![]() ![]() This family includes mTOR (mammalian target of rapamycin), which controls cell growth in response to environmental cues, mitogenic SMG1 (suppressor with morphological effect on genitalia 1), which regulates nonsense-mediated decay of aberrant mRNA. They include DNA-PKcs (theĭNA-dependent protein kinase catalytic subunit), which is crucial for DNA repair of DSBs by nonhomologous end-joining, and In mammals, there are four additional members of the PIKK family that have diverse functions. Mutation in ATR results in Seckel syndrome, a developmental disorder characterized by growth retardation and microcephaly ATR is activated by replication stress, and is an essential gene in budding yeast and mice. ATM is critical for the cellular response to DNA double-strandīreaks (DSBs), and mutations in ATM lead to the neurodegenerative and cancer predisposition disease ataxia telangiectasia Phosphoinositide-3-kinase-related protein kinase (PIKK) family. The central regulators of theĭDR are ataxia telangiectasia-mutated (ATM) and ataxia-telangiectasia and Rad3-related (ATR), two members of the mammalian To address this damageĪnd optimize survival, cells evolved the DNA damage response (DDR), a complex signal transduction network that activates transcriptionĪnd DNA repair, and coordinates cell cycle transitions in order to maintain genomic stability. Organisms experience significant amounts of DNA damage, which threatens their survival on a daily basis. Regulators of PIKK abundance and checkpoint signaling. The components of the TTT complex are mutually dependent on each other, and act as critical Maintenance 2), called the Triple T complex, and phosphoinositide-3-kinase-related protein kinases (PIKKs) such as ataxia TTI1 and TTI2 exist in multiple complexes, including a 2-MDa complex with TEL2 (telomere TTI1 and TTI2 protect cells from spontaneous DNA damage, and are required for the establishment of Here we describe TTI1 (Tel two-interacting protein 1) and TTI2 as highly conserved regulators ![]() Along with a number of known DDR genes, we discovered a large set of novel genes whose depletion ![]() Our current understanding of the DDR network, we performed a genome-wide RNAi screen to identify genes required for resistance In response to DNA damage, cells activate a complex signal transduction network called the DNA damage response (DDR). ![]()
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