The Fn14 immediate-early response gene is induced during liver regeneration and highly expressed in both human and murine hepatocellular carcinomas
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TWEAK induces apoptosis through a death-signaling complex comprising receptor-interacting protein 1 (RIP1), Fas-associated death domain (FADD), and caspase-8TWEAK binding to the Fn14 cysteine-rich domain depends on charged residues located in both the A1 and D2 modulesTWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regenerationThe human Fn14 receptor gene is up-regulated in migrating glioma cells in vitro and overexpressed in advanced glial tumorsThe TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeuticsSoluble Fn14 Is Detected and Elevated in Mouse and Human Kidney DiseaseSolution structure of the cysteine-rich domain in Fn14, a member of the tumor necrosis factor receptor superfamilyCrystal Structure of Human TWEAK in Complex with the Fab Fragment of a Neutralizing Antibody Reveals Insights into Receptor BindingAdvances in anticancer immunotoxin therapyInteraction of TWEAK with Fn14 leads to the progression of fibrotic liver disease by directly modulating hepatic stellate cell proliferationFibroblast 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 myogenesisThe tumor necrosis factor-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling system regulates glioma cell survival via NFkappaB pathway activation and BCL-XL/BCL-W expressionA Bioinformatics Resource for TWEAK-Fn14 Signaling PathwayApoptosis-related genes change their expression with age and hearing loss in the mouse cochlea.A novel role for tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in the development of cardiac dysfunction and failure.TWEAK induces NF-kappaB2 p100 processing and long lasting NF-kappaB activation.Serum soluble TWEAK levels are decreased in treatment naive noncirrhotic chronic hepatitis B patients.Regulation of fibroblast growth factor-inducible 14 (Fn14) expression levels via ligand-independent lysosomal degradationFull-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-kappaB pathwayTWEAK induces liver progenitor cell proliferationDNA methyltransferase 3a and mitogen-activated protein kinase signaling regulate the expression of fibroblast growth factor-inducible 14 (Fn14) during denervation-induced skeletal muscle atrophy.Urinary biomarkers in lupus nephritis.Hedgehog signaling is critical for normal liver regeneration after partial hepatectomy in mice.Regulation of tumor necrosis factor-like weak inducer of apoptosis receptor protein (TWEAKR) expression by Kaposi's sarcoma-associated herpesvirus microRNA prevents TWEAK-induced apoptosis and inflammatory cytokine expression.Predictive gene signature of response to the anti-TweakR mAb PDL192 in patient-derived breast cancer xenograftsFunctional expression of TWEAK and the receptor Fn14 in human malignant ovarian tumors: possible implication for ovarian tumor intervention.TWEAK-independent Fn14 self-association and NF-κB activation is mediated by the C-terminal region of the Fn14 cytoplasmic domainStructural basis and targeting of the interaction between fibroblast growth factor-inducible 14 and tumor necrosis factor-like weak inducer of apoptosisFn14•TRAIL effectively inhibits hepatocellular carcinoma growth.A soluble Fn14-Fc decoy receptor reduces infarct volume in a murine model of cerebral ischemia.Role of Fn14 in acute alcoholic steatohepatitis in mice.TWEAK/Fn14 system and crescent formation in IgA nephropathy.Chronic activation of FXR in transgenic mice caused perinatal toxicity and sensitized mice to cholesterol toxicity.Development of an Fn14 agonistic antibody as an anti-tumor agent.Folic acid supplementary reduce the incidence of adenocarcinoma in a mouse model of colorectal cancer: microarray gene expression profileFn14 receptor promotes invasive potential and metastatic capacity of non-small lung adenocarcinoma cells through the up-regulation of integrin α6Fn14, a Downstream Target of the TGF-β Signaling Pathway, Regulates Fibroblast Activation.Therapeutic potential of the TWEAK/Fn14 pathway in intractable gastrointestinal cancer.Expression of TweakR in breast cancer and preclinical activity of enavatuzumab, a humanized anti-TweakR mAb.TWEAK and the central nervous system.
P2860
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P2860
The Fn14 immediate-early response gene is induced during liver regeneration and highly expressed in both human and murine hepatocellular carcinomas
description
2000 nî lūn-bûn
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2000 թուականի Ապրիլին հրատարակուած գիտական յօդուած
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2000 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2000年の論文
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2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
name
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@ast
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@en
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@nl
type
label
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@ast
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@en
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@nl
prefLabel
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@ast
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@en
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@nl
P2093
P2860
P3181
P1476
The Fn14 immediate-early respo ...... rine hepatocellular carcinomas
@en
P2093
J A Winkles
K A Peifley
S S Thorgeirsson
V M Factor
P2860
P304
P3181
P356
10.1016/S0002-9440(10)64996-6
P407
P577
2000-04-01T00:00:00Z