ATP1B3 protein modulates the restriction of HIV-1 production and nuclear factor K light chain enhancer of activated B cells (NF-κB) activation by BST-2

Hironori Nishitsuji, Ryuichi Sugiyama, Makoto Abe, Hiroshi Takaku

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)4754-4762
Number of pages9
JournalJournal of Biological Chemistry
Volume291
Issue number9
DOIs
Publication statusPublished - 26-02-2016

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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