Human immunodeficiency virus-1 Nef suppresses Hsp70-mediated Tat activation

Ryuichi Sugiyama; Haruki Naganuma; Hironori Nishitsuji; Hiroshi Takaku

doi:10.1016/j.febslet.2011.09.029

Human immunodeficiency virus-1 Nef suppresses Hsp70-mediated Tat activation

Ryuichi Sugiyama
, Haruki Naganuma
, Hironori Nishitsuji
, Hiroshi Takaku

Research output: Contribution to journal › Article › peer-review

15 Citations (Scopus)

Abstract

The human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) contains binding sites for several host transcription factors that contribute to HIV-1 gene expression. Although previous reports have indicated that HIV-1 Nef positively or negatively regulates HIV-1 gene expression, the precise molecular mechanisms by which this occurs remain largely unknown. In this study, we report that Nef suppressed LTR-driven transcription only in the presence of HIV-1 Tat, which was localized to the cytoplasm and degraded by the proteasome. However, the depletion of Hsp70 was found to reduce the suppressive effect of Nef on HIV-1 gene expression. These results suggest that Nef suppresses Hsp70-mediated HIV-1 Tat activation.

Original language	English
Pages (from-to)	3367-3371
Number of pages	5
Journal	FEBS Letters
Volume	585
Issue number	21
DOIs	https://doi.org/10.1016/j.febslet.2011.09.029
Publication status	Published - 04-11-2011
Externally published	Yes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2011.09.029

Cite this

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title = "Human immunodeficiency virus-1 Nef suppresses Hsp70-mediated Tat activation",

abstract = "The human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) contains binding sites for several host transcription factors that contribute to HIV-1 gene expression. Although previous reports have indicated that HIV-1 Nef positively or negatively regulates HIV-1 gene expression, the precise molecular mechanisms by which this occurs remain largely unknown. In this study, we report that Nef suppressed LTR-driven transcription only in the presence of HIV-1 Tat, which was localized to the cytoplasm and degraded by the proteasome. However, the depletion of Hsp70 was found to reduce the suppressive effect of Nef on HIV-1 gene expression. These results suggest that Nef suppresses Hsp70-mediated HIV-1 Tat activation.",

author = "Ryuichi Sugiyama and Haruki Naganuma and Hironori Nishitsuji and Hiroshi Takaku",

note = "Funding Information: We thank Drs. M. Kannagi and T. Hayashi for providing pNef-V5 and its mutants, Dr. I.S.Y. Chen for providing pNL4-3lucΔenv and Dr. A. Ryo for providing pCMV-Myc-Ubi. This work was supported in part by a Grant-in-Aid for High Technology Research (no. 09309011) from the Ministry of Education, Science, Sports, and Culture in Japan, by a Grant-in-Aid for AIDS research from the Ministry of Health, Labor, and Welfare in Japan, and by a Grant from the Ministry of Education, Culture, Sports, Science, and Technology in Japan (MEXT) as part of the Strategic Research Foundation Grant-Aided Project for Private Universities. ",

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doi = "10.1016/j.febslet.2011.09.029",

language = "English",

volume = "585",

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journal = "FEBS Letters",

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T1 - Human immunodeficiency virus-1 Nef suppresses Hsp70-mediated Tat activation

AU - Sugiyama, Ryuichi

AU - Naganuma, Haruki

AU - Nishitsuji, Hironori

AU - Takaku, Hiroshi

N1 - Funding Information: We thank Drs. M. Kannagi and T. Hayashi for providing pNef-V5 and its mutants, Dr. I.S.Y. Chen for providing pNL4-3lucΔenv and Dr. A. Ryo for providing pCMV-Myc-Ubi. This work was supported in part by a Grant-in-Aid for High Technology Research (no. 09309011) from the Ministry of Education, Science, Sports, and Culture in Japan, by a Grant-in-Aid for AIDS research from the Ministry of Health, Labor, and Welfare in Japan, and by a Grant from the Ministry of Education, Culture, Sports, Science, and Technology in Japan (MEXT) as part of the Strategic Research Foundation Grant-Aided Project for Private Universities.

PY - 2011/11/4

Y1 - 2011/11/4

N2 - The human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) contains binding sites for several host transcription factors that contribute to HIV-1 gene expression. Although previous reports have indicated that HIV-1 Nef positively or negatively regulates HIV-1 gene expression, the precise molecular mechanisms by which this occurs remain largely unknown. In this study, we report that Nef suppressed LTR-driven transcription only in the presence of HIV-1 Tat, which was localized to the cytoplasm and degraded by the proteasome. However, the depletion of Hsp70 was found to reduce the suppressive effect of Nef on HIV-1 gene expression. These results suggest that Nef suppresses Hsp70-mediated HIV-1 Tat activation.

AB - The human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) contains binding sites for several host transcription factors that contribute to HIV-1 gene expression. Although previous reports have indicated that HIV-1 Nef positively or negatively regulates HIV-1 gene expression, the precise molecular mechanisms by which this occurs remain largely unknown. In this study, we report that Nef suppressed LTR-driven transcription only in the presence of HIV-1 Tat, which was localized to the cytoplasm and degraded by the proteasome. However, the depletion of Hsp70 was found to reduce the suppressive effect of Nef on HIV-1 gene expression. These results suggest that Nef suppresses Hsp70-mediated HIV-1 Tat activation.

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SN - 0014-5793

VL - 585

SP - 3367

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JO - FEBS Letters

JF - FEBS Letters

IS - 21

ER -

Human immunodeficiency virus-1 Nef suppresses Hsp70-mediated Tat activation

Abstract

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All Science Journal Classification (ASJC) codes

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