The p53 transcription factor regulates multiple biological functions, including growth arrest, DNA repair, and apoptosis. This gene is continuously degraded in the cell under normal conditions. When external or cellular stress causes DNA damage, the genes ATM and ATR are activated and phosphorylate the cell cycle checkpoint proteins CHEK1 and CHEK2. During this process, p53 degradation is inhibited, and p53 protein accumulates in the nucleus. p53 is activated by posttranslational modifications such as acetylation or phosphorylation. Additional cofactors enhance or inhibit the activity of this important transcription factor. Genes targeted by p53 initiate multiple processes such as cell cycle arrest and apoptosis. A wide variety of cancers carry p53 mutations or other defects that dysregulate p53 and its cofactors, making this gene an important and highly-studied tumor suppressor. Analyzing the expression, regulation, and sequence of p53 signaling genes can help determine their relative ...
According to a new study, scientists have safely shut down breast cancer and a form of leukemia in mice by targeting abnormal proteins to which the cancers are addicted.
Human Crif1 is a protein with multiple functions, playing important roles in embryonic development, cellular stress, cell cycle regulation and mitochondrial membrane integrity. CRIF1 is coined to play a regulatory role in the Bone Marrow microenvironment-induced leukemia cell cycle arrest possibly through interacting with CDK2 and acting as a cyclin-dependent kinase inhibitor ...
PLK5兔多克隆抗体(ab93124)可与重组片段样本反应并经WB, ELISA实验严格验证。中国75%以上现货,所有产品均提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
Component of the 9-1-1 cell-cycle checkpoint response complex that plays a major role in DNA repair. The 9-1-1 complex is recruited to DNA lesion upon damage by the RAD17-replication factor C (RFC) clamp loader complex. Acts then as a sliding clamp platform on DNA for several proteins involved in long-patch base excision repair (LP-BER). The 9-1-1 complex stimulates DNA polymerase beta (POLB) activity by increasing its affinity for the 3-OH end of the primer-template and stabilizes POLB to those sites where LP-BER proceeds; endonuclease FEN1 cleavage activity on substrates with double, nick, or gap flaps of distinct sequences and lengths; and DNA ligase I (LIG1) on long-patch base excision repair substrates. The 9-1-1 complex is necessary for the recruitment of RHNO1 to sites of double-stranded breaks (DSB) occurring during the S phase. Isoform 1 possesses 3-,5 double stranded DNA exonuclease activity ...
The cell cycle proteins are key regulators of cell cycle progression whose de-regulation is one of the causes of breast cancer. RNA interference (RNAi) is an endogenous mechanism to regulate gene expression and it could serve as the basis of regulating aberrant proteins including cell cycle proteins. Since the delivery of small interfering RNA (siRNA) is a main barrier for implementation of RNAi therapy, we explored the potential of a non-viral delivery system, 2.0 kDa polyethylenimines substituted with linoleic acid and caprylic acid, for this purpose. Using a library of siRNAs against cell cycle proteins, we identified cell division cycle protein 20 (CDC20), a recombinase RAD51, and serine-threonine protein kinase CHEK1 as effective targets for breast cancer therapy, and demonstrated their therapeutic potential in breast cancer MDA-MB-435, MDA-MB-231 and MCF7 cells with respect to another well-studied cell cycle protein, kinesin spindle protein. We also explored the efficacy of dicer-substrate siRNA
The cell cycle includes 4 main phases: Gap 1 (G1), DNA replication (S), Gap 2 (G2), and mitosis (M). Tight regulation of the transition between these phases halts cell cycle progression if a phase is not properly completed. For example, the G2-M DNA damage checkpoint ensures the fidelity of DNA replication, and arrests the cell cycle to allow time for replication error correction and DNA damage repair. Cell cycle progression is regulated by the cyclic rise and fall of kinase expression, and their interaction with, and action on, their cyclin targets. Cell cycle dysregulation commonly occurs during oncogenesis, and tumor cells often do not arrest the cell cycle when normally required. Key genes that regulate cell cycle progression and checkpoints encode cullins, cyclins, and cyclin-dependent kinases and their inhibitors. Other cell cycle regulatory genes include apoptosis regulators and DNA damage sensors ...
