ArticleThe American journal of pathology2009
Kindlin-1 Is required for RhoGTPase-mediated lamellipodia formation in keratinocytes.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 82 citations in OpenAlex.
- Long-term cytokine exposure remodels the methylome and transcriptome of recessive dystrophic epidermolysis bullosa keratinocytes - a bioinformatic analysis.Frontiers in cell and developmental biology · 2026Article
- Paxillin and Kindlin: Research Progress and Biological Functions.Biomolecules · 2025Review
- FERMT1 suppression induces anti-tumor effects and reduces stemness in glioma cancer cells.Journal of cancer research and clinical oncology · 2024Article
- Kindlin-3 deficiency leads to impaired erythropoiesis and erythrocyte cytoskeleton.Blood advances · 2023Article
- Article
- Kindlin-1 drives early steps of breast cancer metastasis.Cancer communications (London, England) · 2022Article
- Kindlin1 As a Gender and Location-Specific Diagnostic Marker in Gastric Cancer Patients.Iranian journal of pathology · 2022Article
- Migfilin: Cell Adhesion Effect and Comorbidities.OncoTargets and therapy · 2022Review
- Pathogenetic Therapy of Epidermolysis Bullosa: Current State and Prospects.Bulletin of experimental biology and medicine · 2021Review
- A novel frameshift mutation in theExperimental and therapeutic medicine · 2020Article
- Assessment of the risk and characterization of non-melanoma skin cancer in Kindler syndrome: study of a series of 91 patients.Orphanet journal of rare diseases · 2019Article
- Distinct expression profiles and functions of Kindlins in breast cancer.Journal of experimental & clinical cancer research : CR · 2018Article
- Kindlin-1 Regulates Keratinocyte Electrotaxis.The Journal of investigative dermatology · 2016Article
- A Deep-Intronic FERMT1 Mutation Causes Kindler Syndrome: An Explanation for Genetically Unsolved Cases.The Journal of investigative dermatology · 2015Article
- Expression of Kindlin-1 in human hepatocellular carcinoma and its prognostic significance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- The Kindler syndrome: a spectrum of FERMT1 mutations in Iranian families.The Journal of investigative dermatology · 2015Article
- The role of alpha-actinin-4 in human kidney disease.Cell & bioscience · 2015Article
- Oxidative stress and mitochondrial dysfunction in Kindler syndrome.Orphanet journal of rare diseases · 2014Article
- Kindlin-1 controls Wnt and TGF-β availability to regulate cutaneous stem cell proliferation.Nature medicine · 2014Article
- Integrin cytoplasmic tail interactions.Biochemistry · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kindlin-1 is an epithelial-specific member of the novel kindlin protein family, which are regulators of integrin functions. Mutations in the gene that encodes Kindlin-1, FERMT1 (KIND1), cause the Kindler syndrome (KS), a human disorder characterized by mucocutaneous fragility, progressive skin atrophy, ulcerative colitis, photosensitivity, and propensity to skin cancer. Our previous studies indicated that loss of kindlin-1 resulted in abnormalities associated with integrin functions, such as adhesion, proliferation, polarization, and motility of epidermal cells. Here, we disclosed novel FERMT1 mutations in KS and used them, in combination with small-interfering RNA, protein, and imaging studies, to uncover new functions for kindlin-1 in keratinocytes and to discern the molecular pathology of KS. We show that kindlin-1 forms molecular complexes with beta1 integrin, alpha-actinin, migfilin, and focal adhesion kinase and regulates cell shape and migration by controlling lamellipodia formation. Kindlin-1 governs these processes by signaling via Rho family GTPases, and it is required to maintain the pool of GTP-bound, active Rac1, RhoA and Cdc42, and the phosphorylation of their downstream effectors p21-activated kinase 1, LIM kinase, and cofilin. Loss of these kindlin-1 functions forms the biological basis for the epithelial cell fragility and atrophy in the pathology of KS.
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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.