuclear overexpression of p53 protein in transitional cell bladder carcinoma: A marker for disease progression. (labcorp.com)
  • One key protein that coordinates DNA repair with cell cycle progression and apoptosis is the tumor suppressor protein p53. (rupress.org)
  • The p53 tumor suppressor protein plays a crucial role in tumorigenesis by controlling cell-cycle progression and apoptosis. (desafioceroaedes.com)
  • Part of the cell-cycle regulatory function of p53 entails the induction of p21waf-1 (14, 15), an inhibitor of cyclin-dependent kinases, which inhibits cell-cycle progression at both G1 and G2 (16C18). (desafioceroaedes.com)
  • Inactivation of pRb promotes host cell cycle progression into S phase, and inactivation of p53 promotes cell immortalization. (unr.edu)
  • DLEC1 methylation was frequently detected in ESCC tumors and correlated with lymph node metastasis, tumor recurrence and progression, with DLEC1 as the most frequently methylated among the established 3p22.2 tumor suppressors ( RASSF1A, PLCD1 and ZMYND10/BLU ). (thno.org)
  • In general, physicians and dentists know little about what causes oral tumor development and progression. (scielo.br)
  • Recent studies suggest that these nerves play a role in tumor growth and progression. (nih.gov)
  • We wanted to understand the reciprocal tumor-nerve signals that drive cancer progression," Amit says. (nih.gov)
  • ΔNp73 lacks the transactivation domain and possesses a dominant negative activity against p73, as well as p53 ( 15 ). (pnas.org)
  • This architecture of p53 in toto suggests novel mechanisms for structural plasticity, which enables the protein to bind variably spaced DNA target sequences, essential for p53 transactivation and tumour suppressor functions. (whiterose.ac.uk)
  • The p53 protein contains six highly conserved regions, one of which, termed Box I, is located in the N-terminal transactivation domain (amino acid residues 13 and 26). (elsevier.com)
  • Biochemical analyses demonstrate that deletion of residues 13 to 16 significantly increases both the transcriptional transactivation and G 2 arrest-inducing activities of murine p53. (elsevier.com)
  • Residues 13 to 16 appear to function as a regulatory element in p53, modulating p53-dependent transcriptional transactivation and cell-cycle arrest, possibly by affecting the structural stability of the core domain of the protein. (elsevier.com)
  • We investigated a possible influence of the raf kinase on phosphorylation and transactivation of p53. (spandidos-publications.com)
  • Therefore, it is not surprising that the loss of p53 function(s) is linked to the development of human cancer . (clicktocurecancer.info)
  • Mutation and/or allelic loss of p53 is one of the causes of a variety of mesenchymal and epithelial tumors. (abeomics.com)
  • These results suggest that loss of p53 in oral cancer enhances nerve growth and density in the tumor microenvironment. (nih.gov)
  • Loss of p53 drives neuron reprogramming in head and neck cancer. (nih.gov)
  • Monoclonal antibodies, such as cetuximab, can block tumor growth in differen. (bioportfolio.com)
  • In the present studies, we generated polyclonal and monoclonal antibodies to characterize endogenous BRCA2 and identify proteins that form complexes with this protein. (pnas.org)
  • As the 'guardian of the genome', p53 is the main regulator preventing carcinogenic and teratogenic lesions [24, 25]. (clicktocurecancer.info)
  • In addition, the two compounds dramatically decreased transcription of the HPV genome, which was assumed to cause p53 reactivation. (nih.gov)
  • The length of helical viruses can depend on the length of the genome, the DNA or RNA within, since there are often regular structural interactions between the nucleic acids of the genome and the proteins that cover it. (encyclopedia.com)
  • The p53 protein protects the genome in several ways. (medicalnewstoday.com)
  • In this way, p53 counteracts the development of cancer and is therefore also known as the 'guardian of the genome'", says Mangerich. (eurekalert.org)
  • Thus, BRCA2 likely participates with p53 and RAD51 in maintaining genome integrity. (pnas.org)
