Evidence map›Paper›PMID 25066055›Full record

ArticleCell metabolism2014

The ER-associated degradation adaptor protein Sel1L regulates LPL secretion and lipid metabolism.

Haibo Sha, Shengyi Sun, Adam B Francisco, Nicole Ehrhardt, Zhen Xue, Lei Liu, Peter Lawrence, Frits Mattijssen, Robert D Guber, Muhammad S Panhwar and 8 more

Open access · greenAbstract read
In one paragraph

Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

89 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. 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
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. SEL1L-HRD1-mediated ERAD in mammals.Nature cell biology · 2025
    Review
  15. Article
  16. World journal of gastroenterology · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. Article

29 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

18 authors at 6 institutions in 4 countries.

Haibo ShaDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Shengyi SunGraduate Program in Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853, USA.
Adam B FranciscoDepartment of Animal Science, Cornell University, Ithaca, NY 14853, USA.
Nicole EhrhardtDepartment of Biomedical Sciences, Medical Genetics Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Zhen XueDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Lei LiuDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Peter LawrenceDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Frits MattijssenNutrition Metabolism and Genomics Group, Wageningen University, Wageningen 6703HD, the Netherlands.
Robert D GuberDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Muhammad S PanhwarWeill Cornell Medical College in Qatar, P.O. Box 24144, Education City, Doha, Qatar.
J Thomas BrennaDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Hang ShiDepartment of Biology, Georgia State University, Atlanta, GA 30303, USA.
Bingzhong XueDepartment of Biology, Georgia State University, Atlanta, GA 30303, USA.
Sander KerstenDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA; Nutrition Metabolism and Genomics Group, Wageningen University, Wageningen 6703HD, the Netherlands.
André BensadounDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Miklós PéterfyDepartment 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.
Qiaoming LongLaboratory Animal Research Center, Medical College of Soochow University, Suzhou, Jiangsu 215006, China.
Ling QiDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA; Graduate Program in Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853, USA. Electronic address: lq35@cornell.edu.
Cornell University · USCedars-Sinai Medical Center · USGeorgia State University · USSoochow University · CNWageningen University & Research · NLWeill Cornell Medical College in Qatar · QA

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REUE, KAREN · 1985 to 2019
$50.2M
The Lipin Protein Family and Triglyceride Metabolism P01HL090553 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2008 to 2018
$23.3M
Adipokine Signaling in MacrophagesR01DK082582 · NIDDK · CORNELL UNIVERSITY · PI QI, LING · 2009 to 2013
$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
Dissecting the Role of Unfolded Protein Response in Alcoholic Liver DiseaseR21AA020351 · NIAAA · CORNELL UNIVERSITY · PI QI, LING · 2012 to 2013
$389k
Howard Hughes Medical Institute 59107338NCATS NIH HHS UL1 TR000124NCATS NIH HHS UL1TR000124NHLBI NIH HHS NIH P01HL028481NHLBI NIH HHS NIH P01HL090553NHLBI NIH HHS P01 HL028481NHLBI NIH HHS P01 HL090553NIAAA NIH HHS R21 AA020351NIDDK NIH HHS NIH R01DK082582NIDDK NIH HHS R01 DK082582NIDDK NIH HHS R01 DK105393
6 · The paper itself

Abstract

Sel1L is an essential adaptor protein for the E3 ligase Hrd1 in the endoplasmic reticulum (ER)-associated degradation (ERAD), a universal quality-control system in the cell; but its physiological role remains unclear. Here we show that mice with adipocyte-specific Sel1L deficiency are resistant to diet-induced obesity and exhibit postprandial hypertriglyceridemia. Further analyses reveal that Sel1L is indispensable for the secretion of lipoprotein lipase (LPL), independent of its role in Hrd1-mediated ERAD and ER homeostasis. Sel1L physically interacts with and stabilizes the LPL maturation complex consisting of LPL and lipase maturation factor 1 (LMF1). In the absence of Sel1L, LPL is retained in the ER and forms protein aggregates, which are degraded primarily by autophagy. The Sel1L-mediated control of LPL secretion is also seen in other LPL-expressing cell types including cardiac myocytes and macrophages. Thus, our study reports a role of Sel1L in LPL secretion and systemic lipid metabolism.

Indexed as

Lipid MetabolismAdipocytesAnimalsCells, CulturedDiet, High-FatEndoplasmic Reticulum-Associated DegradationFemaleGene DeletionHyperglycemiaIntracellular Signaling Peptides and ProteinsLipoprotein LipaseMaleMembrane ProteinsMiceMice, Inbred C57BLObesityIntracellular Signaling Peptides and ProteinsLipoprotein LipaseLMF1 protein, mouseMembrane ProteinsProtein AggregatesProteinsSel1h protein, mouse

Identifiers

PMID25066055
PMCPMC4156539
OpenAlexW2090294867

What OpenQuestion holds

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Registered trials

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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.