ATM Deficiency Disrupts TCRα Locus Integrity and the Maturation of CD4CD8 Thymocytes
نویسندگان
چکیده
Author contributions: I.M performed most of the research, analyzed data and co-wrote the paper. R.A.G performed some experiments and analyzed data. L.N contributed to the design of the study and supervised experimental work. A.C designed and performed the statistical analysis of the cytogenetics data. C.J.G and J.S.D designed the study, supervised the experimental work and co-wrote the manuscript.
منابع مشابه
ATM deficiency disrupts Tcra locus integrity and the maturation of CD4+CD8+ thymocytes.
Mutations in ATM (ataxia-telangiectasia mutated) cause ataxia-telangiectasia (AT), a disease characterized by neurodegeneration, sterility, immunodeficiency, and T-cell leukemia. Defective ATM-mediated DNA damage responses underlie many aspects of the AT syndrome, but the basis for the immune deficiency has not been defined. ATM associates with DNA double-strand breaks (DSBs), and some evidence...
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Ataxia telangiectasia mutated (ATM) is a protein kinase and a master regulator of DNA-damage responses. Germline ATM inactivation causes ataxia-telangiectasia (A-T) syndrome with severe lymphocytopenia and greatly increased risk for T-cell lymphomas/leukemia. Both A-T and T-cell prolymphoblastic leukemia patients with somatic mutations of ATM frequently carry inv(14;14) between the T-cell recep...
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The ataxia telangiectasia mutated (ATM) kinase and H2AX histone tumor suppressor proteins are each critical for maintenance of cellular genomic stability and suppression of lymphomas harboring clonal translocations. ATM is the predominant kinase that phosphorylates H2AX in chromatin around DNA double-strand breaks, including along lymphocyte Ag receptor loci cleaved during V(D)J recombination. ...
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تاریخ انتشار 2006