  • The tumor suppressor protein p53 exerts its cell cycle-regulatory effects through its ability to function as a sequence-specific DNA-binding transcription factor. (elsevier.com)
  • Herein, we show that p53 physically interacts with specific subregions of steroid receptor coactivator-1 (SRC-1) and its family members, p/ClP (p300/CBP interacting protein), xSRC-3, and AIB1 (amplified in breast cancer), originally isolated as transcription coactivators of nuclear receptors, as demonstrated by the yeast and mammalian two-hybrid tests as well as glutathione S-transferase pull-down assays. (elsevier.com)
  • This inhibition also takes place in the presence of general inhibitors of transcription and/or translation such as the antibiotics rifampin, chloramphenicol, and spectinomycin ( 40 ) and through the inhibition of translation by the Doc protein of prophage P1 ( 21 ). (asm.org)
  • In addition to the zinc that is bound to enzymes, transcription factors, and other proteins, about 10 percent of CNS zinc is in the free form and is associated with presynaptic vesicles of glutamatergic neurons. (nap.edu)
  • In fact, they found that TGF-β halts both the transcription of the p53 gene-the process by which cellular machinery reads the DNA code for a gene-and the subsequent process by which the corresponding p53 protein is produced, known as translation. (labspaces.net)
  • The double-stranded RNA activated protein kinase PKR is a serine/threonine kinase that modulates protein synthesis through the phosphorylation of translation initiation factor eIF-2alpha. (nih.gov)
  • Swaminathan, Robinson and colleagues report that the kinase YopO phosphorylates and thereby constitutively activates the actin-severing host protein gelsolin. (asbmb.org)
  • We have investigated the phosphorylation of p53 by mitogen-activated protein (MAP) kinase, a protein kinase that plays a central role in mediating many mitogenic and differentiation signals. (dundee.ac.uk)
  • Phosphorylation of p53 by MAP kinase occurred at two N-terminal sites, threonine residues 73 and 83. (dundee.ac.uk)
  • Each of these kinase activities co-eluted with myelin basic protein kinase activity and could be inactivated following treatment with protein phosphatase 2A, a serine/threonine phosphatase, or leukocyte antigen receptor, a protein tyrosine phosphatase, suggesting that these activities were members of the MAP kinase family. (dundee.ac.uk)
  • The data suggest that p53 may be phosphorylated by MAP kinase physiologically and that this interaction may be involved in the cell's response to UV exposure, growth factor stimulation, or transformation by oncogenes. (dundee.ac.uk)
  • Proliferative-Enriched for neural stem cell markers, PTEN loss, EGFR amplified or normal, Akt (protein kinase B) cell signaling pathway activation, shorter survival than proneural subgroup. (mdpi.com)
  • This in turn led to calcium influx and to the calcium-mediated activation of protein kinase C/NADPH (nicotinamide adenine dinucleotide phosphate) oxidase as well as nitric oxide synthase (Aimo et al. (nap.edu)
  • Members of the Akt (also known as protein kinase B) family have been implicated in tumorigenesis ever since their discovery as a cellular gene coopted by a transforming retrovirus. (sciencemag.org)
  • Results: Nuclear p53 protein was observed in 16% of the 31 in situ carcinomas, 22% of the 172 sporadic carcinomas, 34% of the 50 tumors from patients with familial breast cancer, 52% of the 23 tumors from patients with the familial breast and ovarian cancer syndrome, and all three tumors from two patients with the Li-Fraumeni syndrome. (elsevier.com)
  • Oncogenic STAT3 signaling activation and 3p22-21.3 locus alteration are common in multiple tumors, especially carcinomas of the nasopharynx, esophagus and lung. (thno.org)
  • Sebaceous carcinomas have significantly increased nuclear staining with p53 and Ki-67 (MIB-1) and reduced levels of BCL2 and p21, in comparison to sebaceous adenomas and sebaceous epitheliomas. (thefreelibrary.com)
  • Sebaceous carcinomas are associated with increased, presumably defective, p53. (thefreelibrary.com)
