Loss of the E3 ubiquitin ligase MKRN1 represses diet-induced metabolic syndrome through AMPK activation
DC Field | Value | Language |
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dc.contributor.author | Lee, Min-Sik | - |
dc.contributor.author | Han, Hyun-Ji | - |
dc.contributor.author | Han, Su Yeon | - |
dc.contributor.author | Kim, Il Young | - |
dc.contributor.author | Chae, Sehyun | - |
dc.contributor.author | Lee, Choong-Sil | - |
dc.contributor.author | Kim, Sung Eun | - |
dc.contributor.author | Yoon, Seul Gi | - |
dc.contributor.author | Park, Jun-Won | - |
dc.contributor.author | Kim, Jung-Hoon | - |
dc.contributor.author | Shin, Soyeon | - |
dc.contributor.author | Jeong, Manhyung | - |
dc.contributor.author | Ko, Aram | - |
dc.contributor.author | Lee, Ho-Young | - |
dc.contributor.author | Oh, Kyoung-Jin | - |
dc.contributor.author | Lee, Yun-Hee | - |
dc.contributor.author | Bae, Kwang-Hee | - |
dc.contributor.author | Koo, Seung-Hoi | - |
dc.contributor.author | Kim, Jea-Woo | - |
dc.contributor.author | Seong, Je Kyung | - |
dc.contributor.author | Hwang, Daehee | - |
dc.contributor.author | Song, Jaewhan | - |
dc.date.accessioned | 2021-09-02T07:36:50Z | - |
dc.date.available | 2021-09-02T07:36:50Z | - |
dc.date.created | 2021-06-16 | - |
dc.date.issued | 2018-08-24 | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/73730 | - |
dc.description.abstract | AMP-activated protein kinase (AMPK) plays a key role in controlling energy metabolism in response to physiological and nutritional status. Although AMPK activation has been proposed as a promising molecular target for treating obesity and its related comorbidities, the use of pharmacological AMPK activators has been met with contradictory therapeutic challenges. Here we show a regulatory mechanism for AMPK through its ubiquitination and degradation by the E3 ubiquitin ligase makorin ring finger protein 1 (MKRN1). MKRN1 depletion promotes glucose consumption and suppresses lipid accumulation due to AMPK stabilisation and activation. Accordingly, MKRN1-null mice show chronic AMPK activation in both liver and adipose tissue, resulting in significant suppression of diet-induced metabolic syndrome. We demonstrate also its therapeutic effect by administering shRNA targeting MKRN1 into obese mice that reverses non-alcoholic fatty liver disease. We suggest that ubiquitin-dependent AMPK degradation represents a target therapeutic strategy for metabolic disorders. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | BROWN ADIPOSE-TISSUE | - |
dc.subject | PROTEIN-KINASE | - |
dc.subject | INSULIN-RESISTANCE | - |
dc.subject | ENERGY SENSOR | - |
dc.subject | RNA-SEQ | - |
dc.subject | LIVER | - |
dc.subject | GENE | - |
dc.subject | HOMEOSTASIS | - |
dc.subject | DEGRADATION | - |
dc.subject | INTEGRATION | - |
dc.title | Loss of the E3 ubiquitin ligase MKRN1 represses diet-induced metabolic syndrome through AMPK activation | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Koo, Seung-Hoi | - |
dc.identifier.doi | 10.1038/s41467-018-05721-4 | - |
dc.identifier.scopusid | 2-s2.0-85052150170 | - |
dc.identifier.wosid | 000442594800006 | - |
dc.identifier.bibliographicCitation | NATURE COMMUNICATIONS, v.9 | - |
dc.relation.isPartOf | NATURE COMMUNICATIONS | - |
dc.citation.title | NATURE COMMUNICATIONS | - |
dc.citation.volume | 9 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | BROWN ADIPOSE-TISSUE | - |
dc.subject.keywordPlus | PROTEIN-KINASE | - |
dc.subject.keywordPlus | INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | ENERGY SENSOR | - |
dc.subject.keywordPlus | RNA-SEQ | - |
dc.subject.keywordPlus | LIVER | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | HOMEOSTASIS | - |
dc.subject.keywordPlus | DEGRADATION | - |
dc.subject.keywordPlus | INTEGRATION | - |
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