Essential roles for early growth response transcription factor Egr-1 in tissue fibrosis and wound healing. - Wikidata - awgldk - TriplyDB

Essential roles for early growth response transcription factor Egr-1 in tissue fibrosis and wound healing.

Essential roles for early growth response transcription factor Egr-1 in tissue fibrosis and wound healing.

http://www.wikidata.org/entity/Q37316485

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Transition from inflammation to proliferation: a critical step during wound healing Animal models of systemic sclerosis: their utility and limitations.Cyclic nucleotide phosphodiesterase 1A: a key regulator of cardiac fibroblast activation and extracellular matrix remodeling in the heart Time-dependent expression and distribution of Egr-1 during skeletal muscle wound healing in rats Live in vivo imaging of Egr-1 promoter activity during neonatal development, liver regeneration and wound healing The transcriptional cofactor nab2 is induced by tgf-Beta and suppresses fibroblast activation: physiological roles and impaired expression in scleroderma.Transcription factor EGR1 directs tendon differentiation and promotes tendon repair.Hepatic fibrosis is enhanced and accompanied by robust oval cell activation after chronic carbon tetrachloride administration to Egr-1-deficient mice Metabolic changes in skin caused by Scd1 deficiency: a focus on retinol metabolism.Gene expression analysis reveals inhibition of radiation-induced TGFβ-signaling by hyperbaric oxygen therapy in mouse salivary glands.Identification of cadherin 11 as a mediator of dermal fibrosis and possible role in systemic sclerosis.Nuclear factor (NF)-κB and its associated pathways are major molecular regulators of blood-induced joint damage in a murine model of hemophilia.The early growth response gene Egr2 (Alias Krox20) is a novel transcriptional target of transforming growth factor-β that is up-regulated in systemic sclerosis and mediates profibrotic responses.Early growth response transcription factors: key mediators of fibrosis and novel targets for anti-fibrotic therapy.Early growth response-2 expression in uterine leiomyoma cells: regulation and function FibronectinEDA promotes chronic cutaneous fibrosis through Toll-like receptor signaling.Early growth response factor-1 limits biliary fibrosis in a model of xenobiotic-induced cholestasis in mice.Osteopontin in systemic sclerosis and its role in dermal fibrosis Fibrosis in systemic sclerosis: common and unique pathobiology.Regulation of Matrix Remodeling by Peroxisome Proliferator-Activated Receptor-γ: A Novel Link Between Metabolism and Fibrogenesis.Early growth response genes signaling supports strong paracrine capability of mesenchymal stem cells.Toll-like receptor 4 signaling augments transforming growth factor-β responses: a novel mechanism for maintaining and amplifying fibrosis in scleroderma.Proteasomal inhibition after injury prevents fibrosis by modulating TGF-β(1) signalling.Increased Expression of EGR-1 in Diabetic Human Adipose Tissue-Derived Mesenchymal Stem Cells Reduces Their Wound Healing Capacity.Tenascin-C drives persistence of organ fibrosis.Elk-3 Contributes to the Progression of Liver Fibrosis by Regulating the Epithelial-Mesenchymal Transition.The systematic analysis of coding and long non-coding RNAs in the sub-chronic and chronic stages of spinal cord injury.Understanding fibrosis in systemic sclerosis: shifting paradigms, emerging opportunities.Egr-1: new conductor for the tissue repair orchestra directs harmony (regeneration) or cacophony (fibrosis).Fibrosis in systemic sclerosis: emerging concepts and implications for targeted therapy.Interstitial lung disease in connective tissue diseases: evolving concepts of pathogenesis and management.Fibroblast abnormalities in the pathogenesis of systemic sclerosis.Molecular basis of organ fibrosis: potential therapeutic approaches.Update on etiopathogenesis of systemic sclerosis.Transforming growth factor β--at the centre of systemic sclerosis.Systematic review of molecular mechanism of action of negative-pressure wound therapy.Functional characterization of SAMD9, a protein deficient in normophosphatemic familial tumoral calcinosis.Matrix remodeling in systemic sclerosis.Identification of Novel Fibrosis Modifiers by In Vivo siRNA Silencing.Factor VII deficiency impairs cutaneous wound healing in mice.

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Essential roles for early growth response transcription factor Egr-1 in tissue fibrosis and wound healing.

http://www.wikidata.org/entity/Q37316485

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scientific article published on 13 August 2009

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Essential roles for early grow ...... ue fibrosis and wound healing.

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Essential roles for early grow ...... ue fibrosis and wound healing.

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Essential roles for early grow ...... ue fibrosis and wound healing.

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Essential roles for early grow ...... ue fibrosis and wound healing.

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Essential roles for early grow ...... ue fibrosis and wound healing.

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Essential roles for early grow ...... ue fibrosis and wound healing.

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AJPATH.2009.090241

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The American Journal of Pathology

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Essential roles for early grow ...... sue fibrosis and wound healing

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Aisha Nair

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Denisa S Melichian

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John Varga

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Katherine Gruner

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Luke Barr

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Mauricio de la Garza

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Minghua Wu

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Shiva Shahrara

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Swati Bhattacharyya

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Thomas A Mustoe

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P2860

Sp1 and Smad proteins cooperate to mediate transforming growth factor-beta 1-induced alpha 2(I) collagen expression in human glomerular mesangial cells

Glial cell-line derived neurotrophic factor-dependent fusimotor neuron survival during development

Luteinizing hormone deficiency and female infertility in mice lacking the transcription factor NGFI-A (Egr-1)

Egr-1, a master switch coordinating upregulation of divergent gene families underlying ischemic stress

Following the molecular pathways toward an understanding of the pathogenesis of systemic sclerosis.

Non-Smad TGF-beta signals.

Proapoptotic Bid is required for pulmonary fibrosis

The transcriptional coactivator and acetyltransferase p300 in fibroblast biology and fibrosis.

Targeted disruption of TGF-beta/Smad3 signaling modulates skin fibrosis in a mouse model of scleroderma.

Systemic sclerosis: a prototypic multisystem fibrotic disorder.

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