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Beschreibung
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ATM (Ataxia Telangiectasia, mutated) is a 350-370 kD member of the PI3/PI4-kinase family. This protein is expressed in the nucleus and endocytotic vesicles. ATM is involved in signal transduction, cell cycle control, DNA repair, and has been proposed as a possible tumor suppressor and protein involved in vesicle transport. ATM is induced by ionizing radiation. This protein can be phosphorylated and acetylated and has been shown to interact with DNA ends, NFKBIA, CTIP, RAD9, P53, ABL1, BRCA1, NIBRIN (NBS1), and TERF1. The ATM protein is part of the BRCA1-associated genome surveillance complex (BASC) containing BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBS1 protein complex, and beta-adaptin. Distribution: Nuclear, endocytotic vesicles Function: Signal transduction, cell cycle control, DNA repair, possible tumor suppressor, possible vesicle/protein transport Modifications: Phosphorylation Synonyms: Ataxia Telangiectasia, Mutated Regulation: Induced by ionizing radiation Structure: PI3/PI4-kinase family, 350-370 kD
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Spezifität
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DNA ends, NFkappaB, CTIP, RAD9, p53, ABL1, BRCA1, NIBRIN (NBS1), TERF1. Part of the BRCA1-associated genome surveillance complex (BASC)containing BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBS1 protein complex, beta-adaptin. reacts with lys41-acetylated atm
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