  • In seeking to determine the structure of p53 bound to DNA, the challenge for the scientists was that their efforts to crystallize the p53 dimer bound to DNA consistently resulted in structures that could not bind to DNA. (bio-medicine.org)
  • Orlova, Elena V. / The structure of p53 tumour suppressor protein reveals the basis for its functional plasticity . (utmb.edu)
  • If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood. (lifeboat.com)
  • Our findings reveal a functional cross-talk between p73 and Wwox tumor suppressor protein. (pnas.org)
  • The p73 protein is a structural and functional homolog of the p53 tumor suppressor protein ( 12 , 13 ). (pnas.org)
  • Donato R. S100: a multigenic family of calcium-modulated proteins of the EF-hand type with intracellular and extracellular functional roles. (springer.com)
  • Structural and functional characterization of the endogenous BRCA2 protein have been hampered by the large size of the protein and the lack of suitable immunological reagents for its detection. (pnas.org)
  • Because an immediate cellular reponse to DNA damage is p53-mediated cell cycle arrest ( 37 ), and RAD51 has been reported to physically associate with p53 ( 38 , 39 ), we also investigated whether a physical and functional relationship could be detected between BRCA2 and p53. (pnas.org)
  • 22 In its absence (mouse p53 -null, in which p53 is no longer functional), neuronal stem cell self-renewal and the number of differentiated neurons increases. (aappublications.org)
  • Normally happening polyphenolic phytochemicals have already been reported to inhibit tumor [12, 13] and Rabbit polyclonal to ABHD14B in addition display potential binding to MDM2 in its hydrophobic grooves [14, 15]. (colinsbraincancer.com)
  • Open up in another windowpane Tipifarnib Fig 1 Framework of p53 binding website of MDM2 (A) Ribbon, (B) Surface area. (colinsbraincancer.com)
  • The crystal structure of MDM2 (PDB ID 1RV1) was from the RCSB proteins data standard bank. (colinsbraincancer.com)
  • Recent evidence shows that several proteins involved in oncogenesis, such as ADP ribosylation factor, oncogenic Ras, RB, and TSG101, also affect the stability of p53 by modulating Mdm2-mediated degradation (reviewed in ref. 7 ). (aacrjournals.org)
  • Mdm2 functions to regulate the tumor suppressor protein p53. (sciencemag.org)
  • All of this now appears to depend on the activity of Akt because phosphorylation of Mdm2 is required for translocation of Mdm2 from the cytoplasm to the nucleus, where it can contact p53. (sciencemag.org)
  • The p53-MDM2 negative feedback loop constitutes the core module of a network of regulatory interactions activated under cellular stress. (ias.ac.in)
  • Coincidentally, estrogen rapidly increased and then decreased MDM2 relative to controls, suggesting temporal modulation of p53 function. (jneurosci.org)
  • Between them, they appear to regulate the function of p53. (medicalnewstoday.com)
  • Demonstrating that neurons express unique, alternatively spliced forms of the proteins that regulate mitochondrial dynamics which confer the proteins with distinct activities. (washington.edu)
  • MicroRNAs are short strands of RNA that regulate protein expression by binding to specific messenger RNA molecules and inhibiting them from their normal function, which is to direct the production of proteins. (nih.gov)
  • In cervical carcinoma, human papilloma virus (HPV) E6 facilitates proteasomal degradation of p53. (nih.gov)
  • The capability to induce degradation of p53 varies between strains, with CagA-positive bacterias being stronger [20,29]. (uberbrain.net)
  • Although CagA most likely does not straight bind to p53, it induces its degradation [29]. (uberbrain.net)
  • Notably, ectopic transfection of CagA is enough to inhibit p53 activity and induce its degradation [20,30]. (uberbrain.net)
  • It was demonstrated that amounts and organic variability of CagA proteins highly impact p53 degradation [32]. (uberbrain.net)
  • These findings resulted in a hypothesis that, at a particular time, degrees of p53 reveal an equilibrium between p53 degradation. (uberbrain.net)
  • Interferon-inducible protein 16: insight into the interaction with tumor suppressor p53. (nih.gov)
