ZBRK1 represses HIV-1 LTR-mediated transcription

Hironori Nishitsuji, Makoto Abe, Reila Sawada, Hiroshi Takaku

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The identification of cellular proteins that interact with the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) provides a basic understanding of HIV-1 gene expression, which is the major determinant regulating virus replication. We show that ZBRK1 negatively regulates the HIV-1 LTR. Ectopic expression of ZBRK1 represses transcriptional activity of the HIV-1 LTR, whereas the depletion of endogenous ZBRK1 leads to activation of the HIV-1 LTR. The repressor activity of ZBRK1 is required for TRIM28 binding. Furthermore, ZBRK1 is bound to the HIV-1 LTR in vivo. These results indicate that ZBRK1 could be involved in a potent intrinsic antiretroviral defense. Structured summary of protein interactions: ZBRK1 physically interacts with TRIM28 by anti tag coimmunoprecipitation (View interaction).

Original languageEnglish
Pages (from-to)3562-3568
Number of pages7
JournalFEBS Letters
Volume586
Issue number20
DOIs
Publication statusPublished - 19-10-2012
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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