ArticleJournal of virology2001
The pathogenicity of human immunodeficiency virus (HIV) type 1 Nef in CD4C/HIV transgenic mice is abolished by mutation of its SH3-binding domain, and disease development is delayed in the absence of Hck.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 121 citations in OpenAlex.
- Rosmarinic acid alleviates bleomycin-induced pulmonary fibrosis in mice by activating the Rap1 pathway.Scientific reports · 2026Article
- Nef as a driver of immunodeficiency and HIV-associated diseases: insights from mouse models.Frontiers in immunology · 2026Review
- A Systematic Compilation of Human SH3 Domains: A Versatile Superfamily in Cellular Signaling.Cells · 2023Review
- NEF-Induced HIV-Associated Nephropathy Through HCK/LYN Tyrosine Kinases.The American journal of pathology · 2023Article
- Collapsing glomerulopathy: unraveling varied pathogeneses.Current opinion in nephrology and hypertension · 2023Review
- Apoptosis regulation by the tyrosine-protein kinase CSK.Frontiers in cell and developmental biology · 2022Review
- μ-Lat: A mouse model to evaluate human immunodeficiency virus eradication strategies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Structure, function, and inhibitor targeting of HIV-1 Nef-effector kinase complexes.The Journal of biological chemistry · 2020Review
- Common Mechanisms of Viral Injury to the Kidney.Advances in chronic kidney disease · 2019Review
- Recent Updates on Mouse Models for Human Immunodeficiency, Influenza, and Dengue Viral Infections.Viruses · 2019Review
- Implications of HIV-1 Nef for "Shock and Kill" Strategies to Eliminate Latent Viral Reservoirs.Viruses · 2018Review
- Bone degradation machinery of osteoclasts: An HIV-1 target that contributes to bone loss.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- All-Round Manipulation of the Actin Cytoskeleton by HIV.Viruses · 2018Review
- HIV-I Nef inhibitors: a novel class of HIV-specific immune adjuvants in support of a cure.AIDS research and therapy · 2017Review
- Src family kinases in chronic kidney disease.American journal of physiology. Renal physiology · 2017Review
- Hallmarks of HIV-1 pathogenesis are modulated by Nef's Secretion Modification Region.Journal of AIDS & clinical research · 2015Article
- Interaction with the Src homology (SH3-SH2) region of the Src-family kinase Hck structures the HIV-1 Nef dimer for kinase activation and effector recruitment.The Journal of biological chemistry · 2014Article
- The accessory factor Nef links HIV-1 to Tec/Btk kinases in an Src homology 3 domain-dependent manner.The Journal of biological chemistry · 2014Article
- Article
- Small molecule inhibitors of the HIV-1 virulence factor, Nef.Drug discovery today. Technologies · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human immunodeficiency virus type 1 (HIV-1) Nef protein is an important determinant of AIDS pathogenesis. We have previously reported that HIV-1 Nef is responsible for the induction of a severe AIDS-like disease in CD4C/HIV transgenic (Tg) mice. To understand the molecular mechanisms of this Nef-induced disease, we generated Tg mice expressing a mutated Nef protein in which the SH3 ligand-binding domain (P(72)XXP(75)XXP(78)) was mutated to A(72)XXA(75)XXQ(78). This mutation completely abolished the pathogenic potential of Nef, although a partial downregulation of the CD4 cell surface expression was still observed in these Tg mice. We also studied whether Hck, one of the effectors previously found to bind to this PXXP motif of Nef, was involved in disease development. Breeding of Tg mice expressing wild-type Nef on an hck(-/-) (knockout) background did not abolish any of the pathological phenotypes. However, the latency of disease development was prolonged. These data indicate that an intact PXXP domain is essential for inducing an AIDS-like disease in CD4C/HIV Tg mice and suggest that interaction of a cellular effector(s) with this domain is required for the induction of this multiorgan disease. Our findings indicate that Hck is an important, but not an essential, effector of Nef and suggest that another factor(s), yet to be identified, may be more critical for disease development.
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