Evidence map›Paper›PMID 24453213›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Sel1L is indispensable for mammalian endoplasmic reticulum-associated degradation, endoplasmic reticulum homeostasis, and survival.

Shengyi Sun, Guojun Shi, Xuemei Han, Adam B Francisco, Yewei Ji, Nuno Mendonça, Xiaojing Liu, Jason W Locasale, Kenneth W Simpson, Gerald E Duhamel and 4 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 145 papers.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed
5.2field-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

145 citing papers in PubMed, 211 citations in OpenAlex.

  1. Trial
  2. Article
  3. Cell autonomous inflammation in VEXAS is mediated by cGAS-STING.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  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
  8. Article
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  10. Review
  11. Article
  12. Article
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  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
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85 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

14 authors at 6 institutions in 4 countries.

Shengyi SunGraduate Program in Biochemistry, Molecular and Cell Biology, Division of Nutritional Sciences, and Department of Animal Science, Cornell University, Ithaca, NY 14853.
Guojun Shi
Xuemei Han
Adam B Francisco
Yewei Ji
Nuno Mendonça
Xiaojing Liu
Jason W Locasale
Kenneth W Simpson
Gerald E Duhamel
Sander Kersten
John R Yates
Qiaoming Long
Ling Qi
Cornell University · USInstitute of Molecular and Cell Biology · RUScripps Research Institute · USWageningen University & Research · NLRuijin Hospital · CNSoochow University · CN

Funding

TrainingP41GM103533 · NIGMS · UNIVERSITY OF WASHINGTON · PI MACCOSS, MICHAEL · 2012 to 2021
$20.7M
Adipokine Signaling in MacrophagesR01DK082582 · NIDDK · CORNELL UNIVERSITY · PI QI, LING · 2009 to 2013
$1.6M
Understanding metabolic flux and the control of mammalian cell growthR00CA168997 · NCI · DUKE UNIVERSITY · PI LOCASALE, JASON W. · 2013 to 2015
$695k
Contribution of Campylobacter jejuni nuclease in Animal Models of Acute InfectionR21AI085332 · NIAID · CORNELL UNIVERSITY · PI DUHAMEL, GERALD E. · 2010 to 2011
$408k
Howard Hughes Medical Institute 59107338NCI NIH HHS CA168997NCI NIH HHS R00 CA168997NIAID NIH HHS R21 AI085332NIAID NIH HHS R21AI085332NIDDK NIH HHS R01 DK082582NIDDK NIH HHS R01DK082582NIGMS NIH HHS P41 GM103533
6 · The paper itself

Abstract

Suppressor/Enhancer of Lin-12-like (Sel1L) is an adaptor protein for the E3 ligase hydroxymethylglutaryl reductase degradation protein 1 (Hrd1) involved in endoplasmic reticulum-associated degradation (ERAD). Sel1L's physiological importance in mammalian ERAD, however, remains to be established. Here, using the inducible Sel1L knockout mouse and cell models, we show that Sel1L is indispensable for Hrd1 stability, ER homeostasis, and survival. Acute loss of Sel1L leads to premature death in adult mice within 3 wk with profound pancreatic atrophy. Contrary to current belief, our data show that mammalian Sel1L is required for Hrd1 stability and ERAD function both in vitro and in vivo. Sel1L deficiency disturbs ER homeostasis, activates ER stress, attenuates translation, and promotes cell death. Serendipitously, using a biochemical approach coupled with mass spectrometry, we found that Sel1L deficiency causes the aggregation of both small and large ribosomal subunits. Thus, Sel1L is an indispensable component of the mammalian Hrd1 ERAD complex and ER homeostasis, which is essential for protein translation, pancreatic function, and cellular and organismal survival.

Indexed as

Endoplasmic Reticulum-Associated DegradationHomeostasisAnimalsAtrophyCell Culture TechniquesCell DeathCell ProliferationCell SurvivalEndoplasmic ReticulumIntracellular Signaling Peptides and ProteinsMammalsMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalPancreas, ExocrineIntracellular Signaling Peptides and ProteinsProteinsSel1h protein, mouseSyvn1 protein, mouseUbiquitin-Protein LigasesERAD tuningER dilationexocrine pancreatic insufficiencyinducible ERAD-deficient modelsstress granule

Identifiers

PMID24453213
PMCPMC3918815
OpenAlexW2169883398

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.