G alpha 13 ablation reprograms myofibers to oxidative phenotype and enhances whole-body metabolism
DC Field | Value | Language |
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dc.contributor.author | Koo, Ja Hyun | - |
dc.contributor.author | Kim, Tae Hyun | - |
dc.contributor.author | Park, Shi-Young | - |
dc.contributor.author | Joo, Min Sung | - |
dc.contributor.author | Han, Chang Yeob | - |
dc.contributor.author | Choi, Cheol Soo | - |
dc.contributor.author | Kim, Sang Geon | - |
dc.date.available | 2020-02-27T16:44:10Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2017-10-02 | - |
dc.identifier.issn | 0021-9738 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/5591 | - |
dc.description.abstract | Skeletal muscle is a key organ in energy homeostasis owing to its high requirement for nutrients. Heterotrimeric G proteins converge signals from cell-surface receptors to potentiate or blunt responses against environmental changes. Here, we show that muscle-specific ablation of G alpha 13 in mice promotes reprogramming of myofibers to the oxidative type, with resultant increases in mitochondrial biogenesis and cellular respiration. Mechanistically, G alpha 13 and its downstream effector RhoA suppressed nuclear factor of activated T cells 1 (NFATc1), a chief regulator of myofiber conversion, by increasing Rho-associated kinase 2-mediated (Rock2-mediated) phosphorylation at Ser243. Ser243 phosphorylation of NFATc1 was reduced after exercise, but was higher in obese animals. Consequently, G alpha 13 ablation in muscles enhanced whole-body energy metabolism and increased insulin sensitivity, thus affording protection from diet-induced obesity and hepatic steatosis. Our results define G alpha 13 as a switch regulator of myofiber reprogramming, implying that modulations of G alpha 13 and its downstream effectors in skeletal muscle are a potential therapeutic approach to treating metabolic diseases. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | AMER SOC CLINICAL INVESTIGATION INC | - |
dc.relation.isPartOf | JOURNAL OF CLINICAL INVESTIGATION | - |
dc.subject | MUSCLE-FIBER-TYPE | - |
dc.subject | INSULIN-RESISTANCE | - |
dc.subject | MITOCHONDRIAL-FUNCTION | - |
dc.subject | NUCLEAR FACTOR | - |
dc.subject | LIPID-CONTENT | - |
dc.subject | EXERCISE | - |
dc.subject | EXPRESSION | - |
dc.subject | CELLS | - |
dc.subject | MICE | - |
dc.subject | PGC-1-ALPHA | - |
dc.title | G alpha 13 ablation reprograms myofibers to oxidative phenotype and enhances whole-body metabolism | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000412017800029 | - |
dc.identifier.doi | 10.1172/JCI92067 | - |
dc.identifier.bibliographicCitation | JOURNAL OF CLINICAL INVESTIGATION, v.127, no.10, pp.3845 - 3860 | - |
dc.identifier.scopusid | 2-s2.0-85030562828 | - |
dc.citation.endPage | 3860 | - |
dc.citation.startPage | 3845 | - |
dc.citation.title | JOURNAL OF CLINICAL INVESTIGATION | - |
dc.citation.volume | 127 | - |
dc.citation.number | 10 | - |
dc.contributor.affiliatedAuthor | Choi, Cheol Soo | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | MUSCLE-FIBER-TYPE | - |
dc.subject.keywordPlus | INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | MITOCHONDRIAL-FUNCTION | - |
dc.subject.keywordPlus | NUCLEAR FACTOR | - |
dc.subject.keywordPlus | LIPID-CONTENT | - |
dc.subject.keywordPlus | EXERCISE | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordPlus | PGC-1-ALPHA | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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