Linked Life Data

10555784

Source:http://linkedlifedata.com/resource/pubmed/id/10555784

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1999-11-24
pubmed:abstractText
Rat pheochromocytoma (PC12) cells exhibit apoptotic cell death when deprived of serum and can be rescued by nerve growth factor (NGF). We characterized AP-1 DNA binding activity in PC12 cells after serum deprivation in the presence or absence of NGF or other neurotrophic agents. There was a decline in AP-1 DNA binding activity concomitant with apoptosis in PC12 cells after serum deprivation. Treatment of serum-deprived PC12 with NGF induced persistent AP-1 binding activity that was blocked by the Trk receptor inhibitor K252a. PC12 cells treated with dibutyryl cyclic AMP or insulin also displayed increased AP-1 DNA binding activity. While NGF somewhat increased c-Fos and c-Jun protein levels transiently, it had a more robust and persistent stimulatory effect on Jun B protein levels. AP-1 transcriptional activity increased after NGF, dibutyryl cAMP, or insulin treatment under serum free conditions. Curcumin, which inhibits AP-1 activity, blocked the NGF-mediated rescue. These results would suggest that the rescue of serum-deprived PC12 cells from apoptosis requires increasing endogenous levels of specific Fos/Jun components of AP-1.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0364-3190
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1431-41
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Prolonged activation of transcription factor AP-1 during NGF-mediated rescue from apoptotic cell death in PC12 cells.
pubmed:affiliation
Department of Human Biological Chemistry and Genetics, The University of Texas Medical Branch, Galveston 77555-0652, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.