Full metadata record
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, Se Hyun | - |
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, So Yeon | - |
dc.contributor.author | Jeong, Man Hyung | - |
dc.contributor.author | Ko, A Ram | - |
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, Jae Whan | - |
dc.date.accessioned | 2018-09-17T12:52:45Z | - |
dc.date.available | 2018-09-17T12:52:45Z | - |
dc.date.created | 2018-09-10 | - |
dc.date.issued | 2018-08 | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11750/9300 | - |
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. © 2018, The Author(s). | - |
dc.language | English | - |
dc.publisher | Nature Publishing Group | - |
dc.title | Loss of the E3 ubiquitin ligase MKRN1 represses diet-induced metabolic syndrome through AMPK activation | - |
dc.type | Article | - |
dc.identifier.doi | 10.1038/s41467-018-05721-4 | - |
dc.identifier.scopusid | 2-s2.0-85052150170 | - |
dc.identifier.bibliographicCitation | Nature Communications, v.9, no.1 | - |
dc.description.isOpenAccess | TRUE | - |
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 | - |
dc.citation.number | 1 | - |
dc.citation.title | Nature Communications | - |
dc.citation.volume | 9 | - |