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  1. Article ; Online: SEL1L-HRD1 interaction is required to form a functional HRD1 ERAD complex.

    Lin, Liangguang Leo / Wang, Huilun Helen / Pederson, Brent / Wei, Xiaoqiong / Torres, Mauricio / Lu, You / Li, Zexin Jason / Liu, Xiaodan / Mao, Hancheng / Wang, Hui / Zhou, Linyao Elina / Zhao, Zhen / Sun, Shengyi / Qi, Ling

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 1440

    Abstract: The SEL1L-HRD1 protein complex represents the most conserved branch of endoplasmic reticulum (ER)-associated degradation (ERAD). Despite recent advances in both mouse models and humans, in vivo evidence for the importance of SEL1L in the ERAD complex ... ...

    Abstract The SEL1L-HRD1 protein complex represents the most conserved branch of endoplasmic reticulum (ER)-associated degradation (ERAD). Despite recent advances in both mouse models and humans, in vivo evidence for the importance of SEL1L in the ERAD complex formation and its (patho-)physiological relevance in mammals remains limited. Here we report that SEL1L variant p.Ser658Pro (SEL1L
    MeSH term(s) Animals ; Mice ; Disease Models, Animal ; Endoplasmic Reticulum-Associated Degradation ; Mammals/metabolism ; Proteins/metabolism ; Proteomics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Sel1h protein, mouse ; Syvn1 protein, mouse (EC 2.3.2.27)
    Language English
    Publishing date 2024-02-16
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-45633-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Publisher Correction: SEL1L-HRD1 interaction is required to form a functional HRD1 ERAD complex.

    Lin, Liangguang Leo / Wang, Huilun Helen / Pederson, Brent / Wei, Xiaoqiong / Torres, Mauricio / Lu, You / Li, Zexin Jason / Liu, Xiaodan / Mao, Hancheng / Wang, Hui / Zhou, Linyao Elina / Zhao, Zhen / Sun, Shengyi / Qi, Ling

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 3241

    Language English
    Publishing date 2024-04-15
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-47251-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Muscle-specific ER-associated degradation maintains postnatal muscle hypertrophy and systemic energy metabolism.

    Abdon, Benedict / Liang, Yusheng / da Luz Scheffer, Débora / Torres, Mauricio / Shrestha, Neha / Reinert, Rachel B / Lu, You / Pederson, Brent / Bugarin-Lapuz, Amara / Kersten, Sander / Qi, Ling

    JCI insight

    2023  Volume 8, Issue 17

    Abstract: The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated ... ...

    Abstract The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and a 30% reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beigeing of adipocytes, and resistance to diet-induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance.
    MeSH term(s) Humans ; Endoplasmic Reticulum-Associated Degradation ; Ubiquitin-Protein Ligases/metabolism ; Proteins/genetics ; Muscles/metabolism ; Energy Metabolism ; Hypertrophy/metabolism
    Chemical Substances Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Proteins ; SEL1L protein, human
    Language English
    Publishing date 2023-08-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.170387
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: SEL1L-HRD1 interaction is prerequisite for the formation of a functional HRD1 ERAD complex.

    Lin, Liangguang Leo / Wei, Xiaoqiong / Wang, Huilun Helen / Pederson, Brent / Torres, Mauricio / Lu, You / Li, Zexin Jason / Liu, Xiaodan / Mao, Hancheng / Wang, Hui / Zhao, Zhen / Sun, Shengyi / Qi, Ling

    bioRxiv : the preprint server for biology

    2023  

    Abstract: The SEL1L-HRD1 protein complex represents the most conserved branch of endoplasmic reticulum (ER)-associated degradation (ERAD); however, definitive evidence for the importance of SEL1L in HRD1 ERAD is lacking. Here we report that attenuation of the ... ...

    Abstract The SEL1L-HRD1 protein complex represents the most conserved branch of endoplasmic reticulum (ER)-associated degradation (ERAD); however, definitive evidence for the importance of SEL1L in HRD1 ERAD is lacking. Here we report that attenuation of the interaction between SEL1L and HRD1 impairs HRD1 ERAD function and has pathological consequences in mice. Our data show that
    Language English
    Publishing date 2023-06-07
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.04.13.536796
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  5. Book ; Online: ER-associated degradation maintains postnatal muscle hypertophy and systemic energy metabolism

    Abdon, Benedict / Liang, Yusheng / da Luz Scheffer, Débora / Torres, Mauricio / Shrestha, Neha / Reinert, Rachel / Lu, You / Pederson, Brent / Bugarin-Lapuz, Amara / Kersten, Sander / Qi, Ling

    2023  

    Abstract: The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum is largely unknown. Here, we report that the SEL1L-HRD1 endoplasmic reticulum (ER)- ...

    Abstract The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum is largely unknown. Here, we report that the SEL1L-HRD1 endoplasmic reticulum (ER)-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and significant reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beiging of adipocytes, and resistance to diet induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance. Overall design: Gene expression was profiled in gastrocnemius muscle isolated from 8-week-old wildtype and muscle-specific Sel1L-deficient mice.

    The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum is largely unknown. Here, we report that the SEL1L-HRD1 endoplasmic reticulum (ER)-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and significant reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized ...
    Keywords Mus musculus
    Subject code 610
    Publisher Wageningen University & Research
    Publishing country nl
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  6. Article ; Online: Muscle-specific ER-associated degradation maintains postnatal muscle hypertrophy and systemic energy metabolism

    Abdon, Benedict / Liang, Yusheng / da Luz Scheffer, Débora / Torres, Mauricio / Shrestha, Neha / Reinert, Rachel / Lu, You / Pederson, Brent / Bugarin-Lapuz, Amara / Kersten, Sander / Qi, Ling

    JCI Insight

    2023  Volume 8, Issue 17

    Abstract: The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated ... ...

    Abstract The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and a 30% reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beigeing of adipocytes, and resistance to diet-induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance.
    Keywords Life Science
    Subject code 610
    Language English
    Publishing country nl
    Document type Article ; Online
    ISSN 2379-3708
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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