In this study, we generated a mutant of SpCdc25 that is severely impaired in its ability to bind to the fission yeast 14-3-3 proteins (Rad 24 and Rad 25). When expressed in fission yeast, this mutant Cdc25 protein localized almost exclusively to the nucleus, in contrast to wild-type Cdc25, which localized to both the cytoplasm and the nucleus. Inhibition of Crm1-mediated nuclear export resulted in the nuclear accumulation of wild-type Cdc25, indicating that wild-type Cdc25 normally shuttles between the nucleus and the cytoplasm. Overproduction of Rad 24 caused wild-type Cdc25 to localize exclusively to the cytoplasm, whereas nuclear localization of the 14-3-3 binding mutant was not altered upon Rad 24 overproduction. Finally, cells expressing the 14-3-3 binding mutant exhibited defective G2/M checkpoint responses. Taken together, these results suggest that 14-3-3 binding regulates the intracellular compartmentalization of Cdc25 and establish that 14-3-3 binding to Cdc25 is required for fission ...
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to repair the damage before continuing to divide. DNA damage checkpoints occur at the G1/S and G2/M boundaries. An intra-S checkpoint also exists. Checkpoint activation is controlled by two master kinases, ATM and ATR. ATM responds to DNA double-strand breaks and disruptions in chromatin structure, whereas ATR primarily responds to stalled replication forks. These kinases phosphorylate downstream targets in a signal transduction cascade, eventually leading to cell cycle arrest. A class of checkpoint mediator proteins including BRCA1, MDC1, and 53BP1 has also been identified. These proteins seem to be required for transmitting the checkpoint activation signal to downstream proteins. p53 is an important downstream target of ATM and ATR, as it is required for inducing apoptosis following DNA damage.[33] At the G1/S checkpoint, p53 functions by deactivating the CDK2/cyclin E ...
The protein encoded by this gene belongs the PI3/PI4-kinase family, and is most closely related to ATM, a protein kinase encoded by the gene mutated in ataxia telangiectasia. This protein and ATM share similarity with Schizosaccharomyces pombe rad3, a cell cycle checkpoint gene required for cell cycle arrest and DNA damage repair in response to DNA damage. This kinase has been shown to phosphorylate checkpoint kinase CHK1, checkpoint proteins RAD17, and RAD9, as well as tumor suppressor protein BRCA1. Mutations of this gene are associated with Seckel syndrome. An alternatively spliced transcript variant of this gene has been reported, however, its full length nature is not known. Transcript variants utilizing alternative polyA sites exist. [provided by RefSeq, Jul 2008 ...
HEADER TRANSFERASE 31-JAN-08 3C5L TITLE POLO-LIKE KINASE 1 POLO BOX DOMAIN IN COMPLEX WITH PPHSPT TITLE 2 PEPTIDE COMPND MOL_ID: 1; COMPND 2 MOLECULE: SERINE/THREONINE-PROTEIN KINASE PLK1; COMPND 3 CHAIN: A; COMPND 4 FRAGMENT: POLO BOX 1, POLO BOX 2, UNP RESIDUES 373-593; COMPND 5 SYNONYM: POLO-LIKE KINASE 1, PLK-1, SERINE/THREONINE- COMPND 6 PROTEIN KINASE 13, STPK13; COMPND 7 EC: 2.7.11.21; COMPND 8 ENGINEERED: YES; COMPND 9 MOL_ID: 2; COMPND 10 MOLECULE: PEPTIDE; COMPND 11 CHAIN: B; COMPND 12 ENGINEERED: YES SOURCE MOL_ID: 1; SOURCE 2 ORGANISM_SCIENTIFIC: HOMO SAPIENS; SOURCE 3 ORGANISM_COMMON: HUMAN; SOURCE 4 ORGANISM_TAXID: 9606; SOURCE 5 GENE: PLK1, PLK; SOURCE 6 EXPRESSION_SYSTEM: ESCHERICHIA COLI; SOURCE 7 EXPRESSION_SYSTEM_TAXID: 562; SOURCE 8 EXPRESSION_SYSTEM_STRAIN: ROSETTA 2; SOURCE 9 EXPRESSION_SYSTEM_VECTOR_TYPE: PLASMID; SOURCE 10 EXPRESSION_SYSTEM_PLASMID: PET28A; SOURCE 11 MOL_ID: 2; SOURCE 12 SYNTHETIC: YES KEYWDS PLK1, POLO-LIKE KINASE 1, POLO BOX DOMAIN, PHOSPHOPEPTIDE, ...
