c-Abl Tyrosine Kinase Is Not Essential for Ataxia Telangiectasia Mutated Functions in Chromosomal Maintenance

c-Abl is activated by DNA damage in an ataxia telangiectasia mutated (ATM)-dependent manner and plays important roles in growth arrest and apoptosis induced by DNA damage. c-Abl also interacts physically and functionally with Rad51, a key molecule in homologous recombinational (HR) DNA repair. To st...

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Veröffentlicht in:	The Journal of biological chemistry 2000-01, Vol.275 (2), p.725-728
Hauptverfasser:	Takao, Noriaki, Mori, Ryoichi, Kato, Hideaki, Shinohara, Akira, Yamamoto, Ken-ichi
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Ataxia Telangiectasia - genetics Ataxia Telangiectasia Mutated Proteins ATM protein Avian Proteins B-Lymphocytes c-Abl protein Cell Cycle Proteins Cell Line Cell Survival Chickens DNA Repair DNA-Binding Proteins - metabolism Genes, abl Karyotyping Male Protein-Serine-Threonine Kinases - deficiency Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins c-abl - deficiency Proto-Oncogene Proteins c-abl - genetics Proto-Oncogene Proteins c-abl - metabolism Rad51 protein Rad51 Recombinase Recombinant Proteins - metabolism Transfection Tumor Suppressor Proteins
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