ArticleThe Journal of cell biology2005
The Rac activator Tiam1 is required for (alpha)3(beta)1-mediated laminin-5 deposition, cell spreading, and cell migration.
Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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.
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Who cites it
50 citing papers in PubMed, 98 citations in OpenAlex.
- Full-Length Laminin-332 Promotes Integrin α3β1-Dependent Cutaneous Wound Closure in a Murine Model.Biomedicines · 2026Article
- Double-sided niche regulation in skin stem cell and cancer: mechanisms and clinical applications.Molecular cancer · 2025Review
- Keratinocyte Integrin α3β1 Promotes Efficient Healing of Wound Epidermis.JID innovations : skin science from molecules to population health · 2025Article
- The epidermal integrin-mediated secretome regulates the skin microenvironment during tumorigenesis and repair.Matrix biology : journal of the International Society for Matrix Biology · 2024Review
- Integrin mutations in blistering skin diseases and related genetically engineered mouse models.Human immunology · 2024Review
- Roles for epithelial integrin α3β1 in regulation of the microenvironment during normal and pathological tissue remodeling.American journal of physiology. Cell physiology · 2024Review
- Contribution of Endothelial Laminin-Binding Integrins to Cellular Processes Associated with Angiogenesis.Cells · 2022Article
- The Rac-GEF Tiam1 Promotes Dendrite and Synapse Stabilization of Dentate Granule Cells and Restricts Hippocampal-Dependent Memory Functions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- MicroRNA-200b/c-3p regulate epithelial plasticity and inhibit cutaneous wound healing by modulating TGF-β-mediated RAC1 signaling.Cell death & disease · 2020Article
- Epidermal activation of the small GTPase Rac1 in psoriasis pathogenesis.Small GTPases · 2019Review
- Intercellular adhesion molecule-1 augments myoblast adhesion and fusion through homophilic trans-interactions.Scientific reports · 2017Article
- Concerted regulation of retinal pigment epithelium basement membrane and barrier function by angiocrine factors.Nature communications · 2017Article
- Integrin-mediated regulation of epidermal wound functions.Cell and tissue research · 2016Review
- The rod domain is not essential for the function of plectin in maintaining tissue integrity.Molecular biology of the cell · 2015Article
- Rho GEFs and GAPs: emerging integrators of extracellular matrix signaling.Small GTPases · 2015Article
- Biological effects of RNAi targeted inhibiting Tiam1 gene expression on cholangiocarcinoma cells.International journal of clinical and experimental pathology · 2015Article
- The small GTPases RhoA and Rac1 regulate cerebellar development by controlling cell morphogenesis, migration and foliation.Developmental biology · 2014Article
- Focal Contact and Hemidesmosomal Proteins in Keratinocyte Migration and Wound Repair.Advances in wound care · 2014Review
- Integrin Regulation of Epidermal Functions in Wounds.Advances in wound care · 2014Review
- I'm coming to GEF you: Regulation of RhoGEFs during cell migration.Cell adhesion & migration · 2014Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Rho-like guanosine triphosphatase Rac1 regulates various signaling pathways, including integrin-mediated adhesion and migration of cells. However, the mechanisms by which integrins signal toward Rac are poorly understood. We show that the Rac-specific guanine nucleotide exchange factor Tiam1 (T-lymphoma invasion and metastasis 1) is required for the integrin-mediated laminin (LN)-5 deposition, spreading, and migration of keratinocytes. In contrast to wild-type keratinocytes, Tiam1-deficient (Tiam1-/-) keratinocytes are unable to adhere to and spread on a glass substrate because they are unable to deposit their own LN5 substrate. Both Tiam1 and V12Rac1 can rescue the defects of Tiam1-/- keratinocytes, indicating that these deficiencies are caused by impaired Tiam1-mediated Rac activation. Tiam1-/- cells are unable to activate Rac upon alpha3beta1-mediated adhesion to an exogenous LN5 substrate. Moreover, Tiam1 deficiency impairs keratinocyte migration in vitro and reepithelialization of excision wounds in mouse skin. Our studies indicate that Tiam1 is a key molecule in alpha3beta1-mediated activation of Rac, which is essential for proper production and secretion of LN5, a requirement for the spreading and migration of keratinocytes.
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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.