赫拉
HEK 293细胞
基因敲除
基因沉默
细胞生物学
分子生物学
转染
细胞培养
生物
化学
基因
生物化学
遗传学
作者
Hironori Nishitsuji,Ryuichi Sugiyama,Makoto Abe,Hiroshi Takaku
标识
DOI:10.1074/jbc.m115.679357
摘要
Here, we identify ATP1B3 and fibrillin-1 as novel BST-2-binding proteins. ATP1B3 depletion in HeLa cells (BST-2-positive cells), but not 293T cells (BST-2-negative cells), induced the restriction of HIV-1 production in a BST-2-dependent manner. In contrast, fibrillin-1 knockdown reduced HIV-1 production in 293T and HeLa cells in a BST-2-independent manner. Moreover, NF-κB activation was enhanced by siATP1B3 treatment in HIV-1- and HIV-1ΔVpu-infected HeLa cells. In addition, ATP1B3 silencing induced high level BST-2 expression on the surface of HeLa cells. These results indicate that ATP1B3 is a co-factor that accelerates BST-2 degradation and reduces BST-2-mediated restriction of HIV-1 production and NF-κB activation.
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