ArticleJournal of virology2008
Modulation of beta-catenin and E-cadherin interaction by Vpu increases human immunodeficiency virus type 1 particle release.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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
9 citing papers in PubMed, 14 citations in OpenAlex.
- The Culprit Behind HBV-Infected Hepatocytes: NTCP.Drug design, development and therapy · 2024Review
- Article
- Upsetting the Balance: When Viruses Manipulate Cell Polarity Control.Journal of molecular biology · 2018Review
- β-Catenin/TCF-4 signaling regulates susceptibility of macrophages and resistance of monocytes to HIV-1 productive infection.Current HIV research · 2014Article
- Human tumour viruses and the deregulation of cell polarity in cancer.Nature reviews. Cancer · 2012Review
- Identification of novel T cell factor 4 (TCF-4) binding sites on the HIV long terminal repeat which associate with TCF-4, β-catenin, and SMAR1 to repress HIV transcription.Journal of virology · 2012Article
- Role of β-catenin and TCF/LEF family members in transcriptional activity of HIV in astrocytes.Journal of virology · 2012Article
- IFN-gamma mediates enhancement of HIV replication in astrocytes by inducing an antagonist of the beta-catenin pathway (DKK1) in a STAT 3-dependent manner.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Role of β-catenin/TCF-4 signaling in HIV replication and pathogenesis: insights to informing novel anti-HIV molecular therapeutics.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Vpu (viral protein U) is a 17-kDa human immunodeficiency virus type 1 (HIV-1) accessory protein that enhances the release of particles from the surfaces of infected cells. Vpu recruits beta-transducin repeat-containing protein (beta-TrCP) and mediates proteasomal degradation of CD4. By sequestering beta-TrCP away from other cellular substrates, Vpu leads to the stabilization of beta-TrCP substrates such as beta-catenin, IkappaBalpha, ATF4, and Cdc25A, but not of other substrates such as Emi1. This study shows that in addition to stabilizing beta-catenin, Vpu leads to the depression of both total and beta-catenin-associated E-cadherin levels through beta-TrCP-dependent stabilization of the transcriptional repressor Snail. We showed that both downregulation of overall E-cadherin levels and dissociation of E-cadherin from beta-catenin result in enhanced viral release. By contrast, the overexpression of E-cadherin or the prevention of the dissociation of E-cadherin from beta-catenin results in depressed levels of virus release. Since E-cadherin is expressed only in dendritic cells and macrophages, and not in T cells, our data suggest that the HIV-1 vpu gene may have evolved to counteract different restrictions to assembly in different cells.
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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.