4.5 Review

ER-associated degradation in health and disease - from substrate to organism

期刊

JOURNAL OF CELL SCIENCE
卷 132, 期 23, 页码 -

出版社

COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.232850

关键词

Sel1L-Hrd1 ERAD; Health; Disease; Constitutive ERAD; Inducible ERAD; ERAD substrate; Quality control; Quantity control; Nuclear gene transcription

资金

  1. National Institutes of Health (NIH) [R01GM113188, R35DM130292, R01DK105393, R01DK111174, R01DK120047, R01DK120330, R01DK117639]
  2. University of Michigan Protein Folding Diseases Initiative
  3. American Diabetes Association (ADA)
  4. American Heart Association Predoctoral Fellowship [16PRE29750001]
  5. Junior Faculty and Career Development Awards from the ADA
  6. Juvenile Diabetes Research Foundation United States of America (JDRF)

向作者/读者索取更多资源

The recent literature has revolutionized our view on the vital importance of endoplasmic reticulum (ER)-associated degradation (ERAD) in health and disease. Suppressor/enhancer of Lin-12-like (Sel1L)-HMG-coA reductase degradation protein 1 (Hrd1)-mediated ERAD has emerged as a crucial determinant of normal physiology and as a sentinel against disease pathogenesis in the body, in a largely substrate- and cell type-specific manner. In this Review, we highlight three features of ERAD, constitutive versus inducible ERAD, quality versus quantity control of ERAD and ERAD-mediated regulation of nuclear gene transcription, through which ERAD exerts a profound impact on a number of physiological processes.

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