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논문 기본 정보

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학술저널
저자정보
Sunhong Kim (KRIBB) Sung Goo Park (KRIBB) 김정훈 (한국생명공학연구원) Bi-Oh Park (Chungbuk National University) Seong Heon Kim (Korea Research Institute of Bioscience and Biotechnology (KRIBB)) Jong Hwan Kim (Korea Research Institute of Bioscience and Biotechnology (KRIBB)) Seon-Young Kim (Korea Research Institue of Bioscience and Biotechnology) Byoung Chul Park (KRIBB) 한상배 (충북대학교 약학대학원)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제44권 제7호
발행연도
2021.1
수록면
458 - 467 (10page)

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GPR43 (also known as FFAR2 or FFA2) is a G-protein-coupled receptor primarily expressed in immune cells, enteroendocrine cells and adipocytes that recognizes short-chain fatty acids, such as acetate, propionate, and butyrate, likely to be implicated in innate immunity and host energy homeostasis. Activated GPR43 suppresses the cAMP level and induces Ca2+ flux via coupling to Gαi and Gαq families, respectively. Additionally, GPR43 is reported to facilitate phosphorylation of ERK through G-protein-dependent pathways and interacts with β-arrestin 2 to inhibit NF-κB signaling. However, other G-protein-dependent and independent signaling pathways involving GPR43 remain to be established. Here, we have demonstrated that GPR43 augments Rho GTPase signaling. Acetate and a synthetic agonist effectively activated RhoA and stabilized YAP/TAZ transcriptional coactivators through interactions of GPR43 with Gαq/11 and Gα12/13. Acetate-induced nuclear accumulation of YAP was blocked by a GPR43-specific inverse agonist. The target genes induced by YAP/TAZ were further regulated by GPR43. Moreover, in THP-1?derived M1-like macrophage cells, the Rho-YAP/TAZ pathway was activated by acetate and a synthetic agonist. Our collective findings suggest that GPR43 acts as a mediator of the Rho-YAP/TAZ pathway.

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