  • Analysis of S2 subunit of SARS-nCoV-2 interaction with tumor suppressor proteins. (cdc.gov)
  • The results disclosed that relatively small changes in tetramer formation, induced by the stabilization or inhibition of homo-tetramerization, could control p53 function. (springer.com)
  • Now, in a new study featured as a "paper of the week" and on the cover of the July 21 issue of the Journal of Biological Chemistry, researchers at The Wistar Institute have successfully determined the three-dimensional structure of the p53 protein bound as a dimer to DNA and used the structure to produce an accurate model of the p53 tetramer bound to DNA. (bio-medicine.org)
  • This suggests that the interface between the two proteins of the dimer is likely as important for the proper functioning of the tetramer as its interface with DNA, which also depends on the interface of the core domains of the two p53 proteins that form a dimer. (bio-medicine.org)
  • Using ATP-stabilised p53, we have employed cryoelectron microscopy and single particle analysis to solve the first three-dimensional structure of the full-length p53 tetramer (resolution 13.7 Å). (whiterose.ac.uk)
  • The p53 molecule is a D2 tetramer, resembling a hollow skewed cube with node-like vertices of two sizes. (whiterose.ac.uk)
  • However, preliminary cross-linking studies do not detect disruption of p53 tetramerization by either LANA or HVS-encoded ORF73, suggesting that p53 inactivation may be by a mechanism independent of tetramer disruption. (unr.edu)
  • Tetramer formation of tumor suppressor protein p53: Structure, function, and applications. (ebi.ac.uk)
  • All known DNA tumor viruses are known to target and inactivate two main cell cycle regulatory proteins, retinoblastoma protein (pRb) and p53. (unr.edu)
  • The DNA tumor virus Kaposi's sarcoma associated herpesvirus (KSHV)-encoded latency-associated nuclear antigen (LANA) was shown to target and inactivate pRb as well as p53. (unr.edu)
  • Cervical cancer is caused by human papilloma virus ( HPV ) expressing E6 and E7 oncoproteins, which are known to inactivate tumor suppressor proteins p53 and pRb, respectively. (healthymuslim.com)
  • Association of p53 protein expression with tumor cell proliferation rate and clinical outcome in node-negative breast cancer. (labcorp.com)
  • Immunohistochemical co-expression of human papillomavirus type 16/18 transforming (E6) oncoprotein and p53 tumour suppressor gene proteins in oesophageal cancer. (bvsalud.org)
  • It exhibited anticancer properties reducing the tumor load via apoptosis and cell cycle arrested in various cancer cell lines and controlled tumor proliferation by blocking tumor inducing gene such as FLT3, Akt gene, ROS and NF- κ B inhibition. (scirp.org)
  • Phase 2 study of treatment selection based on tumor thymidylate synthase expression in previously untreated patients with metastatic colorectal cancer: A trial of the ECOG-ACRIN Cancer Research Group (E4203). (bioportfolio.com)
  • The authors hypothesized that patients with metastatic colorectal cancer (mCRC) who had tumors with low thymidylate synthase (TS-L) expression would have a higher response rate to combined 5-fluoroura. (bioportfolio.com)
  • Tumors or cancer of the COLON or the RECTUM or both. (bioportfolio.com)
  • Aggregation and Prion-Like Properties of Misfolded Tumor Suppressors: Is Cancer a Prion Disease? (ebi.ac.uk)
  • The high-risk human papillomavirus (HPV), which are implicated in the pathogenesis of cervical cancer, produce the E6 protein (8) . (aacrjournals.org)
  • Scientists have cracked a cell mechanism that drives tumor formation in most types of cancer. (medicalnewstoday.com)
  • However, mutated forms of p53, which are common in cancer, behave differently than regular p53. (medicalnewstoday.com)
  • Instead of protecting the cell, they can take on oncogenic, or tumor-promoting, properties and become active drivers of cancer. (medicalnewstoday.com)
  • Normally, if a cell is at risk of turning into a cancer cell, the protein p53 will be activated. (eurekalert.org)
