Wenxia Jiang

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Ataxia telangiectasia (A-T) mutated (ATM) kinase orchestrates deoxyribonucleic acid (DNA) damage responses by phosphorylating numerous substrates implicated in DNA repair and cell cycle checkpoint activation. A-T patients and mouse models that express no ATM protein undergo normal embryonic development but exhibit pleiotropic DNA repair defects. In this(More)
Non-homologous end joining (NHEJ) is a major pathway to repair DNA double-strand breaks (DSBs), which can display different types of broken ends. However, it is unclear how NHEJ factors organize to repair diverse types of DNA breaks. Here, through systematic analysis of the human NHEJ factor interactome, we identify PAXX as a direct interactor of Ku. The(More)
Growth and differentiation of stem cells is thought to be regulated by growth factors and responding protein tyrosine kinase activities. Comparing mitotic stem cells from the adult intestinal epithelium, isolated from the crypts of Lieberkuhn, with isolated differentiated absorbtive cells we find major differences in the levels of phosphotyrosine-containing(More)
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(More)
Fertilization of the sea urchin egg results in the phosphorylation, on tyrosine, of a high molecular weight protein localized in the egg cortex. In the present study, treatment of unfertilized eggs with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate stimulated tyrosine phosphorylation of the high molecular weight cortical protein to levels three- to(More)
Non-homologous end-joining (NHEJ) is the most prominent DNA double strand break (DSB) repair pathway in mammalian cells. PAXX is the newest NHEJ factor, which shares structural similarity with known NHEJ factors-XRCC4 and XLF. Here we report that PAXX is dispensable for physiological NHEJ in otherwise wild-type mice. Yet Paxx-/- mice require XLF and Xlf-/-(More)
Missense mutations in ATM kinase, a master regulator of DNA damage responses, are found in many cancers, but their impact on ATM function and implications for cancer therapy are largely unknown. Here we report that 72% of cancer-associated ATM mutations are missense mutations that are enriched around the kinase domain. Expression of kinase-dead ATM(More)
Bcl11b is a transcription factor important for T cell development and also a tumor-suppressor gene that is hemizygously inactivated in ~10% human T cell acute lymphoblastic leukemia (T-ALL) and several murine T-ALL models, including ATM(-/-) thymic lymphomas. Here we report that heterozygous loss of Bcl11b (Bcl11b(+/-)) unexpectedly reduced lethal thymic(More)
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