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Kindlins: essential regulators of integrin signalling and cell-matrix adhesion
Open accessAbstract
Integrin-mediated cell-ECM (extracellular matrix) adhesion is a fundamental process that controls cell behaviour. For correct cell-ECM adhesion, both the ligand-binding affinity and the spatial organization of integrins must be precisely controlled; how integrins are regulated, however, is not completely understood. Kindlins constitute a family of evolutionarily conserved cytoplasmic components of cell-ECM adhesions that bind to beta-integrin cytoplasmic tails directly and cooperate with talin in integrin activation. In addition, kindlins interact with many components of cell-ECM adhesions--such as migfilin and integrin-linked kinase--to promote cytoskeletal reorganization. Loss of kindlins causes severe defects in integrin signalling, cell-ECM adhesion and cytoskeletal organization, resulting in early embryonic lethality (kindlin-2), postnatal lethality (kindlin-3) and Kindler syndrome (kindlin-1). It is therefore clear that kindlins, together with several other integrin-proximal proteins, are essential for integrin signalling and cell-ECM adhesion regulation.
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“FERMT1 (also known as kindlin-1) directly binds the cytoplasmic tail of β1 integrin to enable signaling and mediate cell spreading and controls murine cutaneous stem cell homeostasis (Kloeker et al., 2004, Larjava et al., 2008, Rognoni et al., 2014).”
From Multimodal Analysis of Composition and Spatial Architecture in Human Squamous Cell Carcinoma (2020) · cites this paper as Larjava et al., 2008
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“FERMT1 (also known as kindlin-1) directly binds the cytoplasmic tail of β1 integrin to enable signaling and mediate cell spreading and controls murine cutaneous stem cell homeostasis (Kloeker et al., 2004, Larjava et al., 2008, Rognoni et al., 2014).”
From Multimodal Analysis of Composition and Spatial Architecture in Human Squamous Cell Carcinoma (2020) · cites this paper as Larjava et al., 2008
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“FERMT1 (also known as kindlin-1) directly binds the cytoplasmic tail of b1 integrin to enable signaling and mediate cell spreading and controls murine cutaneous stem cell homeostasis (Kloeker et al., 2004; Larjava et al., 2008; Rognoni et al., 2014).”
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Metadata
- Authors
- Larjava, H., Plow, E. F., & Wu, C.
- Affiliations
- University of British Columbia (CA)
- Cleveland Clinic (US)
- University of Pittsburgh (US)
- Venue
- The EMBO Reports
- Published
- 2008-11-07
- Volume
- 9
- Issue
- 12
- Pages
- 1203-1208
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC2603460
- OpenAlex
- W2159437476
- Cited by
- 268
- References
- 49
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 7 · 2023: 7 · 2022: 14 · 2021: 16 · 2020: 12 · 2019: 13 · 2018: 11 · 2017: 15 · 2016: 10 · 2015: 12 · 2014: 21 · 2013: 21 · 2012: 16
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- EMBO Reports (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (P01HL073311)
- National Institute of General Medical Sciences (GM 65188, R01GM065188)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK54639, R01DK054639)
- National Institute of Dental and Craniofacial Research (R01DE016099, DE016099)
- Topics
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Skin and Cellular Biology Research
- Keywords
- kindlin, integrin signaling, cell-matrix adhesion, talin, integrin activation, integrin-linked kinase, cytoskeletal organization, Kindler syndrome, kindlin-1, Kindlin-2, kindlin-3, embryonic lethality
- MeSH terms
- Animals, Carrier Proteins, Cell Adhesion, Disease, Humans, Signal Transduction, Integrins, Cell-Matrix Junctions
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