Tastasis, radioresistance and poor prognosis of cancer. Recent studies have shown that the removal of specific phosphorylation events in T2609 and S2056 cluster DNA PKC were necessary for maximum sensitivity at Zellabt Tion induced by radiation, give Similar mutant DNA PKC 0. Involved other than the inhibition of DNA repair, DNA PKc down-regulation was in the induction of cell death was both by apoptosis and induction of autophagy. The exact mechanism of the fa What we induce autophagy DNAPKc k Nnte as a mechanism of radiosensitization requires further exploration. Unlike the two major pathways of DNA repair, a different way, which is primarily used to remove DNA adducts induced in the base unit is the way of excision repair. Upon detection of a product base also cleaves a DNA glycosylase specific adduct N glycosidic bond of the dam Defendants base and created a Web site, apurinic / apyrimidinic. The AP site is then processed by AP endonuclease and repaired. Recently it was shown that soy flavones mediated radiosensitization in the cells of lung cancer by targeting this pathway, which was caused to the importance of AP endonuclease as a target for radiosensitization. DNA-Sch Ending sensors in particular ATM induced by IR is also an important target for intervention. ATM inhibitors also mediated Irbesartan RAAS inhibitor sensitization of cells, mainly due to the inhibition of activation of NFkB. Chk 2, which is downstream Rts of ATM is being investigated as a therapeutic target for radiation sensitization. There are clues that R The ATM-Chk2 activation, ranging from inactivation of Chk2 in AT cells show reports that Chk2 is phosphorylated by ATM at Thr68. Chk2 kinase activity t is induced by increased DNA-Sch Termination by IR, chemotherapeutic agents or other compounds Ht that the DNA-ended sch Directly or indirectly. The activity t of Chk2 h Depends Haupts Chlich of its kinase Cathedral sharing plans.
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