Evidence map›Paper›PMID 30056836›Full record

ReviewTrends in biochemical sciences2018

Quality Control in the Endoplasmic Reticulum: Crosstalk between ERAD and UPR pathways.

Jiwon Hwang, Ling Qi

Open access · greenAbstract readReview
In one paragraph

Review in Trends in biochemical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 365 papers.

0numbers the graph read from it
0cells of the map it votes in
365citing papers in PubMed
19.2field-weighted citation impact, top 1% 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

365 citing papers in PubMed, 586 citations in OpenAlex.

  1. Article
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  4. Review
  5. Biomedicines · 2026
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  12. Single-Cell Proteomics Decodes the Cellular Response to Lysosomal Storage inInternational journal of molecular sciences · 2026
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  15. A Novel Potent and Selective GCN2 Inhibitor, APL-4098, Has Antileukemic Activity through Dysregulation of Mitochondrial Function.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
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  17. Review
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305 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 1 institution in 1 country.

Jiwon HwangDepartment of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48105, USA. Electronic address: jiwonh@med.umich.edu.
Ling QiDepartment of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48105, USA; Division of Metabolism, Endocrinology & Diabetes, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48105, USA. Electronic address: lingq@med.umich.edu.
University of Michigan–Ann Arbor · 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
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 DK120047NIDDK NIH HHS R01 DK120330NIGMS NIH HHS R01 GM113188NIGMS NIH HHS R35 GM130292
6 · The paper itself

Abstract

Endoplasmic reticulum (ER)-associated degradation (ERAD) and the unfolded protein response (UPR) are two key quality-control machineries in the cell. ERAD is responsible for the clearance of misfolded proteins in the ER for cytosolic proteasomal degradation, while UPR is activated in response to the accumulation of misfolded proteins. It has long been thought that ERAD is an integral part of UPR because expression of many ERAD genes is controlled by UPR; however, recent studies have suggested that ERAD has a direct role in controlling the protein turnover and abundance of IRE1α, the most conserved UPR sensor. Here, we review recent advances in our understanding of IRE1α activation and propose that UPR and ERAD engage in an intimate crosstalk to define folding capacity and maintain homeostasis in the ER.

Indexed as

Endoplasmic Reticulum-Associated DegradationUnfolded Protein ResponseCytosolEndoplasmic ReticulumEndoribonucleasesHSP40 Heat-Shock ProteinsHSP47 Heat-Shock ProteinsMembrane ProteinsMolecular ChaperonesProteinsProtein Serine-Threonine KinasesQuality ControlSignal TransductionUbiquitin-Protein LigasesDNAJB9 protein, humanEndoribonucleasesERN1 protein, humanHSP40 Heat-Shock ProteinsHSP47 Heat-Shock ProteinsMembrane ProteinsMolecular ChaperonesProteinsProtein Serine-Threonine KinasesSEL1L protein, humanSYVN1 protein, humanUbiquitin-Protein Ligasesendoplasmic reticulum (ER)ER chaperonesIRE1αprotein degradationprotein foldingSEL1L-HRD1

Identifiers

PMID30056836
PMCPMC6327314
OpenAlexW2811301994

What OpenQuestion holds

Textmetadata
LicenceTDM
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.