Linked Life Data

15322249

Source:http://linkedlifedata.com/resource/pubmed/id/15322249

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-8-23
pubmed:abstractText
Tumor necrosis factor (TNF) receptor 1-associated death domain protein (TRADD) is an adaptor protein known to be involved in the TNF signaling pathway as well as signaling of other members of the TNF receptor superfamily, including DR3, DR6, p75(NTR), and the Epstein-Barr virus latent membrane protein 1. Current knowledge of the function of the adaptor protein has been derived from studies examining its over-expression in either wild-type or mutated forms. In this study, we analyzed the consequences of antisense oligonucleotide (ASO)-mediated depletion of endogenous TRADD on TNF induction of inflammation-related gene products, such as intercellular adhesion molecule-1, and associated kinase signaling pathways in human umbilical vein endothelial cells. A broader perspective of TRADD's role in TNF signaling was indicated by microarray gene expression analysis, where 20 of 24 genes that showed a 5-fold or greater increase in TNF-induced mRNA expression levels displayed a reduction in TNF-induced expression as a consequence of ASO-mediated knockdown of TRADD. Reduced activation of the nuclear factor-kappaB and c-Jun NH(2)-terminal kinase pathways, as measured by IkappaB-alpha protein levels and the extent of c-Jun phosphorylation, was also observed. These results indicate usage of antisense inhibitors of TRADD expression for modulating diseases associated with TRADD-dependent signal transduction pathways.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0026-895X
pubmed:author
pubmed:issnType
Print
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
572-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15322249-Cells, Cultured, pubmed-meshheading:15322249-Dose-Response Relationship, Drug, pubmed-meshheading:15322249-Drug Interactions, pubmed-meshheading:15322249-Endothelium, Vascular, pubmed-meshheading:15322249-Gene Expression, pubmed-meshheading:15322249-Humans, pubmed-meshheading:15322249-Intercellular Adhesion Molecule-1, pubmed-meshheading:15322249-JNK Mitogen-Activated Protein Kinases, pubmed-meshheading:15322249-Mitogen-Activated Protein Kinases, pubmed-meshheading:15322249-NF-kappa B, pubmed-meshheading:15322249-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:15322249-Oligonucleotides, Antisense, pubmed-meshheading:15322249-Proteins, pubmed-meshheading:15322249-Receptors, Tumor Necrosis Factor, pubmed-meshheading:15322249-TNF Receptor-Associated Factor 1, pubmed-meshheading:15322249-Tumor Necrosis Factor-alpha
pubmed:year
2004
pubmed:articleTitle
Effects of antisense oligonucleotide-mediated depletion of tumor necrosis factor (TNF) receptor 1-associated death domain protein on TNF-induced gene expression.
pubmed:affiliation
Isis Pharmaceuticals, Inc., 2292 Faraday Avenue, Carlsbad, CA 92008, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.