Author: Zhao, Bing; Chen, Ye-Guang
Title: Regulation of TGF-ß Signal Transduction Document date: 2014_9_23
ID: 1ag9mnd2_8
Snippet: It has been well established that c-Cbl mutations contribute to leukemia by negatively regulating the activity and stability of receptor tyrosine kinases [45] [46] [47] . Besides, disruption of TGF-signaling, which is a major antiproliferation and prodifferentiation signal for hematopoietic stem/progenitor cells [48] , greatly promotes lymphoblastic and myeloid leukemia in mouse models [49, 50] . We demonstrated that c-Cbl overexpression stabiliz.....
Document: It has been well established that c-Cbl mutations contribute to leukemia by negatively regulating the activity and stability of receptor tyrosine kinases [45] [46] [47] . Besides, disruption of TGF-signaling, which is a major antiproliferation and prodifferentiation signal for hematopoietic stem/progenitor cells [48] , greatly promotes lymphoblastic and myeloid leukemia in mouse models [49, 50] . We demonstrated that c-Cbl overexpression stabilizes T RII and sensitizes leukemia cells to TGF--induced growth inhibition. We also identified a neddylation-activity-defective c-Cbl mutation from leukemia patients, implying that c-Cbl inactivation contributes to leukemia development not only by amplifying the mitogenic signals from RTKs, but also by releasing the antiproliferative effects of TGF-.
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