Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2000-11-3
pubmed:abstractText
The imprinted gene Peg3 encodes a zinc-finger protein which has been proposed to be involved in tumor necrosis factor alpha (TNF) signaling via an interaction with TNF receptor-associated factor 2 (TRAF2). Primary embryonic fibroblasts derived from mice with a null mutation in Peg3 showed no abnormalities in TNF-induced nuclear translocation of nuclear factor kappaB (NF-kappaB) or phosphorylation of the mitogen-activated protein kinases, extracellular signal-regulated kinases 1 and 2, c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38. In addition, the loss of Peg3 function did not increase the sensitivity of the cells to the cytotoxic action of TNF. These results suggest that Peg3 does not play an essential role in TNF signal transduction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0023-6837
pubmed:author
pubmed:issnType
Print
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1509-11
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
The imprinted gene Peg3 is not essential for tumor necrosis factor alpha signaling.
pubmed:affiliation
Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, United Kingdom. lizl@sanger.otago.ac.nz
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't