About: TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity

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About: TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity Goto Sponge NotDistinct Permalink

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scientific article published on 20 February 2003

Attributes	Values
rdf:type	Item
description	wetenschappelijk artikel (nl) наукова стаття, опублікована в лютому 2003 (uk) article scientifique publié en 2003 (fr) im Februar 2003 veröffentlichter wissenschaftlicher Artikel (de) artículu científicu espublizáu en febreru de 2003 (ast) scientific article published on 20 February 2003 (en)
publication date	wds:Q73075512-B89895C8-1781-446A-936F-BCC75D8DB666
publication date	2003-02-20 00:00:00Z (xsd:dateTime)
author name string	wds:Q73075512-10CB8D2E-3EFD-45CF-812E-26B7A34DBE93 wds:Q73075512-257F19BE-3C2A-4468-8A76-F0A28BC9E9A7 wds:Q73075512-8C49F41C-D404-4544-8EA6-FC99DCCEDB24 wds:Q73075512-CA50CBFA-7476-4C72-B146-4E52B9849043 wds:Q73075512-CE19B12F-FE14-406D-A68F-1D9D5EEE8431 wds:Q73075512-D683332F-1E19-4A37-8011-A75E25851DEA wds:Q73075512-E16B7231-C3ED-44E2-AE1B-A8302A07A184 wds:Q73075512-F1C05E1A-D989-44F6-B426-7B7591980877
author name string	Jeffrey A Winkles Shobha Thangada Sharron A N Brown Mark S Williams Heather N Hanscom John Buschman Christine M Richards Patrick J Donohue
rdfs:label	TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity (en) TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity (nl)
skos:prefLabel	TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity (en) TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity (nl)
name	TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity (en) TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity (nl)
author	wds:Q73075512-91A447C5-8C4C-4615-A3A1-2FB57432A2EF
author	Timothy Hla
title	wds:Q73075512-946DA7E6-6D7D-45E2-A19A-0A3ABBAE3CC2
title	TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity (en)
page(s)	wds:Q73075512-94766DB9-A720-4861-B495-A0EF49EF1D6F
page(s)	594-600
instance of	wds:Q73075512-7E762BE5-388C-438F-AADE-1A104DA7AE93
instance of	scholarly article
main subject	wds:Q73075512-E7603E4A-4F33-44E7-A1C7-262CB2845BF1
main subject	chemotaxis
PubMed ID	wds:Q73075512-2D0FC25A-8407-4687-8ED9-6A19E569D6DC
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/12615668
PubMed ID	12615668
published in	wds:Q73075512-31B0FBFE-3B0E-4A63-A481-888C6034CE5A
published in	Arteriosclerosis, Thrombosis, and Vascular Biology
issue	wds:Q73075512-B522F00F-5A1F-4276-829F-C83C4FF830D1
volume	wds:Q73075512-41C6C3ED-6D86-4651-9F65-2457250836A0
issue	4
volume	23
DOI	wds:Q73075512-C50789F7-52B4-46CC-B33D-56352024FCE8
DOI	http://dx.doi.org/10.1161/01.ATV.0000062883.93715.37
DOI	10.1161/01.ATV.0000062883.93715.37
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q73075512
is cites work of	Tumor necrosis factor-like weak inducer of apoptosis increases the permeability of the neurovascular unit through nuclear factor-kappa B pathway activation. Fibroblast growth factor-inducible-14 is induced in axotomized neurons and promotes neurite outgrowth Gene expression profiles of the NCI-60 human tumor cell lines define molecular interaction networks governing cell migration processes TWEAK binding to the Fn14 cysteine-rich domain depends on charged residues located in both the A1 and D2 modules Full-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-kappaB pathway The interaction between tumor necrosis factor-like weak inducer of apoptosis and its receptor fibroblast growth factor-inducible 14 promotes the recruitment of neutrophils into the ischemic brain Development of an Fn14 agonistic antibody as an anti-tumor agent Tweak induces proliferation in renal tubular epithelium: a role in uninephrectomy induced renal hyperplasia Inhibition of the TWEAK/Fn14 pathway attenuates renal disease in nephrotoxic serum nephritis The TWEAK-Fn14 cytokine-receptor axis: discovery, biology and therapeutic targeting TWEAK, a multifunctional cytokine in kidney injury Direct targeting of fibroblast growth factor-inducible 14 protein protects against renal ischemia reperfusion injury Adhesion to substrates induces dendritic cell endothelization and decreases immunological response. 