Involvement of common and cell type-specific pathways in c-fos gene control: stable induction of cAMP in macrophages.
The c-fos proto-oncogene is rapidly and transiently induced by PDGF in fibroblast and by CSF-1 in macrophages. In both cells, the breakdown of phospholipids with the ensuing activation of protein kinase C (PKC) and intracellular release of Ca2+ seems to play a role in the induction of c-fos. The transient induction of c-fos mRNA and protein by PDGF is both increased and prolonged by inhibitors of calmodulin, apparently by inhibiting the degradation of c-fos mRNA. While no response to cyclic nucleotides is observed in fibroblasts, cAMP is a strong inducer of c-fos in macrophages. In contrast to the transient induction by PKC/Ca2+, cAMP induces stable transcription of the c-fos gene for many hours, suggesting the existence of different mechanisms regulating c-fos transcription in the same cell.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002460:Cell Line; D000242:Cyclic AMP / Q000494:pharmacology*; D004789:Enzyme Activation; D005786:Gene Expression Regulation; D008264:Macrophages / Q000378:metabolism*; D051379:Mice; D010743:Phospholipids / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016760:Proto-Oncogene Proteins c-fos; D011519:Proto-Oncogenes; D012333:RNA, Messenger / Q000235:genetics; D013449:Sulfonamides / Q000494:pharmacology; D014158:Transcription, Genetic / Q000187:drug effects; D014268:Trifluoperazine / Q000494:pharmacology
D010743:Phospholipids; D011518:Proto-Oncogene Proteins; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; D013449:Sulfonamides; D014268:Trifluoperazine; C017967:W 7; D000242:Cyclic AMP; D011493:Protein Kinase C; D002118:Calcium