Platelet-activating factor stimulates a fos/jun/AP-1 transcriptional signaling system in human neuroblastoma cells.
Platelet-activating factor (PAF) elicits a rapid and transient activation of the proto-oncogenes c-fos and c-jun in SH-SY5Y neuroblastoma cells, but only to a minor extent in Molt-4 T-lymphocytes. This effect is inhibited by pretreatment of cells with the PAF antagonist BN 52021, suggesting the involvement of a specific receptor. Moreover, PAF treatment can activate gene expression through an AP-1 element, and we propose that genomic trans-activation may occur in target genes containing a functional AP-1 transcription sequence. These results may further understanding of the molecular mechanisms by which PAF contributes to long-term phenotypic changes in the nervous system.
Squinto
S P
SP
Department of Biochemistry, Louisiana State University Medical School, New Orleans.
Block
A L
AL
Braquet
P
P
Bazan
N G
NG
D004268:DNA-Binding Proteins / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D009447:Neuroblastoma; D010972:Platelet Activating Factor / Q000494:pharmacology*; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D014157:Transcription Factors / Q000235:genetics*; D014407:Tumor Cells, Cultured / Q000187:drug effects / Q000378:metabolism*
D004268:DNA-Binding Proteins; D010972:Platelet Activating Factor; D011518:Proto-Oncogene Proteins; D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D014157:Transcription Factors