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 TWEAK-independent Fn14 self-association and NF-κB activation is mediated by the C-terminal region of the Fn14 cytoplasmic domain Tumour necrosis factor-like weak inducer of apoptosis (TWEAK), an important mediator of endothelial inflammation, is associated with the pathogenesis of Henoch-Schonlein purpura The inflammatory response in stroke The Role of the Neuroprotective Factor Npas4 in Cerebral Ischemia A soluble Fn14-Fc decoy receptor reduces infarct volume in a murine model of cerebral ischemia Role of TWEAK in lupus nephritis: a bench-to-bedside review Tumor stroma: a complexity dictated by the hypoxic tumor microenvironment. Tumor necrosis factor-like weak inducer of apoptosis and fibroblast growth factor-inducible 14 mediate cerebral ischemia-induced poly(ADP-ribose) polymerase-1 activation and neuronal death TWEAK-Fn14 pathway inhibition protects the integrity of the neurovascular unit during cerebral ischemia. The interplay between surfaces and soluble factors define the immunologic and angiogenic properties of myeloid dendritic cells. Biomarkers in cardiovascular medicine Apelin, the ligand for the endothelial G-protein-coupled receptor, APJ, is a potent angiogenic factor required for normal vascular development of the frog embryo Tumor necrosis factor-like weak inducer of apoptosis and its potential roles in lupus nephritis Blocking TWEAK-Fn14 interaction inhibits hematopoietic stem cell transplantation-induced intestinal cell death and reduces GVHD. Soluble TWEAK plasma levels as a novel biomarker of endothelial function in patients with chronic kidney disease TWEAK/Fn14 Axis-Targeted Therapeutics: Moving Basic Science Discoveries to the Clinic The human Fn14 receptor gene is up-regulated in migrating glioma cells in vitro and overexpressed in advanced glial tumors Predictive gene signature of response to the anti-TweakR mAb PDL192 in patient-derived breast cancer xenografts Tumor necrosis factor-like weak inducer of apoptosis stimulation of glioma cell survival is dependent on Akt2 function TWEAK and Fn14 in the Neurovascular Unit TWEAK-Fn14 Cytokine-Receptor Axis: A New Player of Myocardial Remodeling and Cardiac Failure TWEAK affects keratinocyte G2/M growth arrest and induces apoptosis through the translocation of the AIF protein to the nucleus TWEAK/Fn14 Axis: A Promising Target for the Treatment of Cardiovascular Diseases. Inflammatory responses in brain ischemia Concerted action of Nrf2-ARE pathway, MRN complex, HMGB1 and inflammatory cytokines - implication in modification of radiation damage In situ formation of poly(vinyl alcohol)-heparin hydrogels for mild encapsulation and prolonged release of basic fibroblast growth factor and vascular endothelial growth factor Innate inflammatory responses in stroke: mechanisms and potential therapeutic targets TWEAK and Fn14 expression in the pathogenesis of joint inflammation and bone erosion in rheumatoid arthritis. Population pharmacokinetic and pharmacodynamic analysis of BIIB023, an anti-TNF-like weak inducer of apoptosis (anti-TWEAK) monoclonal antibody TWEAK/Fn14 pathway modulates properties of a human microvascular endothelial cell model of blood brain barrier The TWEAK-Fn14 system as a potential drug target TWEAK/Fn14 pathway is a novel mediator of retinal neovascularization

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