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How is phagocytosis transcriptionally regulated in macrophages? 


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Phagocytosis in macrophages is transcriptionally regulated through various mechanisms. Activation of transcription factors like TFEB and TFE3 is crucial during bacterial phagocytosis, linking phagocytosis with gene expression changes . Additionally, the presence of all-trans retinoic acid enhances myelin phagocytosis by inducing tissue transglutaminase-2, without affecting the expression of phagocytic receptors . Furthermore, phagocytic TAMs exhibit a distinct gene expression profile associated with oxidative phosphorylation and metabolic changes, impacting tumor-associated macrophage phenotypes . These findings underscore the complexity of transcriptional regulation in macrophages during phagocytosis, involving factors like TFEB, metabolic genes, and retinoic acid signaling.

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Transcriptional factors regulate phagocytosis in macrophages, with diverse subsets influenced by tissue of residence and ontogeny, highlighting the complexity of mononuclear phagocyte development.
Phagocytosis in macrophages is transcriptionally regulated by all-trans retinoic acid (RA) through induction of tissue transglutaminase-2, without altering expression of specific phagocytic receptor genes.
Phagocytosis in macrophages is transcriptionally regulated by a novel PHOX/CD38/MCOLN1/TFEB axis, involving oxidative burst, NAADP generation, Ca2+ efflux, and TFEB-dependent cytokine expression.
Phagocytosis in tumor-associated macrophages (TAMs) leads to upregulation of antigen presentation and metabolic genes, particularly oxidative phosphorylation (OXPHOS), influencing immune suppression and tumor promotion.
Phagocytosis in macrophages is regulated transcriptionally through changes in molecular expression and post-translational modifications, as discussed in the paper.

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