TY - JOUR
T1 - Gα12/13 signaling in metabolic diseases
AU - Yang, Yoon Mee
AU - Kuen, Da Sol
AU - Chung, Yeonseok
AU - Kurose, Hitoshi
AU - Kim, Sang Geon
N1 - Funding Information:
This study was supported by the National Research Foundation (NRF) funded by the Korean government (Ministry of Science, ICT and Future Planning) (#2017K1A1A2004511), and Y.M.Y. was supported by the National Research Foundation (#2020R1C1C1004185).
Publisher Copyright:
© 2020, The Author(s).
PY - 2020/6/1
Y1 - 2020/6/1
N2 - As the key governors of diverse physiological processes, G protein-coupled receptors (GPCRs) have drawn attention as primary targets for several diseases, including diabetes and cardiovascular disease. Heterotrimeric G proteins converge signals from ~800 members of the GPCR family. Among the members of the G protein α family, the Gα12 family members comprising Gα12 and Gα13 have been referred to as gep oncogenes. Gα12/13 levels are altered in metabolic organs, including the liver and muscles, in metabolic diseases. The roles of Gα12/13 in metabolic diseases have been investigated. In this review, we highlight findings demonstrating Gα12/13 amplifying or dampening regulators of phenotype changes. We discuss the molecular basis of G protein biology in the context of posttranslational modifications to heterotrimeric G proteins and the cell signaling axis. We also highlight findings providing insights into the organ-specific, metabolic and pathological roles of G proteins in changes associated with specific cells, energy homeostasis, glucose metabolism, liver fibrosis and the immune and cardiovascular systems. This review summarizes the currently available knowledge on the importance of Gα12/13 in the physiology and pathogenesis of metabolic diseases, which is presented according to the basic understanding of their metabolic actions and underlying cellular and molecular bases.
AB - As the key governors of diverse physiological processes, G protein-coupled receptors (GPCRs) have drawn attention as primary targets for several diseases, including diabetes and cardiovascular disease. Heterotrimeric G proteins converge signals from ~800 members of the GPCR family. Among the members of the G protein α family, the Gα12 family members comprising Gα12 and Gα13 have been referred to as gep oncogenes. Gα12/13 levels are altered in metabolic organs, including the liver and muscles, in metabolic diseases. The roles of Gα12/13 in metabolic diseases have been investigated. In this review, we highlight findings demonstrating Gα12/13 amplifying or dampening regulators of phenotype changes. We discuss the molecular basis of G protein biology in the context of posttranslational modifications to heterotrimeric G proteins and the cell signaling axis. We also highlight findings providing insights into the organ-specific, metabolic and pathological roles of G proteins in changes associated with specific cells, energy homeostasis, glucose metabolism, liver fibrosis and the immune and cardiovascular systems. This review summarizes the currently available knowledge on the importance of Gα12/13 in the physiology and pathogenesis of metabolic diseases, which is presented according to the basic understanding of their metabolic actions and underlying cellular and molecular bases.
UR - http://www.scopus.com/inward/record.url?scp=85087489140&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85087489140&partnerID=8YFLogxK
U2 - 10.1038/s12276-020-0454-5
DO - 10.1038/s12276-020-0454-5
M3 - Review article
C2 - 32576930
AN - SCOPUS:85087489140
VL - 52
SP - 896
EP - 910
JO - Experimental and Molecular Medicine
JF - Experimental and Molecular Medicine
SN - 1226-3613
IS - 6
ER -