MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling
Mitsugumin 53 (MG53) negatively regulates skeletal myogenesis by targeting insulin receptor substrate 1 (IRS-1). Here, we show that MG53 is an ubiquitin E3 ligase that induces IRS-1 ubiquitination with the help of an E2-conjugating enzyme, UBE2H. Molecular manipulations that disrupt the E3-ligase...
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Thư viện Trường Đại học Đà Lạt |
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English |
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MG53, IRS-1 ubiquitination, skeletal myogenesis |
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MG53, IRS-1 ubiquitination, skeletal myogenesis Nguyễn, Thị Huỳnh Nga MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling |
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Mitsugumin 53 (MG53) negatively regulates skeletal myogenesis by targeting insulin receptor
substrate 1 (IRS-1). Here, we show that MG53 is an ubiquitin E3 ligase that induces IRS-1
ubiquitination with the help of an E2-conjugating enzyme, UBE2H. Molecular manipulations
that disrupt the E3-ligase function of MG53 abolish IRS-1 ubiquitination and enhance
skeletal myogenesis. Skeletal muscles derived from the MG53 / mice show an elevated
IRS-1 level with enhanced insulin signalling, which protects the MG53 / mice from
developing insulin resistance when challenged with a high-fat/high-sucrose diet. Muscle
samples derived from human diabetic patients and mice with insulin resistance show normal
expression of MG53, indicating that altered MG53 expression does not serve as a causative
factor for the development of metabolic disorders. Thus, therapeutic interventions that target
the interaction between MG53 and IRS-1 may be a novel approach for the treatment of
metabolic diseases that are associated with insulin resistance. |
| format |
Journal article |
| author |
Nguyễn, Thị Huỳnh Nga |
| author_facet |
Nguyễn, Thị Huỳnh Nga |
| author_sort |
Nguyễn, Thị Huỳnh Nga |
| title |
MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling |
| title_short |
MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling |
| title_full |
MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling |
| title_fullStr |
MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling |
| title_full_unstemmed |
MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling |
| title_sort |
mg53-induced irs-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling |
| publisher |
Springer |
| publishDate |
2022 |
| url |
http://scholar.dlu.edu.vn/handle/123456789/1569 |
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1768306088488206336 |
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oai:scholar.dlu.edu.vn:123456789-15692022-11-09T06:42:01Z MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signalling Nguyễn, Thị Huỳnh Nga MG53, IRS-1 ubiquitination, skeletal myogenesis Mitsugumin 53 (MG53) negatively regulates skeletal myogenesis by targeting insulin receptor substrate 1 (IRS-1). Here, we show that MG53 is an ubiquitin E3 ligase that induces IRS-1 ubiquitination with the help of an E2-conjugating enzyme, UBE2H. Molecular manipulations that disrupt the E3-ligase function of MG53 abolish IRS-1 ubiquitination and enhance skeletal myogenesis. Skeletal muscles derived from the MG53 / mice show an elevated IRS-1 level with enhanced insulin signalling, which protects the MG53 / mice from developing insulin resistance when challenged with a high-fat/high-sucrose diet. Muscle samples derived from human diabetic patients and mice with insulin resistance show normal expression of MG53, indicating that altered MG53 expression does not serve as a causative factor for the development of metabolic disorders. Thus, therapeutic interventions that target the interaction between MG53 and IRS-1 may be a novel approach for the treatment of metabolic diseases that are associated with insulin resistance. 4 2354 1-12 2022-11-09T02:29:50Z 2022-11-09T02:29:50Z 2013 Journal article Bài báo đăng trên tạp chí thuộc ISI, bao gồm book chapter http://scholar.dlu.edu.vn/handle/123456789/1569 10.1038/ncomms3354 en Nature communications 2041-1723 1. Braun, T. & Gautel, M. Transcriptional mechanisms regulating skeletal muscle differentiation, growth and homeostasis. Nat. Rev. Mol. Cell Biol. 12, 349–361 (2011). 2. Sandri, M. Signaling in muscle atrophy and hypertrophy. Physiology (Bethesda) 23, 160–170 (2008). 3. Baker, J., Liu, J. P., Robertson, E. J. & Efstratiadis, A. 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