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
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Pharmacology of manipulating lean body massThe TWEAK-Fn14 pathway: a potent regulator of skeletal muscle biology in health and diseaseCrystal Structure of Human TWEAK in Complex with the Fab Fragment of a Neutralizing Antibody Reveals Insights into Receptor BindingTumor necrosis factor-α regulates distinct molecular pathways and gene networks in cultured skeletal muscle cellsGenomic profiling of messenger RNAs and microRNAs reveals potential mechanisms of TWEAK-induced skeletal muscle wasting in miceTransforming growth factor-beta-activated kinase 1 is an essential regulator of myogenic differentiation.The TWEAK-Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice.Fibroblast growth factor inducible 14 as potential target in patients with alcoholic hepatitisDNA methyltransferase 3a and mitogen-activated protein kinase signaling regulate the expression of fibroblast growth factor-inducible 14 (Fn14) during denervation-induced skeletal muscle atrophy.TWEAK causes myotube atrophy through coordinated activation of ubiquitin-proteasome system, autophagy, and caspases.Tumor necrosis factor-alpha augments matrix metalloproteinase-9 production in skeletal muscle cells through the activation of transforming growth factor-beta-activated kinase 1 (TAK1)-dependent signaling pathwayGenetic ablation of TWEAK augments regeneration and post-injury growth of skeletal muscle in mice.Single muscle fiber gene expression with run taper.Effect of laser therapy on skeletal muscle repair process in diabetic rats.Modulating effect of low level-laser therapy on fibrosis in the repair process of the tibialis anterior muscle in rats.TWEAK-Fn14 pathway activation after exercise in human skeletal muscle: insights from two exercise modes and a time course investigation.The TWEAK-Fn14 system: breaking the silence of cytokine-induced skeletal muscle wasting.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.TNF-like weak inducer of apoptosis (TWEAK) activates proinflammatory signaling pathways and gene expression through the activation of TGF-beta-activated kinase 1The TWEAK-Fn14 cytokine-receptor axis: discovery, biology and therapeutic targetingHeightened muscle inflammation susceptibility may impair regenerative capacity in aging humansIncreased expression of atrogenes and TWEAK family members after severe burn injury in nonburned human skeletal muscle.Overexpression of MHC class I heavy chain protein in young skeletal muscle leads to severe myositis: implications for juvenile myositisProinflammatory cytokine tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) suppresses satellite cell self-renewal through inversely modulating Notch and NF-κB signaling pathways.TWEAK/Fn14 Axis: A Promising Target for the Treatment of Cardiovascular Diseases.TWEAK/Fn14 Signaling Axis Mediates Skeletal Muscle Atrophy and Metabolic Dysfunction.TNF-like weak inducer of apoptosis aggravates left ventricular dysfunction after myocardial infarction in miceExpression of tumor necrosis factor-like weak inducer of apoptosis and fibroblast growth factor-inducible 14 in patients with polymyositis and dermatomyositis.EPO-receptor is present in mouse C2C12 and human primary skeletal muscle cells but EPO does not influence myogenesisThrombospondin-4, tumour necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor Fn14: novel extracellular matrix modulating factors in cardiac remodelling.The TWEAK/Fn14 pathway as an aggravating and perpetuating factor in inflammatory diseases: focus on inflammatory bowel diseases.Role of TWEAK in lupus nephritis: a bench-to-bedside review.Signaling mechanisms in mammalian myoblast fusion.The TWEAK-Fn14 system as a potential drug target.Role of the TWEAK-Fn14-cIAP1-NF-κB Signaling Axis in the Regulation of Myogenesis and Muscle HomeostasisTWEAK and cIAP1 regulate myoblast fusion through the noncanonical NF-κB signaling pathway.Characterization of primary human skeletal muscle cells from multiple commercial sources.Tweak regulates astrogliosis, microgliosis and skeletal muscle atrophy in a mouse model of amyotrophic lateral sclerosis.Muscle Fn14 gene expression is associated with fat-free mass retention during energy deficit at high altitude
P2860
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P2860
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
description
2007 nî lūn-bûn
@nan
2007 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@ast
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@en
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@nl
type
label
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@ast
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@en
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@nl
prefLabel
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@ast
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@en
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@nl
P2093
P2860
P356
P1476
Fibroblast growth factor induc ...... ions of Fn14 during myogenesis
@en
P2093
Charu Dogra
Nia Wedhas
Susan L Hall
Thomas A Linkhart
P2860
P304
15000-15010
P356
10.1074/JBC.M608668200
P407
P50
P577
2007-03-22T00:00:00Z