  • The protein p53 is highly relevant for biomedicine: In one half of all human tumour types, the p53 gene is mutated (irreversibly changed), whereby its cancer-combating function is suppressed. (eurekalert.org)
  • The researchers conducted this study to learn exactly how p53 and TGF-β interact in cancer development. (labspaces.net)
  • Scientists are trying to understand the tumor-nerve relationship in hope that it could lead to better therapies for head and neck cancer. (nih.gov)
  • Its protein product, p53, is a tumor suppressor that acts as a brake on cancer growth. (nih.gov)
  • Using mouse models of oral cancer and laboratory cell cultures, the scientists confirmed the connection between p53 and nerve density. (nih.gov)
  • p53 promotes AKT and SP1-dependent metabolism through the pentose phosphate pathway that inhibits apoptosis in response to Nutlin-3a. (rush.edu)
  • The WWOX gene is a recently cloned tumor suppressor gene that spans the FRA16D fragile region. (pnas.org)
  • This function is lost when the gene is mutated, enabling tumors to grow unrestrained. (nih.gov)
  • Berberine, gallic acid, rutin and mangiferin were screened for binding residues and possible interaction with p53 (PDB ID2VUK). (elsevier.com)
  • Medulloblastoma (MB), a primitive neuroectodermal tumor, is the most common malignant childhood brain tumor and remains incurable in about a third of patients. (aging-us.com)
  • Glioblastoma (GBM), the most common primary malignant brain tumor, is a morphologically heterogenous tumor type. (mdpi.com)
  • p53, a tumor suppressor proteins, has shown to modify the cell routine, apoptosis, and DNA fix to avoid malignant transformation. (colinsbraincancer.com)
  • Banfalvi T, Gilde K, Gergye M, Boldizsar M, Kremmer T, Otto S. Use of serum 5-S-CD and S-100B protein levels to monitor the clinical course of malignant melanoma. (springer.com)
  • Serum S-100b protein as a prognostic marker in malignant cutaneous melanoma. (springer.com)
  • For this purpose, the p53 content of 100 human breast biopsies classified as ductal carcinoma (DCIS), was evaluated by immunohistochemical method. (ac.ir)
  • High concentrations of p53 protein are transiently expressed in human epidermis and superficial dermal fibroblasts following mild ultraviolet irradiation. (abeomics.com)
  • Inactivation of tumor suppressor p53 accompanies the majority of human malignancies. (nih.gov)
  • Anti-TSAP6a was generated against amino acids 16C30 (DSDSSLAKVPDEAPK) of the human TSAP6 protein. (desafioceroaedes.com)
  • Takahashi K, Isobe T, Ohtsuki Y, Akagi T, Sonobe H, Okuyama T. Immunohistochemical study on the distribution of alpha and beta subunits of S-100 protein in human neoplasm and normal tissues. (springer.com)
  • pGFPB2 containing human full-length BRCA2 cDNA fused in-frame with green fluorescent protein (GFP) was constructed as follows. (pnas.org)
  • TGF-β molecules are secreted proteins found in most human t issue s. (labspaces.net)
  • Inactivation of p53 via mutation of its gene is a key step in tumorigenesis. (springer.com)
  • We show that both HIN domains of IFI16 are capable of enhancing p53-DNA complex formation and transcriptional activation via distinctive means. (nih.gov)
  • Both interactions are compatible with the DNA-bound state of p53 and together contribute to the effect of full-length IFI16 on p53-DNA complex formation and transcriptional activation. (nih.gov)
  • The p53 tumor suppressor protein plays a crucial role in influencing cell survival in response to cellular stress and while the p53 pathway is considered a key determinant of anti-tumor responses in many tumors, its role in cell survival in MB is much less well defined. (aging-us.com)
  • Anti-p53 (anti-tumor suppressor gene) antibodies in sera of workers occupationally exposed to vinyl chloride. (greenmedinfo.com)
  • The biochemical properties of Msx1 protein and its fundamental role as an embryonic transcriptional regulator are well established. (aacrjournals.org)
  • Despite our current understanding of protein−DNA recognition, the mechanism(s) underlying the loss in protein−DNA binding affinity/specificity upon single−point mutation are not well understood. (ias.ac.in)