Cell proliferation is essential for many key processes that occur during development including organogenesis, tissue renewal and germline formation. (Bartkova et al., 1997; Clurman and Roberts, 1995; Pines, 1995; Sandhu and Slingerland, 2000). Therefore, the timing of cell division and differentiation must be precisely coordinated with signals that specify morphogenesis, patterning and growth in a temporal, positional and cell type-specific manner (reviewed by Vidwans and Su, 2001). This coordination is executed through regulating both positive and negative regulatory components of the basal cell cycle machinery.. The cell cycle machinery is well conserved among eukaryotes and complex mechanisms ensure that cell cycle progression occurs in a timely and precise sequence. Cyclin-dependent kinases (Cdks) drive progression through the different cell cycle phases (reviewed by Nigg, 2001). In yeasts, these catalytic subunits are regulated through their association with stage-specific cyclin regulatory ...
The Polo Kinase is a central regulator of cell division required for several events of mitosis and cytokinesis. In addition to a kinase domain (KD), Polo-like kinases (Plks) comprise a Polo-Box domain (PBD), which mediates protein interactions with targets and regulators of Plks. In all organisms that contain Plks, one Plk family member fulfills several essential functions in the regulation of cell division, and here we refer to this conserved protein as Polo Kinase (Plk1 in humans). The PBD and the KD are capable of both cooperation and mutual inhibition in their functions. Crystal structures of the PBD, the KD and, recently, a PBD-KD complex have helped understanding the inner workings of the Polo Kinase. In parallel, an impressive array of molecular mechanisms has been found to mediate the regulation of the protein. Moreover, the targeting of Polo Kinase in the development of anti-cancer drugs has yielded several molecules with which to chemically modulate Polo Kinase to study its biological ...
Mitotic cell cycle progression is accomplished through a reproducible sequence of events, DNA replication (S phase) and mitosis (M phase) separated temporally by gaps known as G1 and G2 phases. Cyclin-dependent kinases (CDKs) are key regulatory enzymes, each consisting of a catalytic CDK subunit and an activating cyclin subunit. CDKs regulate the cells progression through the phases of the cell cycle by modulating the activity of key substrates. Downstream targets of CDKs include transcription factor E2F and its regulator Rb. Precise activation and inactivation of CDKs at specific points in the cell cycle are required for orderly cell division. Cyclin-CDK inhibitors (CKIs), such as p16Ink4a, p15Ink4b, p27Kip1, and p21Cip1, are involved in the negative regulation of CDK activities, thus providing a pathway through which the cell cycle is negatively regulated. Eukaryotic cells respond to DNA damage by activating signaling pathways that promote cell cycle arrest and DNA repair. In response to DNA ...
Many anticancer agents induce DNA strand breaks or cause the accumulation of DNA replication intermediates. The protein encoded by ataxia-telangiectasia mutated and Rad 3-related (ATR) generates signals in response to these altered DNA structures and activates cellular survival responses. Accordingly, ATR has drawn increased attention as a potential target for novel therapeutic strategies designed to potentiate the effects of existing drugs. In this study, we use a unique panel of genetically modified human cancer cells to unambiguously test the roles of upstream and downstream components of the ATR pathway in the responses to common therapeutic agents. Upstream, the S-phase-specific cyclin-dependent kinase (Cdk) 2 was required for robust activation of ATR in response to diverse chemotherapeutic agents. While Cdk2-mediated ATR activation promoted cell survival after treatment with many drugs, signaling from ATR directly to the checkpoint kinase Chk1 was required for survival responses to only a ...
