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Alliance"],"accepted":{"date-parts":[[2025,4,28]]},"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:p>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\u2013infected 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.<\/jats:p>","DOI":"10.26508\/lsa.202503231","type":"journal-article","created":{"date-parts":[[2025,5,5]],"date-time":"2025-05-05T12:10:12Z","timestamp":1746447012000},"page":"e202503231","update-policy":"https:\/\/doi.org\/10.26508\/lsa.crossmarkpolicy","source":"Crossref","is-referenced-by-count":4,"title":["SLC38A9 is directly involved in Tat-induced endolysosome dysfunction and senescence in astrocytes"],"prefix":"10.26508","volume":"8","author":[{"given":"Neda","family":"Rezagholizadeh","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, 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