The Hippo signaling pathway consists of an upstream kinase cascade (MST1/2-SAV1-LATS1/2-MOB1) and a downstream nuclear transcriptional-regulator complex (TEADs-YAP-VGLL4), which is known to play an important role in multiple physiological processes, such as tissue homeostasis, organ size, immune response and tumorigenesis.
In a recent study published in Journal of Biological Chemistry, a team led by Dr. ZHANG Lei at Shanghai Institute of Biochemistry and Cell Biology of Chinese Academy of Sciences provided insights into the role of the TEAD4-VGLL4-CtBP2 transcriptional repressor complex in suppression of adipogenesis in murine pre-adipocytes.
Researchers provided compelling evidence for an inhibitory function of TEAD4 during adipogenesis.
They found that the knock-down of TEAD4 significantly promotes adipogenesis dependent on the presence of both CtBP2 and VGLL4, yet independent of YAP. CtBP2 was identified as a novel TEAD4 binding partner, and VGLL4 was found to enhance their interaction as an adaptor protein.
Notably, ChIP-qPCR verified that TEAD4 directly binds to PPARγ promoter at the early stage of adipogenesis.
Collectively, the results uncovered the function of TEAD4 in adipocytes differentiation and provides insights into how the TEAD4-VGLL4-CtBP2 transcriptional complex dynamically controls adipogenesis.
Adipocyte is an important cell type possessing multiple functions in systemic regulation of metabolism. Not only that adipose tissue is critical for energy balance and nutrition homeostasis, dysfunction of adipogenesis also leads to multiple metabolic diseases, such as obesity, diabetes and fatty liver.
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