TY - JOUR
T1 - ZBRK1 represses HIV-1 LTR-mediated transcription
AU - Nishitsuji, Hironori
AU - Abe, Makoto
AU - Sawada, Reila
AU - Takaku, Hiroshi
N1 - Funding Information:
We thank Dr. H. Miyoshi for providing the lentiviral vector system, Dr. T. Suda for providing pNFLAG-Bos, Dr. I.S.Y. Chen for providing pNL4-3lucΔenv and Yoshinori Taniguchi and Takahiro Watanabe for their technical assistance. This work was supported in part by a Grant-in-Aid for Science Research (C) from the Japan Society for the Promotion of Science (JSPS), Japan; by a Grant-in-Aid for AIDS research from the Ministry of Health, Labor, and Welfare, Japan; and by a Grant from the Strategic Research Foundation Grant-aided Project for Private Universities from the Ministry of Education, Culture, Sport, Science, and Technology, Japan (MEXT).
PY - 2012/10/19
Y1 - 2012/10/19
N2 - 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).
AB - 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).
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U2 - 10.1016/j.febslet.2012.08.010
DO - 10.1016/j.febslet.2012.08.010
M3 - Article
C2 - 22975076
AN - SCOPUS:84867572993
SN - 0014-5793
VL - 586
SP - 3562
EP - 3568
JO - FEBS Letters
JF - FEBS Letters
IS - 20
ER -
