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FADD及其磷酸化作用。

FADD and its phosphorylation.

作者信息

Zhang Jing, Zhang Dapeng, Hua Zichun

机构信息

The State Key Laboratory of Pharmaceutical Biotechnology, and Institute of Molecular and Cell Biology, Nanjing Universtiy, Nanjing 210093, China.

出版信息

IUBMB Life. 2004 Jul;56(7):395-401. doi: 10.1080/15216540400008929.

DOI:10.1080/15216540400008929
PMID:15545216
Abstract

The adaptor protein FADD is essential for apoptosis induced by 'death receptors', mediating aggregation and autocatalytic activation of caspase-8. Surprisingly, FADD is also involved in regulating T and B cell development. Accumulating evidences now suggest that FADD and its phosphorylation have additional roles in controlling pathways of cellular activation and proliferation, while the kinase modifying FADD phosphorylation is still unidentified. The cellular localization of FADD may also contribute to define FADD's role in apoptosis or proliferation. FADD may be a pivotal molecule which coupling the opposite cell processes of proliferation and apoptosis. FADD, probably modulated by phosphorylation, may function as a 'cell renewal set point' co-regulating proliferation and apoptosis in parallel.

摘要

衔接蛋白FADD对于“死亡受体”诱导的细胞凋亡至关重要,它介导半胱天冬酶-8的聚集和自催化激活。令人惊讶的是,FADD还参与调节T细胞和B细胞的发育。现在越来越多的证据表明,FADD及其磷酸化在控制细胞激活和增殖途径中具有额外作用,而修饰FADD磷酸化的激酶仍未明确。FADD的细胞定位也可能有助于确定其在细胞凋亡或增殖中的作用。FADD可能是一个关键分子,它将增殖和凋亡这两个相反的细胞过程联系起来。FADD可能受磷酸化调节,或许作为一个“细胞更新设定点”,并行协同调节增殖和凋亡。

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