Aven-Dependent Activation of ATM Following DNA Damage
نویسندگان
چکیده
منابع مشابه
Aven-Dependent Activation of ATM Following DNA Damage
BACKGROUND In response to DNA damage, cells undergo either cell-cycle arrest or apoptosis, depending on the extent of damage and the cell's capacity for DNA repair. Cell-cycle arrest induced by double-stranded DNA breaks depends on activation of the ataxia-telangiectasia (ATM) protein kinase, which phosphorylates cell-cycle effectors such as Chk2 and p53 to inhibit cell-cycle progression. ATM i...
متن کاملReconstitution of an ATM-dependent checkpoint that inhibits chromosomal DNA replication following DNA damage.
Cell cycle checkpoints lead to the inhibition of cell cycle progression following DNA damage. A cell-free system derived from Xenopus eggs has been established that reconstitutes the checkpoint pathway inhibiting DNA replication initiation. DNA containing double-strand breaks inhibits replication initiation in a dose-dependent manner. Upon checkpoint activation, a prereplicative complex is asse...
متن کاملMyc Is Required for Activation of the ATM-Dependent Checkpoints in Response to DNA Damage
BACKGROUND The MYC protein controls cellular functions such as differentiation, proliferation, and apoptosis. In response to genotoxic agents, cells overexpressing MYC undergo apoptosis. However, the MYC-regulated effectors acting upstream of the mitochondrial apoptotic pathway are still unknown. PRINCIPAL FINDINGS In this study, we demonstrate that expression of Myc is required to activate t...
متن کاملATM and Chk2-dependent phosphorylation of MDMX contribute to p53 activation after DNA damage.
The p53 tumor suppressor is activated after DNA damage to maintain genomic stability and prevent transformation. Rapid activation of p53 by ionizing radiation is dependent on signaling by the ATM kinase. MDM2 and MDMX are important p53 regulators and logical targets for stress signals. We found that DNA damage induces ATM-dependent phosphorylation and degradation of MDMX. Phosphorylated MDMX is...
متن کاملAven blocks DNA damage-induced apoptosis by stabilising Bcl-xL.
Induction of apoptosis by DNA-damaging agents involves the activation of mitochondrial apoptotic pathway. Aven has been identified as an antiapoptotic protein and has been shown to activate ATM in response to DNA damage. In this study, we demonstrated that enforced expression of Aven blocks UV-irradiation-, SN-38- or cisplatin-induced apoptosis upstream of mitochondria by stabilising Bcl-xL pro...
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ژورنال
عنوان ژورنال: Current Biology
سال: 2008
ISSN: 0960-9822
DOI: 10.1016/j.cub.2008.05.045