ArticleThe FEBS journal2015
Human X-DING-CD4 mediates resistance to HIV-1 infection through novel paracrine-like signaling.
Article in The FEBS journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Neuroprotective Role of DING Protein in Normal Aging and Alzheimer's Disease.Archives of internal medicine research · 2026Article
- Natural Resistance to HIV Infection: Role of Immune Activation.Immunity, inflammation and disease · 2025Review
- Neuroprotective Role of DING protein in Fetal Alcohol Spectrum Disorders and Depression.Obstetrics and gynecology research · 2025Article
- DING Protein Inhibits Transcription of HIV-1 Gene through Suppression of Phosphorylation of NF-κB p65.Journal of HIV and AIDS · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
X-DING-CD4 is a novel phosphatase mediating antiviral responses to HIV-1 infection. This protein is constitutively expressed and secreted by HIV-1 resistant CD4(+) T cells and its mRNA transcription is up-regulated in peripheral blood mononuclear cells from HIV-1 elite controllers. The secreted/soluble X-DING-CD4 protein form is of particular importance because it blocks virus transcription when added to HIV-1 susceptible cells. The present study aimed to determine the contribution of this factor to the induction of the antiviral response in target cells. We found that soluble X-DING-CD4 enters cells by endocytosis and that influx of this protein induced transcription of interferon-α and endogenous X-DING-CD4 mRNA in transformed CD4(+) T cells and primary macrophages. Treatment of HIV-1 susceptible cells with exogenous X-DING-CD4 caused depletion of phosphorylated p50 and p65 nuclear factor kappa β subunits and a significant reduction in p50/p65 nuclear factor kappa β binding to the HIV-1 long terminal repeat. Taken together, these findings indicate a novel antiviral mechanism mediated by the influx of soluble X-DING-CD4, its signaling to promote self-amplification, and functional duality as an endogenous innate immunity effector and exogenous factor regulating gene expression in bystander cells.
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Registered trials
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