B细胞激活因子
交通2
信号转导
细胞生物学
NF-κB
肿瘤坏死因子α
NFKB1型
细胞因子
生物
转录因子
癌症研究
B细胞
免疫学
肿瘤坏死因子受体
抗体
生物化学
基因
作者
Xiaoyu Tang,Lingling Zhang,Wei Wei
标识
DOI:10.1016/j.imlet.2018.01.010
摘要
B cell activating factor (BAFF) is an important cytokine for the maintenance of B cell development, survival and homeostasis. BAFF/BAFF-R could directly activate nuclear factor kappa B (NF-κB) pathway. Tumour necrosis factor receptor-associated factors (TRAFs) are key regulatory proteins in NF-κB signaling pathways. TRAF1 enhances the activation of tumor necrosis factor receptor 2 (TNF-R2) induced by NF-κB. TRAF2 and TRAF3 signal adapters act cooperatively to control the maturation and survival signals mediated by BAFF receptor. TRAF5 is most homologous to TRAF3, as well as most functionally similar to TRAF2. TRAF6 is also required for the BAFF-mediated activation of NF-κB signal pathway. TRAF7 is involved in signal transduction pathways that lead either to activation or repression of NF-κB transcription factor. In this article, we reviewed the roles of TRAFs in NF-κB signaling pathway mediated by BAFF.
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