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Title:
Control of the G2/M transition | Molecular Biotechnology
Description:
The G2 checkpoint prevents cells from entering mitosis when DNA is damaged, providing an opportunity for repair and stopping the proliferation of damaged cells. Because the G2 checkpoint helps to maintain genomic stability, it is an important focus in understanding the molecular causes of cancer. Many different methods have been used to investigate the G2 checkpoint and uncover some of the underlying mechanisms. Because cell cycle controls are highly conserved, a remarkable synergy between the genetic power of model organisms and biochemical analyses is possible and has uncovered control mechanisms that operate in many diverse species, including humans. CDC2, the cyclin-dependent kinase that normally drives cells into mitosis, is the ultimate target of pathways that mediate rapid arrest in G2 in response to DNA damage. Additional pathways ensure that the arrest is stably maintained. When mammalian cells contain damaged DNA, the p53 tumor suppressor and the Rb family of transcriptional repressors work together to downregulate a large number of genes that encode proteins required for G2 and M. Elimination of these essential cell cycle proteins helps to keep the cells arrested in G2.
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Keywords {🔍}

google, scholar, cas, pubmed, article, cell, dna, biol, checkpoint, kinase, damage, nature, protein, cycle, mol, cdc, control, science, gene, genes, cells, phosphorylation, cancer, yeast, human, dev, cyclin, chem, response, mitotic, sci, mitosis, fission, nuclear, proc, natl, acad, chk, activation, usa, res, complex, stark, taylor, arrest, embo, atm, rad, cellular, nurse,

Topics {✒️}

p130/p107/p105rb-dependent transcriptional repression dna-damage-induced cell-cycle exit p21 waf1/cip1 expression month download article/chapter gadd45-mediated growth suppression cdc2-related protein p40m015 g2-phase dna-damage checkpoint check-point signalling dna double-strand breaks intrinsic dna/chromatin binding p53 c-terminal domain rad3-rad26 complex responds dna damage-induced phosphorylation cell cycle-regulated kinase chk1-encoded protein kinase ran-independent nuclear import purified maturation-promoting factor cell cycle checkpoints s-phase feedback control site-directed cofactor recruitment kinase-inactive atr protein mre 11/rad50/nbs1 complex g1/s-regulated e2f phase-promoting factor phosphorylation van de weyer full article pdf cell cycle controls p53-regulated protein gadd45 related subjects early mitotic events multiple protein kinases lerner research institute histone h1 kinase rad checkpoint pathway cdc34-mediated degradation cdk/cyclin complexes mutated p53 gene mitotic chromosomes induced privacy choices/manage cookies dna damage checkpoint cell cycle checkpoint mo15 gene encodes sea urchin eggs cyclin-dependent kinase cell cycle arrest p130-e2f-4 complex check access dna damage occurs dna damage independently mediate rapid arrest

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      description:The G2 checkpoint prevents cells from entering mitosis when DNA is damaged, providing an opportunity for repair and stopping the proliferation of damaged cells. Because the G2 checkpoint helps to maintain genomic stability, it is an important focus in understanding the molecular causes of cancer. Many different methods have been used to investigate the G2 checkpoint and uncover some of the underlying mechanisms. Because cell cycle controls are highly conserved, a remarkable synergy between the genetic power of model organisms and biochemical analyses is possible and has uncovered control mechanisms that operate in many diverse species, including humans. CDC2, the cyclin-dependent kinase that normally drives cells into mitosis, is the ultimate target of pathways that mediate rapid arrest in G2 in response to DNA damage. Additional pathways ensure that the arrest is stably maintained. When mammalian cells contain damaged DNA, the p53 tumor suppressor and the Rb family of transcriptional repressors work together to downregulate a large number of genes that encode proteins required for G2 and M. Elimination of these essential cell cycle proteins helps to keep the cells arrested in G2.
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