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Receptor-mediated phagocytosis by macrophages induces a calcium-dependent transient increase in c-fos transcription.
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.
Animals, Calcium, Macrophages, Mice, Mice, Inbred C3H, Phagocytosis, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-fos, RNA, Messenger, Receptors, Cell Surface, Tetradecanoylphorbol Acetate, Transcription, Genetic
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