  • Therefore, p53 is altered from overproduction to mutation during the development of hypergastrinemia-induced ECLoma and it may therefore play a role in the cell transformation. (curehunter.com)
  • The intact and complete p53 molecule has eluded previous attempts to obtain its structure, largely due to the intrinsic flexibility of the protein. (whiterose.ac.uk)
  • Presenilin-1, a predisposition gene for familial Alzheimer's disease (5), is usually inhibited by p53 activation and functions as an antiapoptotic molecule (6). (desafioceroaedes.com)
  • TSAP6 represents a molecule up-regulated by p53. (desafioceroaedes.com)
  • Initially, we found that the mazEF module is under the control of ppGpp ( 3 , 13 ), the amino acid starvation signal molecule produced by the RelA protein ( 7 ). (asm.org)
  • Check out links to articles that cite our custom service antibodies, peptides, and proteins in major peer-reviewed journals, organized by research category. (abgent.com)
  • The present work captures p53 bound to DNA in its natural dimeric units and thus allows Marmors tein and colleagues to make new and potentially significant insights into p53 function. (bio-medicine.org)
  • These data provide the groundwork for additional studies on VMY as a therapeutic drug and support further investigations into the intriguing possibility that targeting p53 function may be an effective means of enhancing clinical outcomes in MB. (aging-us.com)
  • p53 is dynamically regulated through various posttranslational modifications (PTMs), which differentially modulate its function and stability. (rcsb.org)
  • Here, we identify homeobox Msx1 as a p53-interacting protein and show its novel function as a p53 regulator. (aacrjournals.org)
  • p53 function is regulated by several mechanisms including post-translational modification, stabilization, protein interactions, and subcellular localization. (aacrjournals.org)
  • Bg7S shares several structural elements with a number of homologous proteins from other seeds, whose function is still uncertain. (bireme.br)
  • Nuclear receptors, such as those that mediate the transcriptional roles of thyroid hormones, glucocorticoids, retinoic acid, vitamin D, and estrogen, are all zinc-finger proteins (Freedman and Luisi, 1993), and function as key players in the CNS. (nap.edu)
  • The p53 protein is well-known for its tumour suppressor function. (ias.ac.in)
  • Initiation of autoimmunity to the p53 tumor suppressor protein by complexes of p53 and SV40 large T antigen. (rupress.org)
  • In this study, high titer ANAs specific for the p53 tumor suppressor protein were induced in mice immunized with purified complexes of murine p53 and the Simian virus 40 large T antigen (SVT), but not in mice immunized with either protein separately. (rupress.org)
  • The latter may have been maintained by self antigen, since the anti-p53, but not the SVT, response in these mice could be boosted by immunizing with murine p53. (rupress.org)
  • p53 tumor suppressor continues to be defined as a proteins interacting with the top T antigen made by simian vacuolating pathogen 40 (SV40). (uberbrain.net)
  • Its epitope maps within the N-terminus (aa 20-25) of p53. (abeomics.com)
  • The C terminus of LANA, the region most highly conserved in ORF73, is shown to be responsible for both pRb and p53 interactions, supporting the hypothesis that these functions are conserved in both homologues. (unr.edu)
  • p53 was mutated at the C-terminus in ECLoma induced by hypergastrinemia. (curehunter.com)
  • Surprisingly, the genetic or chemical silencing of p53 significantly enhanced the cytotoxic effects of both VMY and the DNA damaging drug, doxorubicin. (aging-us.com)
  • In some cases, IHC can serve as surrogate protein markers for underlying genetic events. (thefreelibrary.com)
  • 2,3) Reactivity for adipophilin in sebaceous tumors can also distinguish them from BCC. (thefreelibrary.com)
  • Several of these MAbs did display minor reactivity to other S100 proteins when they were presented in denatured form. (springer.com)
  • However, its role as a regulator of tumor suppressor in adult tissues remains unknown. (aacrjournals.org)