ArticleLife science alliance2025
SLC38A9 is directly involved in Tat-induced endolysosome dysfunction and senescence in astrocytes.
Article in Life science alliance, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Solute carrier membrane transporters: emerging targets in CNS disorders.Nature reviews. Drug discovery · 2026Review
- HIV associated immune aging among people living with HIV: implications for long-term antiretroviral therapy and potential HIV cure interventions in sub-Saharan Africa.Frontiers in immunology · 2026Review
- Stem-cell-derived extracellular vesicles in neurodegeneration and neuroaging: therapeutic potential and challenges.Extracellular vesicles and circulating nucleic acids · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
Cellular senescence contributes to accelerated aging and the development of various neurodegeneration disorders including HIV-associated neurocognitive disorders. The development of HIV-associated neurocognitive disorders is attributed, at least in part, to the CNS persistence of HIV-1 transactivator of transcription (Tat), an essential protein for viral transcription that is actively secreted from HIV-1-infected cells. Secreted Tat enters cells via receptor-mediated endocytosis and induces endolysosome dysfunction and cellular senescence in CNS cells. Given that endolysosome dysfunction represents an early step in exogenous Tat-induced cellular senescence, we tested the hypothesis that Tat induces cellular senescence via an endolysosome-dependent mechanism in human astrocytes. We demonstrated that internalized Tat interacts with an endolysosome-resident arginine sensor SLC38A9 via the arginine-rich basic domain. Such an interaction between Tat and SLC38A9 leads to endolysosome dysfunction, enhanced HIV-1 LTR transactivation, and cellular senescence. These findings suggest that endolysosome dysfunction drives the development of senescence and highlight the novel role of SLC38A9 in Tat-induced endolysosome dysfunction and astrocyte senescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.