ArticleNucleic acids research2020
Host cell factors stimulate HIV-1 transcription by antagonizing substrate-binding function of Siah1 ubiquitin ligase to stabilize transcription elongation factor ELL2.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- TSG101 Promotes SIAH1 Auto-Ubiquitination to Drive Migration and Invasion in Hepatocellular Carcinoma Cells.Journal of cellular and molecular medicine · 2026Article
- Deficiency of SIAH1 promotes the formation of filopodia by increasing the accumulation of FASN in liver cancer.Cell death & disease · 2024Article
- Exploring the Role of Ubiquitin-Proteasome System in the Pathogenesis of Parkinson's Disease.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- Cathepsin K promotes the proliferation of hepatocellular carcinoma cells through induction of SIAH1 ubiquitination and degradation.iScience · 2023Article
- Discovering a New Okadaic Acid Derivative, a Potent HIV Latency Reversing Agent fromMarine drugs · 2023Article
- A modular CRISPR screen identifies individual and combination pathways contributing to HIV-1 latency.PLoS pathogens · 2023Article
- Review
- P-TEFb is degraded by Siah1/2 in quiescent cells.Nucleic acids research · 2022Article
- Design, synthesis, and biological evaluation of 5-((4-(pyridin-3-yl)pyrimidin-2-yl)amino)-1Journal of enzyme inhibition and medicinal chemistry · 2021Article
- Biogenesis of P-TEFb in CD4+ T cells to reverse HIV latency is mediated by protein kinase C (PKC)-independent signaling pathways.PLoS pathogens · 2021Article
- Evaluation of common genetic variants in vitamin E-related pathway genes and colorectal cancer susceptibility.Archives of toxicology · 2021Article
- From Entry to Egress: Strategic Exploitation of the Cellular Processes by HIV-1.Frontiers in microbiology · 2020Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The Siah1 and Siah2 ubiquitin ligases are implicated in diverse biological processes ranging from cellular stress responses, signaling to transcriptional regulation. A key substrate of Siah1 is ELL2, which undergoes proteolysis upon polyubiquitination. ELL2 stimulates transcriptional elongation and is a subunit of the Super Elongation Complex (SEC) essential for HIV-1 transactivation. Previously, multiple transcriptional and post-translational mechanisms are reported to control Siah's expression and activity. Here we show that the activity of Siah1/2 can also be suppressed by host cell factor 1 (HCF1), and the hitherto poorly characterized HCF2, which themselves are not degraded but can bind and block the substrate-binding domain (SBD) of Siah1/2 to prevent their autoubiquitination and trans-ubiquitination of downstream targets including ELL2. This effect stabilizes ELL2 and enhances the ELL2-SEC formation for robust HIV-1 transactivation. Thus, our study not only identifies HCF1/2 as novel activators of HIV-1 transcription through inhibiting Siah1 to stabilize ELL2, but also reveals the SBD of Siah1/2 as a previously unrecognized new target for HCF1/2 to exert this inhibition.
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