Early studies in lower Eukaryotes have defined a role for the members of the NimA related kinase (Nek) family of protein kinases in cell cycle control. Expansion of the Nek family throughout evolution has been accompanied by their broader involvement in checkpoint regulation and cilia biology. Moreover, mutations of Nek family members have been identified as drivers behind the development of ciliopathies and cancer. Recent advances in studying the physiological roles of Nek family members utilizing mouse genetics and RNAi-mediated knockdown are revealing intricate associations of Nek family members with fundamental biological processes. Here, we aim to provide a comprehensive account of our understanding of Nek kinase biology and their involvement in cell cycle, checkpoint control and cancer.
Folia Histochemica et Cytobiologica (FHC) is an international,English-language journal devoted to the developing fields of histochemistry,cytochemistry,cell biology,cell and tissue biology.It is source of the recent research in fields of and cell biology
BC: Thats what the cell cycle does!. FC: Cell Cycle. 1: What is the cell cycle? , The cell cycle is a process in which a cell grows and divides to create a copy of itself. Some orangisms reproduce through the cell cycle and in complex multicellular organisms, the cell cycle is used to allow the organism to grow and to reproduce worn out cells.. 2: Interphase , During interphase, a cell increase in mass, replicates its DNA, and prepares prophase.. 4: Prophase , It is when the loose DNA starts to gather to form chromatid, the DNA copies itself, the spindle fibers start to form, and the cell prepares itself for cell division.. 6: Metaphase , The duplicated chromosomes become aligned in the center of the cell, spindle fibers attach themselves to the centromere of the chromosomes.. 8: Anaphase , The stage of mitosis in which the duplicated sets of chromosomes separate and two indentical groups move to opposite poles of the cell.. 10: Telophase , A nuclear membrane re-forms around each new group of ...
BC: Thats what the cell cycle does!. FC: Cell Cycle. 1: What is the cell cycle? , The cell cycle is a process in which a cell grows and divides to create a copy of itself. Some orangisms reproduce through the cell cycle and in complex multicellular organisms, the cell cycle is used to allow the organism to grow and to reproduce worn out cells.. 2: Interphase , During interphase, a cell increase in mass, replicates its DNA, and prepares prophase.. 4: Prophase , It is when the loose DNA starts to gather to form chromatid, the DNA copies itself, the spindle fibers start to form, and the cell prepares itself for cell division.. 6: Metaphase , The duplicated chromosomes become aligned in the center of the cell, spindle fibers attach themselves to the centromere of the chromosomes.. 8: Anaphase , The stage of mitosis in which the duplicated sets of chromosomes separate and two indentical groups move to opposite poles of the cell.. 10: Telophase , A nuclear membrane re-forms around each new group of ...
Opens the Highlight Feature Bar and highlights feature annotations from the FEATURES table of the record. The Highlight Feature Bar can be used to navigate to and highlight other features and provides links to display the highlighted region separately. Links in the FEATURES table will also highlight the corresponding region of the sequence. More... ...
The mitotic checkpoint protein Bub3 is involved with the essential spindle checkpoint pathway which operates during early embryogenesis. Bub3 is…
... , Authors: Dessen P. Published in: Atlas Genet Cytogenet Oncol Haematol.
In response to genotoxic stress, the DNA damage response, which is governed primarily by the ATM-CHK2, ATR-CHK1, and p38-MK2 (also known as MAPKAPK2) checkpoint effector pathways, becomes activated in order to slow cell-cycle progression and allow time for DNA repair. The CHK1 and MK2 pathways converge on inhibition of cell division cycle 25 (CDC25)-mediated activation of cyclin-dependent kinases, prompting Dietlein and colleagues to hypothesize that simultaneous small-molecule inhibition of CHK1 and MK2 may synergistically silence the DNA damage checkpoint. To systematically characterize combinatorial drug-inhibitor relationships, 96 cancer cell lines were screened with various concentrations of the CHK1 inhibitor PF477736 and the MK2 inhibitor PF3644022, and PreCISE (predictor of chemical inhibitor synergistic effects) software was used to calculate synergism scores based on GI50 drug curves. Synergistic effects between PF477736 and PF3644022 were observed in 33 of 96 cell lines and were ...
