Receptor-mediated phagocytosis by macrophages induces a calcium-dependent transient increase in c-fos transcription
|Published in||Oncogene. 1989, vol. 4, no. 2, p. 237-241|
|Abstract||The transcription of the c-fos gene and the level of c-fos mRNA in mouse peritoneal macrophages are rapidly, strongly and transiently increased after Fc- and C3b-mediated phagocytosis, but not after phagocytosis of latex particles. In order to induce both phagocytosis and a rise in c-fos mRNA, binding to receptors must be followed by mobilization of Ca++ from intracellular Induction of c-fos transcription in macrophages by other agents acting through different intracellular "messengers', i.e. phorbol esters (protein kinase C), cholera toxin (cAMP) and dexamethasone (glucocorticoid receptor) also depends on intracellular Ca++. In all these conditions, induction of c-fos transcription is inhibited by the calmodulin antagonist W7, suggesting a common Ca++-dependent pathway for c-fos gene activation in macrophages.|
|Keywords||Animals — Calcium/ physiology — Macrophages/ immunology — Mice — Mice, Inbred C3H — Phagocytosis — Proto-Oncogene Proteins/ genetics — Proto-Oncogene Proteins c-fos — RNA, Messenger/analysis — Receptors, Cell Surface/physiology — Tetradecanoylphorbol Acetate/pharmacology — Transcription, Genetic|
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|COLLART, Martine et al. Receptor-mediated phagocytosis by macrophages induces a calcium-dependent transient increase in c-fos transcription. In: Oncogene, 1989, vol. 4, n° 2, p. 237-241. https://archive-ouverte.unige.ch/unige:9158|