ArticlePloS one2015
Role of cortactin homolog HS1 in transendothelial migration of natural killer cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- The Role of the Cytoskeleton in Regulating the Natural Killer Cell Immune Response in Health and Disease: From Signaling Dynamics to Function.Frontiers in cell and developmental biology · 2021Review
- Understanding HCMV Latency Using Unbiased Proteomic Analyses.Pathogens (Basel, Switzerland) · 2020Review
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- Article
- Metas-Chip precisely identifies presence of micrometastasis in live biopsy samples by label free approach.Nature communications · 2017Article
- Wnt5a induces ROR1 to complex with HS1 to enhance migration of chronic lymphocytic leukemia cells.Leukemia · 2017Article
- The Arp2/3 complex binding protein HS1 is required for efficient dendritic cell random migration and force generation.Integrative biology : quantitative biosciences from nano to macro · 2017Article
- Bridging the gap: microfluidic devices for short and long distance cell-cell communication.Lab on a chip · 2017Review
- Article
- Endothelial monolayers and transendothelial migration depend on mechanical properties of the substrate.Cytoskeleton (Hoboken, N.J.) · 2014Article
- Article
- Septin and actin contributions to endothelial cell-cell junctions and monolayer integrity.Cytoskeleton (Hoboken, N.J.)Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Natural Killer (NK) cells perform many functions that depend on actin assembly, including adhesion, chemotaxis, lytic synapse assembly and cytolysis. HS1, the hematopoietic homolog of cortactin, binds to Arp2/3 complex and promotes actin assembly by helping to form and stabilize actin filament branches. We investigated the role of HS1 in transendothelial migration (TEM) by NK cells. Depletion of HS1 led to a decrease in the efficiency of TEM by NK cells, as measured by transwell assays with endothelial cell monolayers on porous filters. Transwell assays involve chemotaxis of NK cells across the filter, so to examine TEM more specifically, we imaged live-cell preparations and antibody-stained fixed preparations, with and without the chemoattractant SDF-1α. We found small to moderate effects of HS1 depletion on TEM, including whether the NK cells migrated via the transcellular or paracellular route. Expression of HS1 mutants indicated that phosphorylation of HS1 tyrosines at positions 222, 378 and 397 was required for rescue in the transwell assay, but HS1 mutations affecting interaction with Arp2/3 complex or SH3-domain ligands had no effect. The GEF Vav1, a ligand of HS1 phosphotyrosine, influenced NK cell transendothelial migration. HS1 and Vav1 also affected the speed of NK cells migrating across the surface of the endothelium. We conclude that HS1 has a role in transendothelial migration of NK cells and that HS1 tyrosine phosphorylation may signal through Vav1.
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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.