ArticleScientific reports2016
C4.4A gene ablation is compatible with normal epidermal development and causes modest overt phenotypes.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Comprehensive analysis of exosome gene LYPD3 and prognosis/immune cell infiltration in lung cancer.Translational cancer research · 2024Article
- Review
- c-FOS drives reversible basal to squamous cell carcinoma transition.Cell reports · 2021Article
- Crystal Structures of Human C4.4A Reveal the Unique Association of Ly6/uPAR/α-neurotoxin Domain.International journal of biological sciences · 2020Article
- Evolution and Medical Significance of LU Domain-Containing Proteins.International journal of molecular sciences · 2019Review
- Did evolution create a flexible ligand-binding cavity in the urokinase receptor through deletion of a plesiotypic disulfide bond?The Journal of biological chemistry · 2019Article
- Origin and diversification of the plasminogen activation system among chordates.BMC evolutionary biology · 2019Article
- De novo synthesis of C4.4A in hepatocellular carcinoma promotes migration and invasion of tumor cells.Oncology reports · 2017Article
- Expression and crystallographic studies of the D1D2 domains of C4.4A, a homologous protein to the urokinase receptor.Acta crystallographica. Section F, Structural biology communications · 2017Article
- Expression of C4.4A in an In Vitro Human Tissue-Engineered Skin Model.BioMed research international · 2017Article
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C4.4A is a modular glycolipid-anchored Ly6/uPAR/α-neurotoxin multidomain protein that exhibits a prominent membrane-associated expression in stratified squamous epithelia. C4.4A is also expressed in various solid cancer lesions, where high expression levels often are correlated to poor prognosis. Circumstantial evidence suggests a role for C4.4A in cell adhesion, migration, and invasion, but a well-defined biological function is currently unknown. In the present study, we have generated and characterized the first C4.4A-deficient mouse line to gain insight into the functional significance of C4.4A in normal physiology and cancer progression. The unchallenged C4.4A-deficient mice were viable, fertile, born in a normal Mendelian distribution and, surprisingly, displayed normal development of squamous epithelia. The C4.4A-deficient mice were, nonetheless, significantly lighter than littermate controls predominantly due to differences in fat mass. Congenital C4.4A deficiency delayed migration of keratinocytes enclosing incisional skin wounds in male mice. In chemically induced bladder carcinomas, C4.4A deficiency attenuated the incidence of invasive lesions despite having no effect on total tumour burden. This new C4.4A-deficient mouse line provides a useful platform for future studies on functional aspects of C4.4A in tumour cell invasion in vivo.
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