ArticleJournal of the American Society of Nephrology : JASN2014
The basic domain of HIV-tat transactivating protein is essential for its targeting to lipid rafts and regulating fibroblast growth factor-2 signaling in podocytes isolated from children with HIV-1-associated nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Glycosylated RNAs: discovery and implications in cancer biology.Frontiers in oncology · 2026Review
- HIV-1 Nef synergizes with APOL1-G1 to induce nephrocyte cell death in HIV-related kidney diseases.Disease models & mechanisms · 2025Article
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.Disease models & mechanisms · 2025Article
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.bioRxiv : the preprint server for biology · 2024Article
- APOL1-G2 accelerates nephrocyte cell death by inhibiting the autophagy pathway.Disease models & mechanisms · 2023Article
- A SNARE protective pool antagonizes APOL1 renal toxicity in Drosophila nephrocytes.Cell & bioscience · 2023Article
- Virus-Associated Nephropathies: A Narrative Review.International journal of molecular sciences · 2022Review
- Rho GTPases in kidney physiology and diseases.Small GTPases · 2022Article
- Association of circulating fibroblast growth factor-2 with progression of HIV-chronic kidney diseases in children.Pediatric nephrology (Berlin, Germany) · 2021Article
- Childhood HIV-associated nephropathy: 36 years later.Pediatric nephrology (Berlin, Germany) · 2021Review
- Circulating fibroblast growth factor-2 precipitates HIV nephropathy in mice.Disease models & mechanisms · 2021Article
- Mechanisms of Proteinuria in HIV.Frontiers in medicine · 2021Review
- An HIV-Tat inducible mouse model system of childhood HIV-associated nephropathy.Disease models & mechanisms · 2020Article
- Defining the molecular mechanisms of HIV-1 Tat secretion: PtdIns(4,5)PTraffic (Copenhagen, Denmark) · 2018Review
- All-Round Manipulation of the Actin Cytoskeleton by HIV.Viruses · 2018Review
- Molecular Mechanisms of Injury in HIV-Associated Nephropathy.Frontiers in medicine · 2018Review
- Ablation of FGFR2 in Fibroblasts Ameliorates Kidney Fibrosis after Ischemia/Reperfusion Injury in Mice.Kidney diseases (Basel, Switzerland) · 2017Article
- APOL1-G1 in Nephrocytes Induces Hypertrophy and Accelerates Cell Death.Journal of the American Society of Nephrology : JASN · 2017Article
- Hedgehog pathway plays a vital role in HIV-induced epithelial-mesenchymal transition of podocyte.Experimental cell research · 2017Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Podocyte injury has a critical role in the pathogenesis of HIV-associated nephropathy (HIVAN). The HIV-1 transactivator of transcription (Tat), combined with fibroblast growth factor-2 (FGF-2), can induce the dedifferentiation and proliferation of cultured human podocytes. Cellular internalization of Tat requires interactions with heparan sulfate proteoglycans and cholesterol-enriched lipid rafts (LRs). However, the specific distribution of Tat in human podocytes and its ability to associate with LRs have not been documented. Here, we found that Tat is preferentially recruited to LRs in podocytes isolated from children with HIVAN. Furthermore, we identified arginines in the basic domain (RKKRRQRRR) of Tat as essential for (1) targeting Tat to LRs, (2) Tat-mediated increases in the expression of Rho-A and matrix metalloproteinase-9 in LRs, and (3) Tat-mediated enhancement of FGF-2 signaling in human podocytes and HIV-transgenic mouse kidneys and the exacerbation of renal lesions in these mice. Tat carrying alanine substitutions in the basic domain (AKKAAQAAA) remained localized in the cytosol and did not associate with LRs or enhance FGF-2 signaling in cultured podocytes. These results show the specific association of Tat with LRs in podocytes isolated from children with HIVAN, confirm Tat as a regulator of FGF-2 signaling in LRs, and identify the key domain of Tat responsible for promoting these effects and aggravating renal injury in HIV-transgenic mice. Moreover, these results provide a molecular framework for developing novel therapies to improve the clinical outcome of children with HIVAN.
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