A "traffic control" role for TGFbeta3: orchestrating dermal and epidermal cell motility during wound healing - Wikidata - thesis-toulmin - TriplyDB

A "traffic control" role for TGFbeta3: orchestrating dermal and epidermal cell motility during wound healing

A "traffic control" role for TGFbeta3: orchestrating dermal and epidermal cell motility during wound healing

http://www.wikidata.org/entity/Q24683724

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Keratinocyte-Secreted Heat Shock Protein-90alpha: Leading Wound Reepithelialization and Closure Extracellular Hsp90 (eHsp90) as the actual target in clinical trials: intentionally or unintentionally Cutaneous wound healing: recruiting developmental pathways for regeneration Keratinocyte Migration and a Hypothetical New Role for Extracellular Heat Shock Protein 90 Alpha in Orchestrating Skin Wound Healing Identification of the critical therapeutic entity in secreted Hsp90α that promotes wound healing in newly re-standardized healthy and diabetic pig models Calreticulin: non-endoplasmic reticulum functions in physiology and disease.Functional characterization and gene expression analysis of CD4+ CD25+ regulatory T cells generated in mice treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin.The effect of secretory factors of adipose-derived stem cells on human keratinocytes.Effects of physiological electric fields on migration of human dermal fibroblasts.Amniotic mesenchymal stem cells enhance wound healing in diabetic NOD/SCID mice through high angiogenic and engraftment capabilities.Target-seeking antifibrotic compound enhances wound healing and suppresses scar formation in mice.Transforming growth factor Beta 3 is required for excisional wound repair in vivo Biocompatibilities and biodegradation of poly(3-hydroxybutyrate-co-3-hydroxyvalerate)s produced by a model metabolic reaction-based system.Fibromodulin-deficiency alters temporospatial expression patterns of transforming growth factor-β ligands and receptors during adult mouse skin wound healing.A fragment of secreted Hsp90α carries properties that enable it to accelerate effectively both acute and diabetic wound healing in mice Secreted heat shock protein-90 (Hsp90) in wound healing and cancer.Photoactivated composite biomaterial for soft tissue restoration in rodents and in humans Calreticulin enhances porcine wound repair by diverse biological effects.Prevention and reduction of scarring in the skin by Transforming Growth Factor beta 3 (TGFbeta3): from laboratory discovery to clinical pharmaceutical.Avotermin: a novel antiscarring agent.Transforming growth factor-β3 (TGF-β3) knock-in ameliorates inflammation due to TGF-β1 deficiency while promoting glucose tolerance.Connexin43 carboxyl-terminal peptides reduce scar progenitor and promote regenerative healing following skin wounding.TGF-β3 modulates the inflammatory environment and reduces scar formation following vocal fold mucosal injury in rats.Proteoglycan signaling co-receptors: roles in cell adhesion, migration and invasion.Altered molecular mechanisms of diabetic foot ulcers.Combination of medical needling and non-cultured autologous skin cell transplantation (renovacell) for repigmentation of hypopigmented burn scars in children and young people β1 integrin signaling in asymmetric migration of keratinocytes under mechanical stretch in a co-cultured wound repair model.Transforming Growth Factor-β and Endoglin Signaling Orchestrate Wound Healing TGFβ: A player on multiple fronts in the tumor microenvironment.Multiple self-healing squamous epithelioma is caused by a disease-specific spectrum of mutations in TGFBR1.Expression of TGF-β3 in isolated fibroblasts from foreskin.The role of secreted heat shock protein-90 (Hsp90) in wound healing - how could it shape future therapeutics?Transforming growth factor alpha (TGFalpha)-stimulated secretion of HSP90alpha: using the receptor LRP-1/CD91 to promote human skin cell migration against a TGFbeta-rich environment during wound healing EGFR-mediated expression of aquaporin-3 is involved in human skin fibroblast migration.Increased survivin expression confers chemoresistance to tumor-associated endothelial cells.Delayed wound closure in fibromodulin-deficient mice is associated with increased TGF-β3 signaling.The anti-motility signaling mechanism of TGFβ3 that controls cell traffic during skin wound healing.Treatment of Ischemia-Reperfusion Injury of the Skin Flap Using Human Umbilical Cord Mesenchymal Stem Cells (hUC-MSCs) Transfected with "F-5" Gene Biological activity differences between TGF-β1 and TGF-β3 correlate with differences in the rigidity and arrangement of their component monomers.Extracellular heat shock protein-90alpha: linking hypoxia to skin cell motility and wound healing.

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A "traffic control" role for TGFbeta3: orchestrating dermal and epidermal cell motility during wound healing

http://www.wikidata.org/entity/Q24683724

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2006 nî lūn-bûn

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2006 թուականի Մարտին հրատարակուած գիտական յօդուած

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2006 թվականի մարտին հրատարակված գիտական հոդված

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2006年の論文

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A "traffic control" role for T ...... motility during wound healing

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A "traffic control" role for T ...... motility during wound healing

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A "traffic control" role for T ...... motility during wound healing

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Balaji Bandyopadhyay

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David T Woodley

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Jianhua Fan

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Mei Chen

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Shengxi Guan

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Wei Li

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Yong Li

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P2860

Endoglin is a component of the transforming growth factor-beta receptor system in human endothelial cells

Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death

Scar-free healing: from embryonic mechanisms to adult therapeutic intervention

Mechanisms of TGF-beta signaling from cell membrane to the nucleus

Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease

Smad-dependent and Smad-independent pathways in TGF-beta family signalling

Transforming growth factor-beta in human platelets. Identification of a major storage site, purification, and characterization

Abnormal lung development and cleft palate in mice lacking TGF-beta 3 indicates defects of epithelial-mesenchymal interaction

Signal transduction by members of the transforming growth factor-beta superfamily

Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response

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1093-105

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10.1083/JCB.200507111

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172

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16549496

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2063766

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