Evidence map›Paper›PMID 31792042›Full record

ReviewJournal of cell science2019

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

Asmita Bhattacharya, Ling Qi

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cell science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

79 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  3. Review
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  7. SEL1L-HRD1 ERAD-autophagy interplay maintains mitochondrial homeostasis in brown adipocytes.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  13. Review
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  20. SEL1L-HRD1-mediated ERAD in mammals.Nature cell biology · 2025
    Review

19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Asmita BhattacharyaDepartment of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48105, USA.ORCID 0000-0002-5669-8036
Ling QiDepartment of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48105, USA lingq@med.umich.edu.ORCID 0000-0001-8229-0184
Cornell University · USUniversity of Michigan · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Secretory Pathway Protein Degradation Maintains Insulin Biogenesis + SecretionR01DK111174 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ARVAN, PETER, QI, LING · 2016 to 2024
$5.5M
Novel Role of Hepatic SEL1L-HRD1 ERAD in FGF21 Gene TranscriptionR01DK120330 · NIDDK · UNIVERSITY OF VIRGINIA · PI Deyu Fang, Ling Qi · 2018 to 2026
$4.9M
Interplay Between SERPINB1 and TLR2/TLR4 in Beta Cell RegenerationR01DK117639 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ARVAN, PETER, KULKARNI, ROHIT N. · 2019 to 2023
$3.0M
Regulation of Mitochondrial Dynamics by ERAD: Administrative SupplementR35GM130292 · NIGMS · UNIVERSITY OF VIRGINIA · PI QI, LING · 2019 to 2023
$2.5M
Defining the Central Role of ER-Associated Degradation (ERAD) in Neuroendocrine CellsR01DK120047 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI QI, LING · 2018 to 2021
$1.6M
The Role of Sel1L and ER Quality Control in AdipocytesR01DK105393 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI QI, LING · 2015 to 2018
$1.4M
REGULATION OF IRE1A SIGNALING BY THE SEL1L-HRD1 ERAD COMPLEXR01GM113188 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI QI, LING · 2015 to 2018
$1.2M
NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK105393NIDDK NIH HHS R01 DK111174NIDDK NIH HHS R01 DK117639NIDDK NIH HHS R01 DK120047NIDDK NIH HHS R01 DK120330NIGMS NIH HHS R01 GM113188NIGMS NIH HHS R35 GM130292
6 · The paper itself

Abstract

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.

Indexed as

AnimalsEndoplasmic Reticulum-Associated DegradationHumansModels, BiologicalProteinsUbiquitin-Protein LigasesProteinsSEL1L protein, humanSYVN1 protein, humanUbiquitin-Protein LigasesConstitutive ERADDiseaseERAD substrate, Quality controlHealthInducible ERADNuclear gene transcriptionQuantity controlSel1L-Hrd1 ERAD

Identifiers

PMID31792042
PMCPMC6918741
OpenAlexW2991437291

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.