ArticlePloS one2013
Dynamics of physical interaction between HIV-1 Nef and ASK1: identifying the interacting motif(s).
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- HIV-1 infection does not confer intrinsic resistance to cell death induced by cytotoxic T lymphocytes.bioRxiv : the preprint server for biology · 2026Article
- Crystallographic mining of ASK1 regulators to unravel the intricate PPI interfaces for the discovery of small molecule.Computational and structural biotechnology journal · 2022Review
- Mechanisms of Human Immunodeficiency Virus-Associated Lymphocyte Regulated Cell Death.AIDS research and human retroviruses · 2020Review
- Killing of Latently HIV-Infected CD4 T Cells by Autologous CD8 T Cells Is Modulated by Nef.Frontiers in immunology · 2018Article
- ASK1 restores the antiviral activity of APOBEC3G by disrupting HIV-1 Vif-mediated counteraction.Nature communications · 2015Article
- Proteomic profiling of SupT1 cells reveal modulation of host proteins by HIV-1 Nef variants.PloS one · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FasL mediated preferential apoptosis of bystander CTLs while protection of infected CD4(+)T cells remains one of the hallmarks of immune evasion during HIV infection. The property of infected host cells to evade cell-autonomous apoptosis emanates from ability of HIV-1Nef-protein to physically interact with ASK-1 and thereby inhibit its enzymatic activity. The specific domains of HIV-1Nef through which it may interact with ASK1 and thereby impair the ASK1 activity remain unidentified so far and represent a major challenge towards developing clear understanding about the dynamics of this interaction. Using mammalian two hybrid screen in association with site directed mutagenesis and competitive inhibitor peptides, we identified constituent minimal essential domain (152 DEVGEANN 159) through which HIV-1Nef interacts with ASK1 and inhibits its function. Furthermore our study also unravels a novel alternate mechanism underlying HIV-1 Nef mediated ASK1 functional modulation, wherein by potentiating the inhibitory ser(967) phosphorylation of ASK1, HIV-1Nef negatively modulated ASK1 function.
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Registered trials
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