海词词典,最权威的学习词典,专业出版cell cycle proteims是什么意思,cell cycle proteims的用法,cell cycle proteims翻译和读音等详细讲解。海词词典:学习变容易,记忆很深刻。
Equity mission statement The Australian Cell Cycle Meeting aims to promote the highest standard of research in the areas of cell cycle, DNA damage response and telomeres. To this end, the Australian Cell Cycle Meeting endeavours to foster a culture of inclusion and equity in all of its activities, including conference organisation, conference participation, and…
E2-2 alteration influences cell cycle exit of progenitors in vivo. (A)E2-2 overexpression increased cell cycle exit (EdU+Ki67-/EdU+) among the progenitor cell
CELL CYCLE CHECKPOINTS The cell cycle has regulatory points called checkpoint. A check point is one of several points in the eukaryotic cell cycle at which the progression of a cell to the next stage in the cell cycle can be halted until conditions are favourable (e.g. the DNA is repaired). These checkpoints occur near […]. ...
Cell cycle in somatic cells vs. ESCs. (a) Cell cycle regulation in somatic cells: mitogen signaling through MAPK path
Time‐lapse imaging of cell‐cycle phase transitions reveals that phase durations are uncoupled and can be modeled as an Erlang process. Phase coupling can be forced by perturbing a strong cell‐cycle regulator acting on multiple phases.. See full publication here.. ...
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numerous post-translational modifications lead to stabil- In contrast to the key role of p53 in maintenance of the isation of the p53 protein and activation of its DNA-induced G1 arrest, no specific roles for p53 or p21 sequence-specific DNA binding [9,30]. Only then can p53 have been implicated in the control of the intra-S-phase efficiently stimulate transcription of cell-cycle inhibitors checkpoint. This is perhaps not so surprising as the such as p21 (Figure 2). Furthermore, the p21 protein has to S-phase checkpoint, manifested by a decreased rate of accumulate to levels sufficiently high to inhibit the CDK- DNA synthesis after generation of DSBs, is by definition a containing complexes, before cell-cycle progression transient phenomenon [5]. The absence of the mainte- becomes efficiently blocked. Although p53 has recently nance component during S phase, contrary to the G1 and been described binding to 5′ untranslated region of CDK4 G2 checkpoints, might be beneficial for the cells by ...
Cell cycle analysis is commonly used in biomedical research studies and clinical diagnosis. It helps in distinguishing cells that are in different phases of cell cycle and used to determine the cellular response to biological stimulations and various drug
A ready-to-use reverse transfection format RNAi screening library targeting human cell cycle regulation genes. Just resuspend pre-dispensed siRNA, and add cells. Optimization plates are available.
The cell cycle constitutes a series of stages that allow a cell to double its cellular components and divide into two daughter cells. Cell cycle and division are crucial for development of a multicellular organism, as well as...
Research groupsCell biology and Biotechnology Role of Hsp90 in cell cycle control and ageing Dr Andrés Garzón Villar. ..
Cell cycle: Cell cycle, the ordered sequence of events that occur in a cell in preparation for cell division. The cell cycle is a four-stage process in which the cell increases in size (gap 1, or G1, stage), copies its DNA (synthesis, or S, stage), prepares to divide (gap 2, or G2, stage), and divides
Introduction to Cell Cycle: The cell cycle is the process by which a cell replicates its genetic material and synthesized the other elements of the cell
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The cell membrane The DNA Hello, today we will be learning about the cell cycle. The cell cycle is a process that cells go through in order to divide.
