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    Beta-catenin, which plays a critical role in both the cytoskeleton and in transcriptional regulation in various adherent cell types, undergoes degradation during adherent cell apoptosis. Although beta-catenin has been reported to be present in Jurkat T-acute lymphoblastic leukemia cells, the role of beta-catenin and its regulation in hematologic malignancies have not been examined. The data presented here demonstrate that treatment of the T cell leukemia Jurkat with the apoptosis inducers anti-Fas, TRAIL, staurosporin, and etoposide induced proteolytic cleavage of beta-catenin, as did TRAIL and staurosporin in U937 myeloblastic leukemia cells. In Jurkat cells, beta-catenin was cleaved at both the N- and C-termin ... 전체 초록 보기

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      UCI(KEPA) : I410-ECN-0101-2009-470-012374602