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Fig. 3 | Journal of Biomedical Science

Fig. 3

From: E26 transformation-specific transcription variant 5 in development and cancer: modification, regulation and function

Fig. 3

ETV5 in fertility and embryonic development, metabolic processes, and the immune system. A In Sertoli cells, FGF2 induces CXCL12 expression via the transcriptional regulation of ETV5. CXCL12, CCL9, GDNF and FGF2 released from Sertoli cells interact with receptors located on spermatogonial stem cells (SSCs) and activate intracellular signal cascades, which promote ETV5 expression and contribute to the self-renewal of SSCs. In addition, activated ETV5 promotes the transcription of the GDNF receptor RET. B ETV5 regulates insulin secretion and fatty acid metabolism in pancreatic beta cells and hepatocytes. ETV5 also regulated the energy balance in the brain. C1 In Th17 cells, ETV5 is upregulated by STAT3 and STAT4. Elevated ETV5 levels promote IL17 production by binding to its promoter and recruiting histone acetyltransferase p300. In Th2 cells, ETV5 promotes IL10 expression. In Th9 cells, the upregulation of ETV5 by STAT6 and interferon regulatory factor 4 (IRF4) facilitates IL9 secretion. C2 In TFH cells, overexpressed ETV5 induced by CIC activates MAF expression in STAT3-dependent mechanism, contributing to TFH cells differentiation. In B-cell progenitors, BCR-ALB enhanced aPKC λ activates ERK and ETV5, which transcriptionally upregulates SATB homoebox 2 (SATB2) to inhibit B-cell differentiation and maturation. CHD1L chromodomain helicase DNA binding protein 1 like and DEAD-box helicase 5, CCR1 C-C-receptor type 1, SYTL3 synaptotagmin-like 3, EXOC6 exocyst-6, GC glucocorticoids, ACSL1 acyl-CoA synthetase long chain family member 1

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