ER 相关降解衔接蛋白 Sel1L 调节 LPL 分泌和脂质代谢。,Cell Metabolism

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ER 相关降解衔接蛋白 Sel1L 调节 LPL 分泌和脂质代谢。
Cell Metabolism ( IF 27.7 ) Pub Date : 2014-Sep-02 , DOI: 10.1016/j.cmet.2014.06.015
Haibo Sha ₁ , Shengyi Sun ₂ , Adam B Francisco ₃ , Nicole Ehrhardt ₄ , Zhen Xue ₁ , Lei Liu ₁ , Peter Lawrence ₁ , Frits Mattijssen ₅ , Robert D Guber ₁ , Muhammad S Panhwar ₆ , J Thomas Brenna ₁ , Hang Shi ₇ , Bingzhong Xue ₇ , Sander Kersten ₈ , André Bensadoun ₁ , Miklós Péterfy ₉ , Qiaoming Long ₁₀ , Ling Qi ₁₁

Affiliation

Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Graduate Program in Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853, USA.
Department of Animal Science, Cornell University, Ithaca, NY 14853, USA.
Department of Biomedical Sciences, Medical Genetics Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Nutrition Metabolism and Genomics Group, Wageningen University, Wageningen 6703HD, the Netherlands.
Weill Cornell Medical College in Qatar, P.O. Box 24144, Education City, Doha, Qatar.
Department of Biology, Georgia State University, Atlanta, GA 30303, USA.
Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA; Nutrition Metabolism and Genomics Group, Wageningen University, Wageningen 6703HD, the Netherlands.
Department of Biomedical Sciences, Medical Genetics Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Laboratory Animal Research Center, Medical College of Soochow University, Suzhou, Jiangsu 215006, China.
Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA; Graduate Program in Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853, USA.

Sel1L 是内质网 (ER) 相关降解 (ERAD) 中 E3 连接酶 Hrd1 的重要衔接蛋白，这是细胞中的通用质量控制系统；但其生理作用尚不清楚。在这里，我们表明具有脂肪细胞特异性 Sel1L 缺陷的小鼠对饮食诱导的肥胖具有抵抗力，并表现出餐后高甘油三酯血症。进一步的分析表明，Sel1L 对于脂蛋白脂肪酶 (LPL) 的分泌是必不可少的，而与其在 Hrd1 介导的 ERAD 和 ER 稳态中的作用无关。Sel1L 与由 LPL 和脂肪酶成熟因子 1 (LMF1) 组成的 LPL 成熟复合物发生物理相互作用并使其稳定。在不存在 Sel1L 的情况下，LPL 保留在 ER 中并形成蛋白质聚集体，主要通过自噬降解。Sel1L 介导的 LPL 分泌控制也见于其他表达 LPL 的细胞类型，包括心肌细胞和巨噬细胞。因此，我们的研究报告了 Sel1L 在 LPL 分泌和全身脂质代谢中的作用。

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