Drag the Labels Onto the Diagram to Identify the Stages Of the Cell Cycle. - Drag the Labels Onto the Diagram to Identify the Stages Of the Cell Cycle. , Ponents Of Blood Article
View mouse Spdye4b Chr5:143181017-143205075 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
A seemingly obscure gene in the female fruit fly that is only active in cells that will become eggs has led researchers at the Stowers Institute for Medical Research to the discovery of a atypical protein that lures, traps, and inactivates the powerful Polo kinase, widely considered the master regulator of cell division. Its human homolog, Polo-like kinase-1, is misregulated in many types of cancer.
The longest phase of the cell cycle is the Gap 1 phase, or G1 phase. During this phase, the cell gears up for cell division by amassing more organelles and getting larger....
At least four distinct polo-like kises exist in mammalian cells: PLK1, PLK2, PLK3, and PLK4/SAK . PLK1 apparently plays many roles during mitosis,…
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Cell Cycle DB103 DB009 DB010 DB011 DB012 DB104 DB105 DB013 DB106 DB014 DB015 DB114 DB018 DB016 DB017 DB051 DB095
Hi ladies Im in need of some advice!! Ive had 28 day cycles since I got my period when I was 15 (Im now 24) but my last 4 cycles have been 26 day cycles and now Im a week late, not pregnant 1) hubby was away this month and 2) dr did
In the budding yeast Saccharomyces cerevisiae, unnatural stabilization of the cyclin-dependent kinase inhibitor Sic1 during meiosis can trigger extra rounds of DNA replication. When programmed DNA double-strand breaks are generated but not repaired due to absence of DMC1, a pathway involving the checkpoint gene RAD17 prevents this DNA rereplication. Further genetic analysis has now revealed that prevention of DNA rereplication also requires MEC1, which encodes a protein kinase that serves as a central checkpoint regulator in several pathways including the meiotic recombination checkpoint response. Downstream of MEC1, MEK1 is required through its function to inhibit repair between sister chromatids. By contrast, meiotic recombination checkpoint effectors that regulate gene expression and cyclin-dependent kinase activity are not necessary. Phosphorylation of histone H2A, which is catalyzed by Mec1 and the related Tel1 protein kinase in response to DNA double-strand breaks and can help coordinate ...
Summary The ring-shaped cohesin complex brings together distant DNA domains to maintain, express, and segregate the genome. Establishing specific chromosomal linkages depends on cohesin recruitment to defined loci. One such locus is the budding yeast centromere, which is a paradigm for targeted cohesin loading. The kinetochore, a multiprotein complex that connects centromeres to microtubules, drives the recruitment of high levels of cohesin to link sister chromatids together. We have exploited this system to determine the mechanism of specific cohesin recruitment. We show that phosphorylation of the Ctf19 kinetochore protein by a conserved kinase, DDK, provides a binding site for the Scc2/4 cohesin loading complex, thereby directing cohesin loading to centromeres. A similar mechanism targets cohesin to chromosomes in vertebrates. These findings represent a complete molecular description of targeted cohesin loading, a phenomenon with wide-ranging importance in chromosome segregation and, in ...
The cellular response to DNA damage is critical for maintenance of genomic integrity and inhibition of tumorigenesis. Mutations or aberrant expression of the E3 ubiquitin ligase EDD have been observed in a number of carcinomas and we recently reported that EDD modulates activity of the DNA damage checkpoint kinase, CHK2. Here, we demonstrate that EDD is necessary for G(1)/S and intra S phase DNA damage checkpoint activation and for the maintenance of G(2)/M arrest after double strand DNA breaks. Defective checkpoint activation in EDD-depleted cells led to radio-resistant DNA synthesis, premature entry into mitosis, accumulation of polyploid cells, and cell death via mitotic catastrophe. In addition to decreased CHK2 activation in EDD-depleted cells, the expression of several key cell cycle mediators including Cdc25A/C and E2F1 was altered, suggesting that these checkpoint defects may be both CHK2-dependent and -independent. These data support a role for EDD in the maintenance of genomic stability,