TWEAKing tissue remodeling by a multifunctional cytokine: role of TWEAK/Fn14 pathway in health and disease.
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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-8Structure of the extracellular domains of human and Xenopus Fn14: implications in the evolution of TWEAK and Fn14 interactionsBrd2 gene disruption causes "metabolically healthy" obesity: epigenetic and chromatin-based mechanisms that uncouple obesity from type 2 diabetesTWEAK and the progression of renal disease: clinical translationThe TWEAK-Fn14 pathway: a potent regulator of skeletal muscle biology in health and 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 BindingInflammation induced loss of skeletal muscleInteraction of TWEAK with Fn14 leads to the progression of fibrotic liver disease by directly modulating hepatic stellate cell proliferationTWEAK/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.Serum soluble TWEAK levels are decreased in treatment naive noncirrhotic chronic hepatitis B patients.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 degradationSkin-resident T cells sense ultraviolet radiation-induced injury and contribute to DNA repair.Immune and myodegenerative pathomechanisms in inclusion body myositisTWEAK appears as a modulator of endometrial IL-18 related cytotoxic activity of uterine natural killers.Serum sCD163 levels are associated with type 2 diabetes mellitus and are influenced by coffee and wine consumption: results of the Di@bet.es study.TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis.Full-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-kappaB pathwayThe expression of BAFF, APRIL and TWEAK is altered in eczema skin but not in the circulation of atopic and seborrheic eczema patientsRegulation 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.PGC1α plays a critical role in TWEAK-induced cardiac dysfunction.TWEAK-independent Fn14 self-association and NF-κB activation is mediated by the C-terminal region of the Fn14 cytoplasmic domainDevelopment of human serine protease-based therapeutics targeting Fn14 and identification of Fn14 as a new target overexpressed in TNBC.Structural basis and targeting of the interaction between fibroblast growth factor-inducible 14 and tumor necrosis factor-like weak inducer of apoptosisTWEAK-Fn14 as a mediator of acute kidney injury.TWEAK and Fn14 expression in the pathogenesis of joint inflammation and bone erosion in rheumatoid arthritis.The tumor necrosis factor superfamily of cytokines in the inflammatory myopathies: potential targets for therapy.Development of an Fn14 agonistic antibody as an anti-tumor agent.TWEAK/Fn14 Signaling Involvement in the Pathogenesis of Cutaneous Disease in the MRL/lpr Model of Spontaneous Lupus.Resistin: functional roles and therapeutic considerations for cardiovascular disease.Transcriptome signature of resistance exercise adaptations: mixed muscle and fiber type specific profiles in young and old adults.The fibroblast growth factor-inducible 14 receptor is highly expressed in HER2-positive breast tumors and regulates breast cancer cell invasive capacitySoluble TNF-Like Weak Inducer of Apoptosis as a New Marker in Preeclampsia: A Pilot Clinical Study.The TWEAK receptor Fn14 is a therapeutic target in melanoma: immunotoxins targeting Fn14 receptor for malignant melanoma treatmentNeuropsychiatric disease in murine lupus is dependent on the TWEAK/Fn14 pathway.Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Accelerates the Progression of Renal Fibrosis in Lupus Nephritis by Activating SMAD and p38 MAPK in TGF-β1 Signaling PathwayTWEAK-binding autoantibodies are generated during psoriatic arthritis and are not influenced by anti-TNF therapy
P2860
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P2860
TWEAKing tissue remodeling by a multifunctional cytokine: role of TWEAK/Fn14 pathway in health and disease.
description
2007 nî lūn-bûn
@nan
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
2007年论文
@zh
2007年论文
@zh-cn
name
TWEAKing tissue remodeling by ...... pathway in health and disease.
@en
type
label
TWEAKing tissue remodeling by ...... pathway in health and disease.
@en
prefLabel
TWEAKing tissue remodeling by ...... pathway in health and disease.
@en
P2093
P1433
P1476
TWEAKing tissue remodeling by ...... pathway in health and disease.
@en
P2093
Aniela Jakubowski
Jennifer S Michaelson
Kyungmin Hahm
Linda C Burkly
Timothy S Zheng
P356
10.1016/J.CYTO.2007.09.007
P577
2007-10-01T00:00:00Z