ArticleJournal of neurovirology2009
Association of FAK activation with lentivirus-induced disruption of blood-brain barrier tight junction-associated ZO-1 protein organization.
Article in Journal of neurovirology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 30 citations in OpenAlex.
- Tumor removal limits prostate cancer cell dissemination in bone and osteoblasts induce cancer cell dormancy through focal adhesion kinase.Journal of experimental & clinical cancer research : CR · 2023Article
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- Blood-brain barrier-restricted translocation ofeLife · 2021Article
- Lack of susceptibility in neonatally infected rhesus macaques to simian immunodeficiency virus-induced encephalitis.Journal of neurovirology · 2019Article
- Culture Model for Non-human Primate Choroid Plexus.Frontiers in cellular neuroscience · 2019Article
- MARCKS-related protein regulates cytoskeletal organization at cell-cell and cell-substrate contacts in epithelial cells.Journal of cell science · 2018Article
- Disruption of outer blood-retinal barrier by Toxoplasma gondii-infected monocytes is mediated by paracrinely activated FAK signaling.PloS one · 2017Article
- Effect of human immunodeficiency virus on blood-brain barrier integrity and function: an update.Frontiers in cellular neuroscience · 2015Review
- Novel 3D analysis of Claudin-5 reveals significant endothelial heterogeneity among CNS microvessels.Microvascular research · 2013Article
- Cytokines and chemokines at the crossroads of neuroinflammation, neurodegeneration, and neuropathic pain.Mediators of inflammation · 2013Review
- Focal adhesion kinase-Tyr407 and -Tyr397 exhibit antagonistic effects on blood-testis barrier dynamics in the rat.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Viral disruption of the blood-brain barrier.Trends in microbiology · 2012Review
- Microglia activation by SIV-infected macrophages: alterations in morphology and cytokine secretion.Journal of neurovirology · 2012Article
- An inverted blood-brain barrier model that permits interactions between glia and inflammatory stimuli.Journal of neuroscience methods · 2012Article
- Contribution of a single host genetic locus to mouse adenovirus type 1 infection and encephalitis.mBio · 2012Article
- MCP-3/CCL7 production by astrocytes: implications for SIV neuroinvasion and AIDS encephalitis.Journal of neurovirology · 2011Article
- Molecular mechanisms of neuroinvasion by monocytes-macrophages in HIV-1 infection.Retrovirology · 2010Review
- Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Expression of tight junction proteins between brain microvascular endothelial cells (BMECs) of the blood-brain barrier (BBB) is lost during development of human immunodeficiency virus (HIV) encephalitis (HIVE). Although many studies have focused on the strains of virus that induce neurological sequelae or on the macrophages/microglia that are associated with development of encephalitis, the molecular signaling pathways within the BMECs involved have yet to be resolved. We have previously shown that there is activation and disruption of an in vitro BBB model using lentivirus-infected CEMx174 cells. We and others have shown similar disruption in vivo. Therefore, it was of interest to determine if the presence of infected cells could disrupt intact cerebral microvessels immediately ex vivo, and if so, which signaling pathways were involved. The present data demonstrate that disruption of tight junctions between BMECs is mediated through activation of focal adhesion kinase (FAK) by phosphorylation at TYR-397. Inhibition of FAK activation is sufficient to prevent tight junction disruption. Thus, it may be possible to inhibit the development of HIVE by using inhibitors of FAK.
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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.