ArticleScience signaling2018
Crk adaptor proteins mediate actin-dependent T cell migration and mechanosensing induced by the integrin LFA-1.
Article in Science signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Mechanosensing by T cells promotes a tissue-resident memory transcriptional program.Nature immunology · 2026Article
- Integrin-mediated mechanotransduction in the tumor microenvironment: macrophage-centered signaling mechanisms and immune remodeling.Journal of translational medicine · 2026Review
- Piezo1 as a mechanical checkpoint in T cell immunotherapy for solid tumors.Frontiers in pharmacology · 2026Review
- Advances in ligand-based surface engineering strategies for fine-tuning T cell mechanotransduction toward efficient immunotherapy.Biophysical journal · 2025Review
- The scaffold protein CasL restrains membrane blebbing and promotes T cell migration.Journal of cell science · 2025Article
- Live imaging in zebrafish reveals tissue-specific strategies for amoeboid migration.Development (Cambridge, England) · 2025Article
- Focus on mechano-immunology: new direction in cancer treatment.International journal of surgery (London, England) · 2025Review
- Inhibition of Mac-1 allows human macrophages to migrate against the direction of shear flow on ICAM-1.Molecular biology of the cell · 2024Article
- Mechanical regulation of lymphocyte activation and function.Journal of cell science · 2024Review
- Evidence and therapeutic implications of biomechanically regulated immunosurveillance in cancer and other diseases.Nature nanotechnology · 2024Review
- Piezo1 mechanosensing regulates integrin-dependent chemotactic migration in human T cells.eLife · 2024Article
- Motility and tumor infiltration are key aspects of invariant natural killer T cell anti-tumor function.Nature communications · 2024Article
- Structural mapping of PEAK pseudokinase interactions identifies 14-3-3 as a molecular switch for PEAK3 signaling.Nature communications · 2023Article
- Tuning immunity through tissue mechanotransduction.Nature reviews. Immunology · 2023Review
- Cell adhesion molecules and immunotherapy in advanced non-small cell lung cancer: Current process and potential application.Frontiers in oncology · 2023Review
- Not all (cells) who wander are lost: Upstream migration as a pervasive mode of amoeboid cell motility.Frontiers in cell and developmental biology · 2023Review
- Separation of GVL from GVHD -location, location, location.Frontiers in immunology · 2023Review
- Keratocytes migrate against flow with a roly-poly-like mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The magnitude of LFA-1/ICAM-1 forces fine-tune TCR-triggered T cell activation.Science advances · 2022Article
- Cytotoxic T Lymphocyte Activation Signals Modulate Cytoskeletal Dynamics and Mechanical Force Generation.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
T cell entry into inflamed tissue involves firm adhesion, spreading, and migration of the T cells across endothelial barriers. These events depend on "outside-in" signals through which engaged integrins direct cytoskeletal reorganization. We investigated the molecular events that mediate this process and found that T cells from mice lacking expression of the adaptor protein Crk exhibited defects in phenotypes induced by the integrin lymphocyte function-associated antigen 1 (LFA-1), namely, actin polymerization, leading edge formation, and two-dimensional cell migration. Crk protein was an essential mediator of LFA-1 signaling-induced phosphorylation of the E3 ubiquitin ligase c-Cbl and its subsequent interaction with the phosphatidylinositol 3-kinase (PI3K) subunit p85, thus promoting PI3K activity and cytoskeletal remodeling. In addition, we found that Crk proteins were required for T cells to respond to changes in substrate stiffness, as measured by alterations in cell spreading and differential phosphorylation of the force-sensitive protein CasL. These findings identify Crk proteins as key intermediates coupling LFA-1 signals to actin remodeling and provide mechanistic insights into how T cells sense and respond to substrate stiffness.
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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.