ArticleThe Journal of biological chemistry2013
Inhibition of HIV-1 transcription and replication by a newly identified cyclin T1 splice variant.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- A Truncated Isoform of Cyclin T1 Could Contribute to the Non-Permissive HIV-1 Phenotype of U937 Promonocytic Cells.Viruses · 2024Article
- In silico prediction of HIV-1-host molecular interactions and their directionality.PLoS computational biology · 2022Article
- The landscape of alternative splicing in HIV-1 infected CD4 T-cells.BMC medical genomics · 2020Article
- Immune regulator ABIN1 suppresses HIV-1 transcription by negatively regulating the ubiquitination of Tat.Retrovirology · 2017Article
- Genome editing of the HIV co-receptors CCR5 and CXCR4 by CRISPR-Cas9 protects CD4Cell & bioscience · 2017Article
- Genome editing of CXCR4 by CRISPR/cas9 confers cells resistant to HIV-1 infection.Scientific reports · 2015Article
- Hematopoietic Stem and Immune Cells in Chronic HIV Infection.Stem cells international · 2015Review
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
A variety of cellular factors participates in the HIV-1 life cycle. Among them is the well characterized cyclin T1 (CYCT1). CycT1 binds to cyclin-dependent kinase 9 (CDK9) and forms the positive transcription elongation factor-b (P-TEFb). P-TEFb is then recruited by HIV-1 TAT to the HIV-1 long terminal repeat (LTR) promoter and subsequently leads to phosphorylation of the C-terminal domain of RNA polymerase II (pol II), enhanced processivity of pol II, and transcription of a full-length HIV-1 RNA. In this study, we report the identification of a new CYCT1 splice variant, designated as CYCT1b, and accordingly we renamed CYCT1 as CYCT1a. CYCT1b was detected in several cell lines, including primary human CD4 T cells, and its expression was subject to cell cycle regulation. Similar to CYCT1a, CYCT1b was primarily localized in the nucleus. CYCT1b expression was found to be inversely correlated with HIV-1 gene expression and replication. This inverse correlation appeared to involve TAT transactivation, CDK9 binding, and subsequent recruitment of P-TEFb to the HIV-1 LTR promoter and pol II C-terminal domain phosphorylation. In agreement with these findings, CYCT1b expression led to direct inhibition of TAT-transactivated transcription of the HIV-1 LTR promoter. Taken together, these results show that the newly identified CYCT1b splice variant inhibits HIV-1 transcription and may provide new clues for the development of anti-HIV strategies.
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