TWEAK and Fn14: new molecular targets for cancer therapy?
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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-8The TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeuticsSolution 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 BindingRegulation 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.Functional 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 domainFn14•TRAIL effectively inhibits hepatocellular carcinoma growth.Expression of endoplasmic reticulum stress proteins is a candidate marker of brain metastasis in both ErbB-2+ and ErbB-2- primary breast tumorsFolic acid supplementary reduce the incidence of adenocarcinoma in a mouse model of colorectal cancer: microarray gene expression profileTherapeutic potential of the TWEAK/Fn14 pathway in intractable gastrointestinal cancer.Identification of aurintricarboxylic acid as a selective inhibitor of the TWEAK-Fn14 signaling pathway in glioblastoma cellsThe HER2- and heregulin β1 (HRG)-inducible TNFR superfamily member Fn14 promotes HRG-driven breast cancer cell migration, invasion, and MMP9 expression.The TWEAK-Fn14 cytokine-receptor axis: discovery, biology and therapeutic targetingNuclear Factor κB is Required for Tumor Growth Inhibition Mediated by Enavatuzumab (PDL192), a Humanized Monoclonal Antibody to TweakR.A further TWEAK to multiple sclerosis pathophysiology.Elevated expression of Fn14 in non-small cell lung cancer correlates with activated EGFR and promotes tumor cell migration and invasion.IAPs, TNF, inflammation and Jürg Tschopp; a personal perspective.Exploring in silico affinity of flavonoids and tannins to human fibroblast growth factorinducible14 (Fn14), a member of TNF receptor super family.Tnfrsf12a-Mediated Atherosclerosis Signaling and Inflammatory Response as a Common Protection Mechanism of Shuxuening Injection Against Both Myocardial and Cerebral Ischemia-Reperfusion Injuries.
P2860
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P2860
TWEAK and Fn14: new molecular targets for cancer therapy?
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2006 nî lūn-bûn
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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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2006年论文
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name
TWEAK and Fn14: new molecular targets for cancer therapy?
@ast
TWEAK and Fn14: new molecular targets for cancer therapy?
@en
type
label
TWEAK and Fn14: new molecular targets for cancer therapy?
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TWEAK and Fn14: new molecular targets for cancer therapy?
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prefLabel
TWEAK and Fn14: new molecular targets for cancer therapy?
@ast
TWEAK and Fn14: new molecular targets for cancer therapy?
@en
P2093
P1433
P1476
TWEAK and Fn14: new molecular targets for cancer therapy?
@en
P2093
Jeffrey A Winkles
Michael E Berens
Nhan L Tran
P356
10.1016/J.CANLET.2005.03.048
P407
P577
2006-04-01T00:00:00Z