ArticleThe American journal of pathology2006
A keratinocyte hypermotility/growth-arrest response involving laminin 5 and p16INK4A activated in wound healing and senescence.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 71 citations in OpenAlex.
- Article
- Immortalization of patient-derived lip cells for establishing 3D lip models.Frontiers in cell and developmental biology · 2024Article
- Escape from Cellular Senescence Is Associated with Chromosomal Instability in Oral Pre-Malignancy.Biology · 2023Review
- Molecular Mechanisms of Malignant Transformation of Oral Submucous Fibrosis by Different Betel Quid Constituents-Does Fibroblast Senescence Play a Role?International journal of molecular sciences · 2022Review
- Impact of Aging on the Ovarian Extracellular Matrix and Derived 3D Scaffolds.Nanomaterials (Basel, Switzerland) · 2022Article
- The Balance between Differentiation and Terminal Differentiation Maintains Oral Epithelial Homeostasis.Cancers · 2021Review
- Expression of Laminin γ2 Proteolytic Fragments in Murine Skin Following Exposure to Sulfur Mustard.Anatomical record (Hoboken, N.J. : 2007) · 2020Article
- Understanding Transcriptional Networks Regulating Initiation of Cutaneous Wound Healing.The Yale journal of biology and medicine · 2020Review
- Human papillomavirus genotypes and p16 expression in oral leukoplakia and squamous cell carcinoma.International journal of clinical and experimental pathology · 2019Article
- Long-Term In Vitro Expansion of Epithelial Stem Cells Enabled by Pharmacological Inhibition of PAK1-ROCK-Myosin II and TGF-β Signaling.Cell reports · 2018Article
- Increased expression of p16 in both oral and genital lichen planus.Medicina oral, patologia oral y cirugia bucal · 2018Article
- Expression of Laminin 332 in Vesicant Skin Injury and Wound Repair.Clinical dermatology (Wilmington, Del.) · 2018Article
- Conserved genes and pathways in primary human fibroblast strains undergoing replicative and radiation induced senescence.Biological research · 2016Article
- Topical Administration of Acylated Homoserine Lactone Improves Epithelialization of Cutaneous Wounds in Hyperglycaemic Rats.PloS one · 2016Article
- Investigation of human embryonic stem cell-derived keratinocytes as an in vitro research model for mechanical stress dynamic response.Stem cell reviews and reports · 2015Article
- Focal Contact and Hemidesmosomal Proteins in Keratinocyte Migration and Wound Repair.Advances in wound care · 2014Review
- The molecular balancing act of p16(INK4a) in cancer and aging.Molecular cancer research : MCR · 2014Review
- Topical application of recombinant type VII collagen incorporates into the dermal-epidermal junction and promotes wound closure.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Article
- HPV16 E7 protein and hTERT proteins defective for telomere maintenance cooperate to immortalize human keratinocytes.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Keratinocytes become migratory to heal wounds, during early neoplastic invasion, and when undergoing telomere-unrelated senescence in culture. All three settings are associated with expression of the cell cycle inhibitor p16INK4A (p16) and of the basement membrane protein laminin 5 (LN5). We have investigated cause-and-effect relationships among laminin 5, p16, hypermotility, and growth arrest. Plating primary human keratinocytes on the gamma2 precursor form of laminin 5 (LN5') immediately induced directional hypermotility at approximately 125 microm/hour, followed by p16 expression and growth arrest. Cells deficient in p16 and either p14ARF or p53 became hypermotile in response to LN5' but did not arrest growth. Plating on LN5' triggered smad nuclear translocation, and all LN5' effects were blocked by a transforming growth factor (TGF) beta receptor I (TGFbetaRI) kinase inhibitor. In contrast, plating cells on collagen I triggered a TGFbetaRI kinase-independent hypermotility unaccompanied by smad translocation or growth arrest. Plating on control surfaces with TGFbeta induced hypermotility after a 1-day lag time and growth arrest by a p16-independent mechanism. Keratinocytes serially cultured with TGFbetaRI kinase inhibitor exhibited an extended lifespan, and immortalization was facilitated following transduction to express the catalytic subunit of telomerase (TERT). These results reveal fundamental features of a keratinocyte hyper-motility/growth-arrest response that is activated in wound healing, tumor suppression, and during serial culture.
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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.