ArticleRetrovirology2013
N-terminal Slit2 inhibits HIV-1 replication by regulating the actin cytoskeleton.
Article in Retrovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Mechanisms of HAHV-1 Interaction with Hemocytes inBiology · 2025Article
- Emerging roles of deubiquitinating enzymes in actin cytoskeleton and tumor metastasis.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Fibroblast-derived CXCL12 increases vascular permeability in a 3-D microfluidic model independent of extracellular matrix contractility.Frontiers in bioengineering and biotechnology · 2022Article
- SLIT2/ROBO1-signaling inhibits macropinocytosis by opposing cortical cytoskeletal remodeling.Nature communications · 2020Article
- Inhibitory Effect of Slit2-N on VEGF165-induced proliferation of vascular endothelia via Slit2-N-Robo4-Akt pathway in choroidal neovascularization.Cell cycle (Georgetown, Tex.) · 2019Article
- Peptide regulation of cofilin activity in the CNS: A novel therapeutic approach for treatment of multiple neurological disorders.Pharmacology & therapeutics · 2017Review
- Chemokines and Chemokine Receptors: Accomplices for Human Immunodeficiency Virus Infection and Latency.Frontiers in immunology · 2017Review
- Slit2N Inhibits Transmission of HIV-1 from Dendritic Cells to T-cells by Modulating Novel Cytoskeletal Elements.Scientific reports · 2015Article
- Cataloguing of Potential HIV Susceptibility Factors during the Menstrual Cycle of Pig-Tailed Macaques by Using a Systems Biology Approach.Journal of virology · 2015Article
- Distinct requirements for HIV-cell fusion and HIV-mediated cell-cell fusion.The Journal of biological chemistry · 2015Article
- miR-29b defines the pro-/anti-proliferative effects of S100A7 in breast cancer.Molecular cancer · 2015Article
- Renal endothelial injury and microvascular dysfunction in acute kidney injury.Seminars in nephrology · 2015Review
- Targeting strategies for delivery of anti-HIV drugs.Journal of controlled release : official journal of the Controlled Release Society · 2014Review
- Slit2N and Robo4 regulate lymphangiogenesis through the VEGF-C/VEGFR-3 pathway.Cell communication and signaling : CCS · 2014Article
- Regulatory T Cells Diminish HIV Infection in Dendritic Cells - Conventional CD4(+) T Cell Clusters.Frontiers in immunology · 2014Article
- Slit2-Robo4 pathway modulates lipopolysaccharide-induced endothelial inflammation and its expression is dysregulated during endotoxemia.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Novel anti-HIV therapeutics targeting chemokine receptors and actin regulatory pathways.Immunological reviews · 2013Review
- Emerging therapeutic strategies to prevent infection-related microvascular endothelial activation and dysfunction.Virulence · 2013Review
- Genistein interferes with SDF-1- and HIV-mediated actin dynamics and inhibits HIV infection of resting CD4 T cells.Retrovirology · 2013Article
- HIV restriction in quiescent CD4⁺ T cells.Retrovirology · 2013Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSlit2 is a ~ 200 kDa secreted glycoprotein that has been recently shown to regulate immune functions. However, not much is known about its role in HIV (human immunodeficiency virus)-1 pathogenesis.
resultsIn the present study, we have shown that the N-terminal fragment of Slit2 (Slit2N) (~120 kDa) inhibits replication of both CXCR4 and CCR5-tropic HIV-1 viruses in T-cell lines and peripheral blood T-cells. Furthermore, we demonstrated inhibition of HIV-1 infection in resting CD4+ T-cells. In addition, we showed that Slit2N blocks cell-to-cell transmission of HIV-1. We have shown that Slit2N inhibits HIV-1 infection by blocking viral entry into T-cells. We also ruled out Slit2N-mediated inhibition of various other steps in the life cycle including binding, integration and viral transcription. Elucidation of the molecular mechanism revealed that Slit2N mediates its functional effects by binding to Robo1 receptor. Furthermore, we found that Slit2N inhibited Gp120-induced Robo1-actin association suggesting that Slit2N may inhibit cytoskeletal rearrangements facilitating HIV-1 entry. Studies into the mechanism of inhibition of HIV-1 revealed that Slit2N abrogated HIV-1 envelope-induced actin cytoskeletal dynamics in both T-cell lines and primary T-cells. We further showed that Slit2N specifically attenuated the HIV-1 envelope-induced signaling pathway consisting of Rac1, LIMK and cofilin that regulates actin polymerization.
conclusionsTaken together, our results show that Slit2N inhibits HIV-1 replication through novel mechanisms involving modulation of cytoskeletal dynamics. Our study, thus, provides insights into the role of Slit2N in HIV-1 infection and underscores its potential in limiting viral replication in T-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.