ArticlePLoS biology2020
Structural basis of human full-length kindlin-3 homotrimer in an auto-inhibited state.
Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 32 citations in OpenAlex.
- Structural basis of kindlin-3 in leukocyte adhesion deficiency III.Journal of thrombosis and haemostasis : JTH · 2026Article
- Kindlin-3 sustains cytokine interleukin-2 signaling by linking its receptor to integrin LFA-1.The Journal of biological chemistry · 2026Article
- Kindlin Regulates Mechanosensitive Activation and Adhesion Assembly of Integrin beta6.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hydrophobicity-Driven Disruption Mechanism in Kindlin-3 Induced by Leukocyte Adhesion Deficiency Mutation.ACS omega · 2025Article
- Focal adhesion in the tumour metastasis: from molecular mechanisms to therapeutic targets.Biomarker research · 2025Review
- Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1.Cell communication and signaling : CCS · 2025Article
- Myosin light chain 6 (Myl6) interacts with kindlin-3 and is required to support integrin αJournal of thrombosis and haemostasis : JTH · 2024Article
- ConFERMing the role of talin in integrin activation and mechanosignaling.Journal of cell science · 2023Article
- Molecular basis for integrin adhesion receptor binding to p21-activated kinase 4 (PAK4).Communications biology · 2022Article
- The structural basis of β2 integrin intra-cellular multi-protein complexes.Biophysical reviews · 2022Review
- Review
- Genetic analysis suggests a surface of PAT-4 (ILK) that interacts with UNC-112 (kindlin).G3 (Bethesda, Md.) · 2022Article
- Review
- Bottom-up reconstitution of focal adhesion complexes.The FEBS journal · 2022Review
- Review
- Mechanism of integrin activation by talin and its cooperation with kindlin.Nature communications · 2022Article
- How integrin phosphorylations regulate cell adhesion and signaling.Trends in biochemical sciences · 2022Review
- Paxillin binding to the PH domain of kindlin-3 in platelets is required to support integrin αIIbβ3 outside-in signaling.Journal of thrombosis and haemostasis : JTH · 2021Article
- Review
- Kindlin3 regulates biophysical properties and mechanics of membrane to cortex attachment.Cellular and molecular life sciences : CMLS · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kindlin-1, -2, and -3 directly bind integrin β cytoplasmic tails to regulate integrin activation and signaling. Despite their functional significance and links to several diseases, structural information on full-length kindlin proteins remains unknown. Here, we report the crystal structure of human full-length kindlin-3, which reveals a novel homotrimer state. Unlike kindlin-3 monomer, which is the major population in insect and mammalian cell expression systems, kindlin-3 trimer does not bind integrin β cytoplasmic tail as the integrin-binding pocket in the F3 subdomain of 1 protomer is occluded by the pleckstrin homology (PH) domain of another protomer, suggesting that kindlin-3 is auto-inhibited upon trimer formation. This is also supported by functional assays in which kindlin-3 knockout K562 erythroleukemia cells reconstituted with the mutant kindlin-3 containing trimer-disrupting mutations exhibited an increase in integrin-mediated adhesion and spreading on fibronectin compared with those reconstituted with wild-type kindlin-3. Taken together, our findings reveal a novel mechanism of kindlin auto-inhibition that involves its homotrimer formation.
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.