ArticleJournal of virology1999
Ikappakappa mediates NF-kappaB activation in human immunodeficiency virus-infected cells.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 33 citations in OpenAlex.
- Dual antiviral and anti-inflammatory effects of BAY 11-7082 in SARS-CoV-2 infection via inhibition of the canonical NF-κB signaling pathway.Scientific reports · 2026Article
- Quantitative Proteomics Reveal That CB2R Agonist JWH-133 Downregulates NF-κB Activation, Oxidative Stress, and Lysosomal Exocytosis from HIV-Infected Macrophages.International journal of molecular sciences · 2024Article
- Regulation of CYBB Gene Expression in Human Phagocytes by a Distant Upstream NF-κB Binding Site.Journal of cellular biochemistry · 2015Article
- Macrophage derived cystatin B/cathepsin B in HIV replication and neuropathogenesis.Current HIV research · 2014Review
- A high throughput RNAi screen reveals determinants of HIV-1 activity in host kinases.International journal of clinical and experimental pathology · 2014Article
- Inhibition of NF-κB activity by HIV-1 Vpr is dependent on Vpr binding protein.Journal of cellular physiology · 2013Article
- Human immunodeficiency virus type 1 Vpu and cellular TASK proteins suppress transcription of unintegrated HIV-1 DNA.Virology journal · 2012Article
- Molecular Understanding of HIV-1 Latency.Advances in virology · 2012Article
- Caveolin 1 inhibits HIV replication by transcriptional repression mediated through NF-κB.Journal of virology · 2011Article
- Stromal down-regulation of macrophage CD4/CCR5 expression and NF-κB activation mediates HIV-1 non-permissiveness in intestinal macrophages.PLoS pathogens · 2011Article
- Molecular mechanisms of HIV-1 persistence in the monocyte-macrophage lineage.Retrovirology · 2010Review
- Regulation of HIV-1 transcription in cells of the monocyte-macrophage lineage.Retrovirology · 2009Review
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- Inhibition of human immunodeficiency virus type 1 replication in latently infected cells by a novel IkappaB kinase inhibitor.Antimicrobial agents and chemotherapy · 2006Article
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- Pneumocystis activates human alveolar macrophage NF-kappaB signaling through mannose receptors.Infection and immunity · 2004Article
- NF-kappaB cis-acting motifs of the human immunodeficiency virus (HIV) long terminal repeat regulate HIV transcription in human macrophages.Journal of virology · 2001Article
- Transcription of the RelB gene is regulated by NF-kappaB.Oncogene · 2001Article
- Enhanced proteolysis of IkappaBalpha and IkappaBbeta proteins in astrocytes by Moloney murine leukemia virus (MoMuLV)-ts1 infection: a potential mechanism of NF-kappaB activation.Journal of neurovirology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human monocytes and macrophages are persistent reservoirs of human immunodeficiency virus (HIV) type-1. Persistent HIV infection of these cells results in increased levels of NF-kappaB in the nucleus secondary to increased IkappaBalpha, IkappaBbeta, and IkappaBepsilon degradation, a mechanism postulated to regulate viral persistence. To characterize the molecular mechanisms regulating HIV-mediated degradation of IkappaB, we have sought to identify the regulatory domains of IkappaBalpha targeted by HIV infection. Using monocytic cells stably expressing different transdominant molecules of IkappaBalpha, we determined that persistent HIV infection of these cells targets the NH2 but not the COOH terminus of IkappaBalpha. Further analysis demonstrated that phosphorylation at S32 and S36 is necessary for HIV-dependent IkappaBalpha degradation and NF-kappaB activation. Of the putative N-terminal IkappaBalpha kinases, we demonstrated that the Ikappakappa complex, but not p90(rsk), is activated by HIV infection and mediates HIV-dependent NF-kappaB activation. Analysis of viral replication in cells that constitutively express IkappaBalpha negative transdominant molecules demonstrated a lack of correlation between virus-induced NF-kappaB (p65/p50) nuclear translocation and degree of viral persistence in human monocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.