CD3-epsilon overexpressed in prothymocytes acts as an oncogene.
作者： Baoping Wang , Jian She , Mariolina Salio , Deborah Allen , Elizabeth Lacy
DOI: 10.1007/BF03401669
关键词:
摘要: Background Upon engagement of the T cell receptor for antigen, its associated CD3 proteins recruit signal transduction molecules, which in turn regulate lymphocyte proliferation, apoptosis, and thymocyte development. Because some transducing molecules recruited by CD3-e, i.e., p56lck p59fyn, are oncogenic since we previously found that overexpression CD3-e transgenes causes a block NK development, tested hypothesis aberrant signaling leads both to abnormal death lymphomagenesis.
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