Linked Life Data

12485902

Source:http://linkedlifedata.com/resource/pubmed/id/12485902

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-12-17
pubmed:abstractText
Thalidomide has been shown to have both antiinflammatory and antiangiogenic effects in several diseases. However, its cellular target and mechanism of action are poorly understood. We investigated the action mechanism of thalidomide through the NFkappaB pathway. Thalidomide inhibited interleukin (IL) 1beta-induced NFkappaB transcriptional activation and IL-8 production in Caco-2 colon cancer cells. In addition, thalidomide suppressed NFkappaB nuclear translocation, IkappaB degradation, and NFkappaB-inducing kinase (NIK)-induced NFkappaB transcriptional activation. These results suggest that the molecular target of the effects of thalidomide may be IkappaB phosphorylation by IkappaB kinase (IKK), whose activation follows NIK activation and precedes IkappaB degradation in the NFkappaB pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
973
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
414-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Thalidomide suppresses the interleukin 1beta-induced NFkappaB signaling pathway in colon cancer cells.
pubmed:affiliation
Department of Internal Medicine and Institute of Gastroenterology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't