报告题目：Role of CD44 in MIF mediated signal pathway

报告时间：2012年11月30日上午10:00

报告地点：智能实验楼大会议室

报 告 人：时雪荣 博士（Walter Reed Army Institute of Research, USA）

报告主要内容：The macrophage migration inhibitory factor (MIF) receptor (CD74) was cloned but the signaling mechanism is not evident. We hypothesized that signaling requires an additional molecule such as CD44, which activates nonreceptor tyrosine kinases. We utilized the CD74- and CD44-deficient COS-7/M6 cell to create stable transfectants expressing CD74, CD44, and a truncated CD44 lacking its intracytoplasmic signaling domain. CD74 alone mediated MIF binding; however, MIF-induced ERK1 and ERK2 kinase phosphorylation required the coexpression of full-length CD44. Investigations that used siRNA or kinase inhibitors indicate that MIF-induced ERK1 and ERK2 activation through CD44 required the Src tyrosine kinase. Studies of CD74, CD44, and CD74-CD44 transformants and corresponding mutant cells showed that CD74 and CD44 were necessary for MIF protection from apoptosis. These data establish CD44 as an integral member of the CD74 receptor complex leading to MIF signal transduction.

科技处

浙江省亚热带森林培育国家重点实验室培育基地

2012年月11月28日