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  1. Artikel ; 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  Band 15, Heft 1, Seite(n) 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-Begriff(e) Animals ; Mice ; Disease Models, Animal ; Endoplasmic Reticulum-Associated Degradation ; Mammals/metabolism ; Proteins/metabolism ; Proteomics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
    Chemische Substanzen Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Sel1h protein, mouse ; Syvn1 protein, mouse (EC 2.3.2.27)
    Sprache Englisch
    Erscheinungsdatum 2024-02-16
    Erscheinungsland England
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; 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  Band 15, Heft 1, Seite(n) 3241

    Sprache Englisch
    Erscheinungsdatum 2024-04-15
    Erscheinungsland England
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  3. Artikel ; 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  Band 8, Heft 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-Begriff(e) Humans ; Endoplasmic Reticulum-Associated Degradation ; Ubiquitin-Protein Ligases/metabolism ; Proteins/genetics ; Muscles/metabolism ; Energy Metabolism ; Hypertrophy/metabolism
    Chemische Substanzen Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Proteins ; SEL1L protein, human
    Sprache Englisch
    Erscheinungsdatum 2023-08-03
    Erscheinungsland United States
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: 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
    Sprache Englisch
    Erscheinungsdatum 2023-06-07
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.04.13.536796
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Buch ; 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 ...
    Schlagwörter Mus musculus
    Thema/Rubrik (Code) 610
    Verlag Wageningen University & Research
    Erscheinungsland nl
    Dokumenttyp Buch ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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  6. Artikel ; 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  Band 8, Heft 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.
    Schlagwörter Life Science
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsland nl
    Dokumenttyp Artikel ; Online
    ISSN 2379-3708
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

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