ArticleNature medicine2009
Kindlin-3 is required for beta2 integrin-mediated leukocyte adhesion to endothelial cells.
Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers.
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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
219 citing papers in PubMed, 358 citations in OpenAlex.
- Peripheral blood mononuclear cell proteome changes in patients with myelodysplastic syndrome.BioMed research international · 2015Trial
- Trial
- Regulation of cell adhesion and migration by Kindlin-3 cleavage by calpain.The Journal of biological chemistry · 2012Trial
- CRISPR/Cas9-mediated loss of FERMT3 reveals kindlin-3-independent neutrophil activity in LAD-III.Journal of human immunity · 2026Article
- Beyond Integrin Activation: Kindlin-3 as an Organiser of Immune Receptor Signalling.International journal of molecular sciences · 2026Review
- Plasticity of the infant immune system during the perinatal period.Nature reviews. Immunology · 2026Review
- Structural basis of kindlin-3 in leukocyte adhesion deficiency III.Journal of thrombosis and haemostasis : JTH · 2026Article
- Kindlins in the cardiovascular system: from development to pathogenesis.Frontiers in cardiovascular medicine · 2026Review
- Biomarkers for predicting immunotherapy response and resistance in glioblastoma.Frontiers in immunology · 2026Review
- The cytoskeletal control of B cell receptor and integrin signaling in normal B cells and chronic lymphocytic leukemia.FEBS letters · 2025Review
- Kindlin-3 phosphorylation is crucial for thrombosis and hemostasisResearch and practice in thrombosis and haemostasis · 2025Article
- Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1.Cell communication and signaling : CCS · 2025Article
- β2-integrins as biomarkers in urothelial cancer.PloS one · 2025Article
- Regulation of actin cytoskeletal dynamics in T cell development and function.Frontiers in immunology · 2025Review
- Neutrophil diversity and function in health and disease.Signal transduction and targeted therapy · 2024Review
- Myosin light chain 6 (Myl6) interacts with kindlin-3 and is required to support integrin αJournal of thrombosis and haemostasis : JTH · 2024Article
- Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024Review
- SKAP2 acts downstream of CD11b/CD18 and regulates neutrophil effector function.Frontiers in immunology · 2024Article
- A myristoylated alanine-rich C-kinase substrate (MARCKS) inhibitor peptide attenuates neutrophil outside-in βCell adhesion & migration · 2023Article
- Distinct bidirectional regulation of LFA1 and α4β7 by Rap1 and integrin adaptors in T cells under shear flow.Cell reports · 2023Article
159 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Integrin activation is essential for the function of all blood cells, including platelets and leukocytes. The blood cell-specific FERM domain protein Kindlin-3 is required for the activation of the beta1 and beta3 integrins on platelets. Impaired activation of beta1, beta2 and beta3 integrins on platelets and leukocytes is the hallmark of a rare autosomal recessive leukocyte adhesion deficiency syndrome in humans called LAD-III, characterized by severe bleeding and impaired adhesion of leukocytes to inflamed endothelia. Here we show that Kindlin-3 also binds the beta2 integrin cytoplasmic domain and is essential for neutrophil binding and spreading on beta2 integrin-dependent ligands such as intercellular adhesion molecule-1 and the complement C3 activation product iC3b. Moreover, loss of Kindlin-3 expression abolished firm adhesion and arrest of neutrophils on activated endothelial cells in vitro and in vivo, whereas selectin-mediated rolling was unaffected. Thus, Kindlin-3 is essential to activate the beta1, beta2 and beta3 integrin classes, and loss of Kindlin-3 function is sufficient to cause a LAD-III-like phenotype in mice.
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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.