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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Tumor necrosis factor receptor superfamily, member 12a

Fn14, TWEAK receptor, TweakR, Tnfrsf12a
human homolog is a receptor that binds TWEAK, a member of the TNF family, and is involved in cell proliferation, adhesion and angiogenesis [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: CAN, V1a, HAD, NF-kappaB, PrP
Papers using Fn14 antibodies
Quercetin accumulates in nuclear structures and triggers specific gene expression in epithelial cells.
Smalley Keiran, In PLoS ONE, 2010
... was used for the FN14 cell surface expression experiment, and FITC-conjugated mouse mAb (ITEM-4) anti-human FN14 from Santa Cruz Biotechnology (Covalab, Paris, France) and ...
TWEAK-FN14 signaling induces lysosomal degradation of a cIAP1–TRAF2 complex to sensitize tumor cells to TNFα
Silke John et al., In The Journal of Cell Biology, 2006
... Antibodies used in this study for flow cytometry were anti-FN14 (Abcam), Goat anti–mouse RPE (Millipore), ...
Papers on Fn14
Clinical Effect of Cardiac Shock Wave Therapy on Myocardial Ischemia in Patients With Ischemic Heart Failure.
Yuan et al., Shanghai, China. In J Cardiovasc Pharmacol Ther, Jan 2016
Furthermore, we demonstrated that CSWT resulted in a significant increase in the expression of promoters of neovascularization (vascular endothelial growth factor A [VEGF-A], VEGF-B, chemokine (C-X-C motif) ligand 1 [CXCL1], CXCL2, CXCL3 and TNFRSF12A) and a notable decrease in the expression of a mediator of cell apoptosis (mitogen-activated protein kinase 9).
FN14 and GRP94 expression are prognostic/predictive biomarkers of brain metastasis outcome that open up new therapeutic strategies.
Sierra et al., Barcelona, Spain. In Oncotarget, Nov 2015
GRP94 and FN14 are predictive biomarkers over-expressed in primary breast carcinomas that metastasized in brain.
The TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeutics.
Winkles et al., Baltimore, United States. In Oncogene, Sep 2015
UNASSIGNED: Fibroblast growth factor-inducible 14 (Fn14; TNFRSF12A) is the cell surface receptor for the tumor necrosis factor (TNF) family member TNF-like weak inducer of apoptosis (TWEAK).
TNF-like weak inducer of apoptosis promotes blood brain barrier disruption and increases neuronal cell death in MRL/lpr mice.
Putterman et al., United States. In J Autoimmun, Jun 2015
Furthermore, knockout (KO) of the TWEAK receptor, Fn14, in the MRL/lpr lupus mouse strain markedly attenuates neuropsychiatric disease, as demonstrated by significant reductions in depressive-like behavior and improved cognitive function.
A small molecule PAI-1 functional inhibitor attenuates neointimal hyperplasia and vascular smooth muscle cell survival by promoting PAI-1 cleavage.
Higgins et al., Albany, United States. In Cell Signal, May 2015
The mechanism through which cleaved PAI-1 (CL-PAI-1) stimulates apoptosis appears to involve the TNF-α family member TWEAK (TNF-α weak inducer of apoptosis) and it's cognate receptor, fibroblast growth factor (FGF)-inducible 14 (FN14).
Refeeding with glucose rather than fructose elicits greater hepatic inflammatory gene expression in mice.
Gonoi et al., Chiba, Japan. In Nutrition, May 2015
Refeeding with agar gel containing α-cornstarch or glucose increased the liver expression of Tlr2, proinflammatory genes (Cxcl2, Cxcl10, Cxcl1, Nfkb1, Nfkb2, RelB, Sectm1α, Il1β), stress response genes (Atf3, Asns, Gadd45 a, Perk, Inhbe), detoxification genes (Hmox1, Gsta1, Abca8b), genes involved in tissue regeneration (Gdf15, Krt23, Myc, Tnfrsf12a, Mthfd2), and genes involved in tumor suppression (p53, Txnrd1, Btg2).
Fn14 receptor promotes invasive potential and metastatic capacity of non-small lung adenocarcinoma cells through the up-regulation of integrin α6.
Watts et al., In Neoplasma, 2014
KEYWORDS: Fn14, TNFRSF12A, non-small cell lung cancer, H460 cells, motility, tumor formation and metastasis, integrin α6.
