ArticleVirology2010
Alternate receptor usage of neuropilin-1 and glucose transporter protein 1 by the human T cell leukemia virus type 1.
Article in Virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- VEGFR2 dimerization kinetics on the cell surface determined by microscopy and mathematical modeling.Biophysical journal · 2026Article
- Neuropilin-1 expression modulates infection susceptibility to murine cytomegalovirus at the materno-fetal interface.Journal of virology · 2025Article
- The Assembly of HTLV-1-How Does It Differ from HIV-1?Viruses · 2024Review
- ASFV infection induces lipid metabolic disturbances and promotes viral replication.Frontiers in microbiology · 2024Article
- Review
- Human T-cell leukemia virus type 1 Tax-deregulated autophagy pathway and c-FLIP expression contribute to resistance against death receptor-mediated apoptosis.Journal of virology · 2014Article
- Functional analyse of GLUT1 and GLUT12 in glucose uptake in goat mammary gland epithelial cells.PloS one · 2013Article
- Neuropilins: expression and roles in the epithelium.International journal of experimental pathology · 2012Review
- Cellular Factors Involved in HTLV-1 Entry and Pathogenicit.Frontiers in microbiology · 2012Article
- Review
- Current concepts regarding the HTLV-1 receptor complex.Retrovirology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies have demonstrated that neuropilin 1 (NP-1) is involved in HTLV-1 entry; however, the role NP-1 plays in this process is not understood. We demonstrated that ectopic expression of human NP-1 but not NP-2 cDNA increased susceptibility to HTLV-1. SiRNA-mediated inhibition of NP-1 expression correlated with significant reduction of HTLV-1 Env-mediated fusion. The vascular endothelial growth factor (VEGF(165)) caused downmodulation of surface NP-1 and inhibited HTLV-1 infection of U87 cells. In contrast, VEGF(165) partially inhibited infection of primary astrocytes and had no significant effect on infection of HeLa cells. VEGF(165) and antibodies to the glucose transporter protein 1 (anti-GLUT-1) were both needed to block infection of primary astrocytes, however, only anti-GLUT-1 antibodies were sufficient to block infection of HeLa cells. HTLV-1 Env forms complexes with both NP-1 and GLUT-1 in primary human astrocytes. The alternate usage of these two cellular receptors may have important implications regarding HTLV-1 neuro-tropism.
Indexed as
Identifiers
What OpenQuestion holds
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.