Autophosphorylation at serine 1987 is dispensable for murine Atm activation in vivo

The ATM (ataxia telangiectasia mutated) protein kinase is activated under physiological and pathological conditions that induce DNA double-strand breaks (DSBs). Loss of ATM or failure of its activation in humans and mice lead to defective cellular responses to DSBs, such as cell cycle checkpoints, r...

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Veröffentlicht in:	Nature 2006-09, Vol.443 (7108), p.222-225
Hauptverfasser:	Pellegrini, Manuela, Celeste, Arkady, Difilippantonio, Simone, Guo, Rong, Wang, Weidong, Feigenbaum, Lionel, Nussenzweig, André
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Ataxia Telangiectasia Mutated Proteins Biological and medical sciences Cell cycle Cell Cycle Proteins - chemistry Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Deoxyribonucleic acid DNA DNA Damage DNA-Binding Proteins - chemistry DNA-Binding Proteins - deficiency DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Fundamental and applied biological sciences. Psychology Genomic Instability Humanities and Social Sciences Infertility Kinases letter Lymphocytes - cytology Lymphocytes - metabolism Mice Molecular and cellular biology Molecular genetics multidisciplinary Mutagenesis. Repair Mutant Proteins - chemistry Mutant Proteins - genetics Mutant Proteins - metabolism Mutants Mutation Phosphorylation Phosphoserine - metabolism Physiology Protein-Serine-Threonine Kinases - chemistry Protein-Serine-Threonine Kinases - deficiency Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Proteins Rodents Science Science (multidisciplinary) Transgenes - genetics Tumor Suppressor Proteins - chemistry Tumor Suppressor Proteins - deficiency Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism
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