ArticleImmunology letters2008
The critical role of human transcriptional repressor CTCF mRNA up-regulation in the induction of anti-HIV-1 responses in CD4(+) T cells.
Article in Immunology letters, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Single-cell transcriptomics identifies prothymosin α restriction of HIV-1 in vivo.Science translational medicine · 2023Article
- Are BET Inhibitors yet Promising Latency-Reversing Agents for HIV-1 Reactivation in AIDS Therapy?Viruses · 2021Review
- Human X-DING-CD4 mediates resistance to HIV-1 infection through novel paracrine-like signaling.The FEBS journal · 2015Article
- The interplay between the X-DING-CD4, IFN-α and IL-8 gene activity in quiescent and mitogen- or HIV-1-exposed PBMCs from HIV-1 elite controllers, AIDS progressors and HIV-negative controls.Innate immunity · 2014Article
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- Native X-DING-CD4 protein secreted by HIV-1 resistant CD4+ T cells blocks activity of IL-8 promoter in human endothelial cells infected with enteric bacteria.Innate immunity · 2012Article
- Identification of X-DING-CD4, a new member of human DING protein family that is secreted by HIV-1 resistant CD4(+) T cells and has anti-viral activity.Biochemical and biophysical research communications · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We have employed our CD4(+) T cell model named HIV-1 resistance factor (HRF(+)) to study the inducible anti-HIV-1 responses mediated through novel soluble molecules. We found that exposure to the soluble products of HRF(+) cells activated CCCTC-binding factor (CTCF) mRNA expression in HIV-1 susceptible primary and transformed CD4(+) T cells and overlapped with their acquisition of transient resistance to virus. Conversely, the interference with the expression of CTCF gene in HRF(+) cells reversed the resistant phenotype and eliminated the biological potential of their cell culture supernatant to induce "HRF-like" activity in target cells. Band-shift analysis upon the nuclear fractions from HIV-1 resistant cells showed that CTCF protein bound to HIV-1 promoter and this binding prevented the formation of NF-kappaB/LTR complex. This evidence suggests that CTCF is an intracellular effector of HRF activity and that the acquisition of resistance to HIV-1 in CD4(+) T cells is a consequence of the prior activation of CTCF gene by the soluble entity secreted by HRF(+) cells.
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Registered trials
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