TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration - Test2 - elhamkhani - TriplyDB

TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration

TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration

http://www.wikidata.org/entity/Q24670970

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C3orf58, a novel paracrine protein, stimulates cardiomyocyte cell-cycle progression through the PI3K-AKT-CDK7 pathway The TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeutics Pharmacology of manipulating lean body mass Historical perspectives on tumor necrosis factor and its superfamily: 25 years later, a golden journey TWEAK and the progression of renal disease: clinical translation The TWEAK-Fn14 pathway: a potent regulator of skeletal muscle biology in health and disease Crystal Structure of Human TWEAK in Complex with the Fab Fragment of a Neutralizing Antibody Reveals Insights into Receptor Binding Repair Injured Heart by Regulating Cardiac Regenerative Signals Interaction of TWEAK with Fn14 leads to the progression of fibrotic liver disease by directly modulating hepatic stellate cell proliferation Fibroblast growth factor inducible 14 (Fn14) is required for the expression of myogenic regulatory factors and differentiation of myoblasts into myotubes. Evidence for TWEAK-independent functions of Fn14 during myogenesis Regulatory circuitry of TWEAK-Fn14 system and PGC-1α in skeletal muscle atrophy program.A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway TWEAK Regulates Muscle Functions in a Mouse Model of RNA Toxicity.TWEAK/Fn14, a pathway and novel therapeutic target in myotonic dystrophy.A novel role for tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in the development of cardiac dysfunction and failure.TNF-like weak inducer of apoptosis (TWEAK) promotes beta cell neogenesis from pancreatic ductal epithelium in adult mice.Modulation of ozone-sensitive genes in alpha-tocopherol transfer protein null mice Fibroblast growth factor-inducible 14 (Fn14) is expressed in the lower genital tract and may play a role in amplifying inflammation during infection.Regulation of fibroblast growth factor-inducible 14 (Fn14) expression levels via ligand-independent lysosomal degradation The TWEAK-Fn14 dyad is involved in age-associated pathological changes in skeletal muscle The TWEAK-Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice.Immune and myodegenerative pathomechanisms in inclusion body myositis DNA methyltransferase 3a and mitogen-activated protein kinase signaling regulate the expression of fibroblast growth factor-inducible 14 (Fn14) during denervation-induced skeletal muscle atrophy.Hedgehog signaling is critical for normal liver regeneration after partial hepatectomy in mice.Genetic ablation of TWEAK augments regeneration and post-injury growth of skeletal muscle in mice.Single muscle fiber gene expression with run taper.Activation of stem cells in hepatic diseases.PGC1α plays a critical role in TWEAK-induced cardiac dysfunction.Tumor necrosis factor-like weak inducer of apoptosis or Fn14 deficiency reduce elastase perfusion-induced aortic abdominal aneurysm in mice.TWEAK-Fn14 pathway activation after exercise in human skeletal muscle: insights from two exercise modes and a time course investigation.Muscle inflammation susceptibility: a prognostic index of recovery potential after hip arthroplasty?Development of an Fn14 agonistic antibody as an anti-tumor agent.The TWEAK-Fn14 system: breaking the silence of cytokine-induced skeletal muscle wasting.Tweak induces proliferation in renal tubular epithelium: a role in uninephrectomy induced renal hyperplasia Trpc1 ion channel modulates phosphatidylinositol 3-kinase/Akt pathway during myoblast differentiation and muscle regeneration.Blocking TWEAK-Fn14 interaction inhibits hematopoietic stem cell transplantation-induced intestinal cell death and reduces GVHD.Transcriptome signature of resistance exercise adaptations: mixed muscle and fiber type specific profiles in young and old adults.TWEAK and TRAF6 regulate skeletal muscle atrophy.Therapeutic potential of the TWEAK/Fn14 pathway in intractable gastrointestinal cancer.The role of TWEAK/Fn14 signaling in the MPTP-model of Parkinson's disease.

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P2860

TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration

http://www.wikidata.org/entity/Q24670970

description

2006 nî lūn-bûn

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2006 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

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2006 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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SJ.EMBOJ.7601441

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The EMBO Journal

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TWEAK, via its receptor Fn14, ...... d skeletal muscle regeneration

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Beth Browning

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Christine A Kostek

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Hideo Yagita

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Jeffrey A Winkles

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Jennifer S Michaelson

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Linda C Burkly

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Mahasweta Girgenrath

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Martin L Scott

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Monica Wang

http://www.w3.org/2001/XMLSchema#string

Norm Allaire

http://www.w3.org/2001/XMLSchema#string

P2860

A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis

The Fn14 immediate-early response gene is induced during liver regeneration and highly expressed in both human and murine hepatocellular carcinomas

Expression profiling of cytokines and related genes in regenerating skeletal muscle after cardiotoxin injection: a role for osteopontin

Immortalization of mouse myogenic cells can occur without loss of p16INK4a, p19ARF, or p53 and is accelerated by inactivation of Bax

Diseased muscles that lack dystrophin or laminin-alpha2 have altered compositions and proliferation of mononuclear cell populations

Proinflammatory activity of TWEAK on human dermal fibroblasts and synoviocytes: blocking and enhancing effects of anti-TWEAK monoclonal antibodies

TWEAK induces angiogenesis and proliferation of endothelial cells

Dual role for TWEAK in angiogenic regulation

The TNF and TNF receptor superfamilies: integrating mammalian biology

Muscle satellite cells

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24

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25

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Pascal Schneider

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2006-11-23T00:00:00Z

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6672724

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17124496

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