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Choi, Jang Hyun
Lab of Diabetes and Metabolism Lab.
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dc.citation.endPage 1620 -
dc.citation.number 8 -
dc.citation.startPage 1608 -
dc.citation.title MOLECULAR AND CELLULAR BIOLOGY -
dc.citation.volume 33 -
dc.contributor.author Koh, Ara -
dc.contributor.author Lee, Mi Nam -
dc.contributor.author Yang, Yong Ryoul -
dc.contributor.author Jeong, Heeyoon -
dc.contributor.author Ghim, Jaewang -
dc.contributor.author Noh, Jeongeun -
dc.contributor.author Kim, Jaeyoon -
dc.contributor.author Ryu, Dongryeol -
dc.contributor.author Park, Sehoon -
dc.contributor.author Song, Parkyong -
dc.contributor.author Koo, Seung-Hoi -
dc.contributor.author Leslie, Nick R. -
dc.contributor.author Berggren, Per-Olof -
dc.contributor.author Choi, Jang Hyun -
dc.contributor.author Suh, Pann-Ghill -
dc.contributor.author Ryu, Sung Ho -
dc.date.accessioned 2023-12-22T04:08:37Z -
dc.date.available 2023-12-22T04:08:37Z -
dc.date.created 2013-06-28 -
dc.date.issued 2013-04 -
dc.description.abstract Muscle atrophy occurs under various catabolic conditions, including insulin deficiency, insulin resistance, or increased levels of glucocorticoids. This results from reduced levels of insulin receptor substrate 1 (IRS-1), leading to decreased phosphatidylinositol 3-kinase activity and thereby activation of FoxO transcription factors. However, the precise mechanism of reduced IRS-1 under a catabolic condition is unknown. Here, we report that C1-Ten is a novel protein tyrosine phosphatase (PTPase) of IRS-1 that acts as a mediator to reduce IRS-1 under a catabolic condition, resulting in muscle atrophy. C1-Ten preferentially dephosphorylated Y612 of IRS-1, which accelerated IRS-1 degradation. These findings suggest a novel type of IRS-1 degradation mechanism which is dependent on C1-Ten and extends our understanding of the molecular mechanism of muscle atrophy under catabolic conditions. C1-Ten expression is increased by catabolic glucocorticoid and decreased by anabolic insulin. Reflecting these hormonal regulations, the muscle C1-Ten is upregulated in atrophy but downregulated in hypertrophy. This reveals a previously unidentified role of C1-Ten as a relevant PTPase contributing to skeletal muscle atrophy. -
dc.identifier.bibliographicCitation MOLECULAR AND CELLULAR BIOLOGY, v.33, no.8, pp.1608 - 1620 -
dc.identifier.doi 10.1128/MCB.01447-12 -
dc.identifier.issn 0270-7306 -
dc.identifier.scopusid 2-s2.0-84876333589 -
dc.identifier.uri https://scholarworks.unist.ac.kr/handle/201301/2701 -
dc.identifier.url http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84876333589 -
dc.identifier.wosid 000317272500011 -
dc.language 영어 -
dc.publisher AMER SOC MICROBIOLOGY -
dc.title C1-Ten Is a Protein Tyrosine Phosphatase of Insulin Receptor Substrate 1 (IRS-1), Regulating IRS-1 Stability and Muscle Atrophy -
dc.type Article -
dc.relation.journalWebOfScienceCategory Biochemistry & Molecular Biology; Cell Biology -
dc.relation.journalResearchArea Biochemistry & Molecular Biology; Cell Biology -
dc.description.journalRegisteredClass scie -
dc.description.journalRegisteredClass scopus -
dc.subject.keywordPlus PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY -
dc.subject.keywordPlus FOXO TRANSCRIPTION FACTORS -
dc.subject.keywordPlus HUMAN SKELETAL-MUSCLE -
dc.subject.keywordPlus GROWTH-FACTOR-II -
dc.subject.keywordPlus SIGNAL-TRANSDUCTION -
dc.subject.keywordPlus IN-VIVO -
dc.subject.keywordPlus UBIQUITIN LIGASES -
dc.subject.keywordPlus GENE-EXPRESSION -
dc.subject.keywordPlus CELL-SURVIVAL -
dc.subject.keywordPlus RESISTANCE -

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