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发布于:2020-11-27 10:59:07  访问:0 次 回复:0 篇
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Lmu Neuroscience
Acting with accessory proteins, these kinases set up signaling platforms on the chromatin that anks DNA lesions.DNAPK does not have a clearly established role in regulating cellcycle progression.ATM and ATR, in contrast, control multiple responses to DNA damage, including regulation of DNA synthesis and repair proteins, regulation of transcription of the genes involved in DNA synthesis and repair, and regulation of cellcycle progression.Initiating mitosis with broken chromosomes results in gross genome instability, which is a feature of cancer in humans and is usually lethal in singlecelled microorganisms. Indeed, in yeasts a single unrepaired DSB is sufcient to induce a robust checkpoint response that prevents the onset of mitosis even as cells continue to grow beyond the size at which they normally divide. Nbs, which is only found in eukaryotes, directly binds ATM. Once localized at DNA ends, ATM phosphorylates proteins involved in cellcycle checkpoints, DNA repair, and chromatin structure. These ssDNA tails are rapidly bound by heterotrimeric replication protein A. RPA is essential for homologydirected repair of DNA damage, but it is also a recruitment factor for ATR. Both ATR and are required for checkpoint signaling.Furthermore, in budding yeast, ectopically targeting both buy Nucleotide Compound Library complexes to the same locus is sufcient for checkpoint activation, which suggests that recruitment of the two complexes to sites of damage is necessary and sufcient for checkpoint signaling. ATM and ATR share multiple substrates, including histone HAX.This ssDNA is bound by RPA, which elicits a checkpoint response by ATRATRIP and their orthologs. Chk similarly regulates Y dephosphorylation in response to replication fork arrest. Many of these stresses activate the p MAPK pathway. RESOLUTION OF G CHECKPOINT ARRESTS G checkpoint arrests are generally reversible.Once the problem is resolved, the checkpoint is inactivated and the cell can proceed with mitosis.This inactivation appears to be a passive process in which resolution of the checkpointinitiating event removes the signal that activates the checkpoint kinases, allowing constitutive phosphatases to remove the phosphates from their substrates and reset the system.In situations in which the problem cannot be resolved, cells can adapt to the checkpoint signal and enter mitosis in the presence of ongoing checkpoint signaling.Such adaptation generally appears to be a failure of checkpoint function, as opposed to a regulated attenuation of checkpoint signaling. As cells continue to grow during a checkpoint arrest, it is likely that the mitosispromoting activities that link the onset of mitosis to attainment of a sufcient cell size eventually overcome reasch Anti-cancer Clinical Compound Library mitosisinhibiting activity of the checkpoint.A failure to activate these circuits can lead to premature resumption of cell division in the presence of DNA damage. This decision to commit to cell division is implemented by signaling pathways that regulate the various processes of cell division, in particular mitosis and cytokinesis.They also regulate organelles and other cytoplasmic components in ways that are less well understood.The transition from G phase to mitosis involves reorganization of the nucleus, the condensation of the chromosomes, and the formation of the mitotic spindle. These events are triggered by CDK and culminate with the mitotic chromosomes aligned on the metaphase plate.
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