Kindlin-1 controls Wnt and TGF-β availability to regulate cutaneous stem cell proliferation
Open accessAbstract
Kindlin-1 is an integrin tail binding protein that controls integrin activation. Mutations in the FERMT-1 gene, which encodes for Kindlin-1, lead to Kindler syndrome in man, which is characterized by skin blistering, premature skin aging and skin cancer of unknown etiology. Here we show that loss of Kindlin-1 in mouse keratinocytes recapitulates Kindler syndrome and also produces enlarged and hyperactive stem cell compartments, which lead to hyperthickened epidermis, ectopic hair follicle development and increased skin tumor susceptibility. Mechanistically, Kindlin-1 controls keratinocyte adhesion through β1-class integrins and proliferation and differentiation of cutaneous epithelial stem cells by promoting α(v)β(6) integrin-mediated transforming growth factor-β (TGF-β) activation and inhibiting Wnt-β-catenin signaling through integrin-independent regulation of Wnt ligand expression. Our findings assign Kindlin-1 the previously unknown and essential task of controlling cutaneous epithelial stem cell homeostasis by balancing TGF-β-mediated growth-inhibitory signals and Wnt-β-catenin-mediated growth-promoting signals.
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FERMT1 directly binds the cytoplasmic tail of β1 integrin to enable signaling and mediate cell spreading.
“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 Rognoni et al., 2014
The Introduction (page unavailable) says Kindlins bind β-integrin tails and promote integrin activation, and the Abstract reports that Kindlin-1 controls murine cutaneous stem-cell homeostasis. But the Results attribute the observed spreading defect specifically to αvβ6 integrin; they report normal spreading of Kindlin-1-deficient keratinocytes on fibronectin. These passages do not establish that direct binding to the β1 tail mediates cell spreading. (LLM, conf=0.85)
Experimental — accuracy not yet measuredFERMT1 controls murine cutaneous stem cell homeostasis.
“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 Rognoni et al., 2014
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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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- Authors
- Rognoni, E., Widmaier, M., Jakobson, M., Ruppert, R., Ussar, S., Katsougkri, D., Böttcher, R. T., Lai-Cheong, J. E., Rifkin, D. B., McGrath, J. A., & Fässler, R.
- Affiliations
- Max Planck Institute of Biochemistry (DE)
- NYU Langone Health (US)
- King's College London (GB)
- Corresponding author
- Fässler, Reinhard
- ORCID
- Venue
- Nature Medicine
- Published
- 2014-03-30
- Volume
- 20
- Issue
- 4
- Pages
- 350-359
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3982140
- OpenAlex
- W2076368781
- Cited by
- 140
- References
- 73
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 7 · 2023: 4 · 2022: 11 · 2021: 11 · 2020: 13 · 2019: 11 · 2018: 13 · 2017: 14 · 2016: 18 · 2015: 18 · 2014: 6
- FWCI
- 9.30
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- Max Planck Digital Library (submittedVersion, other-oa)
- Research Portal (King's College London) (submittedVersion)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion)
- Funders
- Wellcome Trust
- National Institute for Health and Care Research
- King's College London
- Max-Planck-Gesellschaft
- National Institutes of Health
- National Cancer Institute (R01CA034282, CA034282)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Skin and Cellular Biology Research
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Health Sciences › Medicine › Urology › Hair Growth and Disorders
- Keywords
- kindlin-1, Kindler syndrome, FERMT1, keratinocytes, stem cell proliferation, Wnt/β-catenin signaling, TGF-beta activation, integrin αvβ6, beta1 integrin, keratinocyte adhesion, epidermal hyperplasia, skin cancer predisposition, mouse model
- MeSH terms
- Animals, Antigens, Neoplasm, Blister, Carrier Proteins, Cell Adhesion, Disease Models, Animal, Epidermolysis Bullosa, Mice, Transgenic, Periodontal Diseases, Photosensitivity Disorders, Skin, Skin Neoplasms, Stem Cells, Signal Transduction, Keratinocytes, Integrins, Transforming Growth Factor beta, Hair Follicle, Integrin beta1, Cell Proliferation, Wnt Proteins, beta Catenin, Mice, Wnt Signaling Pathway
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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