Comparison of cytokine expressions in acute myocardial infarction and stable angina stages of coronary artery disease.
Ding et al., Shanghai, China. In Int J Clin Exp Med, 2014
RESULTS: Compared with SA patients and the controls respectively, in AMI patients, IFNα2, IFNαR1, IFNαR2, IFNγR1, IFNγR2, L1β, IL16, IL18, Cxcl1, Cxcl2, Cxcl6, CxcR2, CxcR4, LIGHT, TNFR1, LT-βR, CD137, TRAILR, and TWEAKR mRNA expressions were significantly up-regulated (P<0.05), while Ccl5, Ccl24, Ccl28, CcR5, TWEAK, CD40, CD27, and BAFFR mRNA expressions were significantly down-regulated (P<0.05).
Transcriptomic and Functional Pathway Analysis of Human Cervical Carcinoma Cancer Cells Response to Microtubule Inhibitor.
Ma et al., Shanghai, China. In J Cancer, 2014
Northern blots also confirmed that KRT-7, FN14, IER3, and ID1 were deregulated in VBL-treated KB-3 cells.
The tumor necrosis factor superfamily members TWEAK, TNFSF15 and fibroblast growth factor-inducible protein 14 are upregulated in proliferative diabetic retinopathy.
Geboes et al., Riyadh, Saudi Arabia. In Ophthalmic Res, 2014
TWEAK activity is mediated via binding to fibroblast growth factor-inducible molecule 14 (Fn14).
TWEAK/Fn14 promotes the proliferation and collagen synthesis of rat cardiac fibroblasts via the NF-кB pathway.
Sui et al., Jinan, China. In Mol Biol Rep, 2012
TWEAK/Fn14 axis increased cell proliferation and collagen synthesis by activating the NF-small ka, CyrillicB pathway and increasing MMP-9 activity
The TWEAK/Fn14 pathway as an aggravating and perpetuating factor in inflammatory diseases: focus on inflammatory bowel diseases.
Burkly et al., Tokyo, Japan. In J Leukoc Biol, 2012
This review describes an emerging role of the TWEAK/Fn14 pathway in autoimmune and inflammatory diseases, with a particular focus on inflammatory bowel diseases.
Elevated expression of Fn14 in non-small cell lung cancer correlates with activated EGFR and promotes tumor cell migration and invasion.
Winkles et al., Phoenix, United States. In Am J Pathol, 2012
Elevated expression of Fn14 in non-small cell lung cancer correlates with activated EGFR and promotes tumor cell migration and invasion.
TWEAK and TRAF6 regulate skeletal muscle atrophy.
Paul et al., Louisville, United States. In Curr Opin Clin Nutr Metab Care, 2012
Adult skeletal muscles express minimal levels of Fn14, the bona fide TWEAK receptor.
The TWEAK-Fn14 system: breaking the silence of cytokine-induced skeletal muscle wasting.
Kumar et al., Louisville, United States. In Curr Mol Med, 2012
Adult skeletal muscle express very low to minimal levels of TWEAK receptor, Fn14.
The cytokine tumor necrosis factor-like weak inducer of apoptosis and its receptor fibroblast growth factor-inducible 14 have a neuroprotective effect in the central nervous system.
Yepes et al., Atlanta, United States. In J Neuroinflammation, 2011
Thie results of this study indicated that the interaction between TWEAK and Fn14 triggers the activation of a cell signaling pathway that results in the induction of tolerance to lethal hypoxia and ischemia.
Extracellular SH3 domain containing proteins--features of a new protein family.
Bosserhoff et al., Bochum, Germany. In Curr Protein Pept Sci, 2008
MIA was shown to interact with fibronectin, and MIA-interacting peptide ligands identified by phage display screening are similar to the consensus sequence of type III human fibronectin repeats, especially FN14.
Tumor necrosis factor family receptors regulating bone turnover: new observations in osteoblastic and osteoclastic cell lines.
Blair et al., Pittsburgh, United States. In Ann N Y Acad Sci, 2007
TNF receptors in osteoblasts and preosteoblasts include TNFR1 (p55), DR3 (TNFR25), DR5 (TRAIL-R2) and Fas, and possibly FN14 and DR4 (TRAIL-R1).
A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis.
Fanslow et al., Seattle, United States. In Immunity, 2001
We report cloning of a receptor for TWEAK (TweakR) from a human umbilical vein endothelial cell (HUVEC) library.
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