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By Shan S. Wong

Collage of Texas future health technological know-how heart, Houston. Biochemistry - complicated examine assessment.

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The G1 checkpoint is activated by ATM signalling to Chk2 and p53, among other targets, preventing the replication of damaged DNA by blocking entry into S-phase. ATM promotes Homologous recombination repair by recruiting BRCA1 to DSBs, but can also antagonize BRCA1 and promote NHEJ by recruiting 53BP1. Defects in the function of p53 may contribute to the genetic instability that appears to drive neoplastic evolution. The decatenation checkpoint is another G2 phase checkpoint that has been reported to be defective in a large proportion (68 %) of melanoma cell-lines (Brooks et al.

ATM and ATR are related kinases that phosphorylate a number of mediators which are mostly cell cycle specific and associate with damage sensors, signal transducers and effectors at particular phases of the cell cycle, and as a consequence, provide signal transduction specificity. ATM and ATR are both members of the PI-3K-like kinase family (PIKK) of protein kinases that also includes DNA dependent protein kinase (DNA-PK) and mammalian target of rapamaycin (mTOR). The ATM signalling cascade includes 53BP1, MDC1, BRCA1, MCPH1, and PTIP, while mediators of ATR signalling include TopBP1, and Claspin (reviewed in Marechal and Zou 2013).

Given that DNA repair defects are early drivers of many solid tumors, there is great interest in developing therapeutics that exploit these potential weaknesses based on synthetic lethality and sensitivity. Because unrepaired DSBs are generally lethal to cells, there has been significant focus on DSB repair pathways and genotoxins that directly or indirectly induce DSBs. However, we should not restrict our thinking to just these pathways and agents, as there are many pathways to death or even senescence, which achieve the same goal of preventing tumor growth and spread.

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