ArticleProceedings of the National Academy of Sciences of the United States of America2011
Beta1 integrin cytoplasmic tyrosines promote skin tumorigenesis independent of their phosphorylation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Dynamic regulation of integrin β1 phosphorylation supports invasion of breast cancer cells.Nature cell biology · 2025Article
- The human retroviral-like aspartic protease 1 (ASPRV1): From in vitro studies to clinical correlations.The Journal of biological chemistry · 2024Review
- Ligand-independent integrin β1 signaling supports lung adenocarcinoma development.JCI insight · 2022Article
- New insights into the phosphorylation of the threonine motif of the β1 integrin cytoplasmic domain.Life science alliance · 2022Article
- The potential of functionalized dressing releasing flavonoids facilitates scar-free healing.Frontiers in medicine · 2022Review
- Roles of Integrins in Gastrointestinal Cancer Metastasis.Frontiers in molecular biosciences · 2021Review
- Rabgap1 promotes recycling of active β1 integrins to support effective cell migration.Journal of cell science · 2020Article
- Interplay between Cell-Surface Receptors and Extracellular Matrix in Skin.Biomolecules · 2020Review
- Accumulation of tissue factor in endothelial cells promotes cellular apoptosis through over-activation of Src1 and involves β1-integrin signalling.Apoptosis : an international journal on programmed cell death · 2020Article
- Integrin Signaling in Cancer: Mechanotransduction, Stemness, Epithelial Plasticity, and Therapeutic Resistance.Cancer cell · 2019Review
- Distinct expression profiles and functions of Kindlins in breast cancer.Journal of experimental & clinical cancer research : CR · 2018Article
- FAK auto-phosphorylation site tyrosine 397 is required for development but dispensable for normal skin homeostasis.PloS one · 2018Article
- Talin regulates integrin β1-dependent and -independent cell functions in ureteric bud development.Development (Cambridge, England) · 2017Article
- Myosin-1E interacts with FAK proline-rich region 1 to induce fibronectin-type matrix.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Review
- Tumor Cell Adhesion As a Risk Factor for Sentinel Lymph Node Metastasis in Primary Cutaneous Melanoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015Article
- Contributions of the integrin β1 tail to cell adhesive forces.Experimental cell research · 2015Article
- Kindler syndrome in mice and men.Cancer biology & therapy · 2014Article
- Integrin cytoplasmic tail interactions.Biochemistry · 2014Review
- β1 integrins with individually disrupted cytoplasmic NPxY motifs are embryonic lethal but partially active in the epidermis.The Journal of investigative dermatology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β1 integrin tyrosine phosphorylation by oncogenic kinases, such as Src, has been predicted to induce tumorigenesis by disrupting adhesion and modifying integrin signaling. We directly tested this hypothesis by subjecting mice with "nonphosphorylatable" tyrosine-to-phenylalanine substitutions in the conserved β1 cytoplasmic tail NPxY motifs to a model of cutaneous carcinogenesis in the presence or absence of elevated Src activity. We found that hydrophobic phenylalanine substitutions of both tyrosines diminished the binding of tail-interacting proteins, including talins and kindlins, resulting in reduced β1-mediated adhesion, focal adhesion kinase (FAK) signaling, and epidermal progenitor cell-derived skin tumors. However, increased Src activity drove tumor formation independent of the phenylalanine substitutions by enhancing FAK activity, which in turn maintained the epidermal progenitor state and blocked keratinocyte differentiation. We conclude that a Src/FAK signaling unit inhibits differentiation to promote tumorigenesis downstream of β1 integrin and independent of β1 integrin tyrosine phosphorylation.
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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.