作者: Surender Kharbanda , Pramod Pandey , Shengfang Jin , Satoshi Inoue , Ajit Bharti
DOI: 10.1038/386732A0
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摘要: How DNA damage is converted into intracellular signals that can control cell behaviour unknown. The c-Abl protein tyrosine kinase activated by ionizing radiation and certain other DNA-damaging agents1–5, whereas the DNA-dependent (DNA-PK), consisting of a serine/threonine Ku DNA-binding subunits, requires double-strand breaks or lesions for activation6–8. Here we demonstrate interacts constitutively with DNA-PK. Ionizing stimulates binding to DNA-PK induces an association antigen. We show phosphorylates activates in vitro. Cells deficient are defective activation induced radiation. In potential feedback mechanism, DNA-PK, but not Ku, Phosphorylation inhibits ability form complex DNA. also treatment cells results phosphorylation dependent on c-Abl. Our support hypothesis there functional interactions between response damage.