Evidence map›Paper›PMID 26631554›Full record

ArticleMolecular biology of the cell2016

Epithelial Sel1L is required for the maintenance of intestinal homeostasis.

Shengyi Sun, Rohan Lourie, Sara B Cohen, Yewei Ji, Julia K Goodrich, Angela C Poole, Ruth E Ley, Eric Y Denkers, Michael A McGuckin, Qiaoming Long and 3 more

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

41 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  3. 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
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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

13 authors at 3 institutions in 3 countries.

Shengyi SunDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853 Graduate Program in Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853 ss2475@cornell.edu lq35@cornell.edu.
Rohan LourieImmunity, Infection and Inflammation Program, Mater Medical Research Institute, Mater Health Services, South Brisbane, Queensland 4101, Australia.
Sara B CohenDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
Yewei JiDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853.
Julia K GoodrichGraduate Program in Genetics, Genomics and Development, Cornell University, Ithaca, NY 14853.
Angela C PooleDepartment of Microbiology, Cornell University, Ithaca, NY 14853 Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853.
Ruth E LeyGraduate Program in Genetics, Genomics and Development, Cornell University, Ithaca, NY 14853 Department of Microbiology, Cornell University, Ithaca, NY 14853 Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853.
Eric Y DenkersDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
Michael A McGuckinImmunity, Infection and Inflammation Program, Mater Medical Research Institute, Mater Health Services, South Brisbane, Queensland 4101, Australia.
Qiaoming LongLaboratory Animal Research Center, Medical College of Soochow University, Suzhou 215006, Jiangsu, China.
Gerald E DuhamelDepartment of Biomedical Sciences, Cornell University, Ithaca, NY 14853.
Kenneth W SimpsonDepartment of Clinical Science, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.
Ling QiDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853 Graduate Program in Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853 ss2475@cornell.edu lq35@cornell.edu.
Cornell University · USMater Health Services · AUSoochow University · CN

Funding

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
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 InstituteNIAID NIH HHS R21 AI085332NIAID NIH HHS R21AI085332NIAID NIH HHS R21AI09061NIDDK NIH HHS 1R01DK105393NIDDK NIH HHS R01 DK105393NIGMS NIH HHS 1R01GM113188NIGMS NIH HHS R01 GM113188
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is an incurable chronic idiopathic disease that drastically decreases quality of life. Endoplasmic reticulum (ER)-associated degradation (ERAD) is responsible for the clearance of misfolded proteins; however, its role in disease pathogenesis remains largely unexplored. Here we show that the expression of SEL1L and HRD1, the most conserved branch of mammalian ERAD, is significantly reduced in ileal Crohn's disease (CD). Consistent with this observation, laboratory mice with enterocyte-specific Sel1L deficiency (Sel1L(ΔIEC)) develop spontaneous enteritis and have increased susceptibility to Toxoplasma gondii-induced ileitis. This is associated with profound defects in Paneth cells and a disproportionate increase of Ruminococcus gnavus, a mucolytic bacterium with known association with CD. Surprisingly, whereas both ER stress sensor IRE1α and effector CHOP are activated in the small intestine of Sel1L(ΔIEC) mice, they are not solely responsible for ERAD deficiency-associated lesions seen in the small intestine. Thus our study points to a constitutive role of Sel1L-Hrd1 ERAD in epithelial cell biology and the pathogenesis of intestinal inflammation in CD.

Indexed as

AnimalsApoptosisDuodenumEndoplasmic Reticulum-Associated DegradationEndoplasmic Reticulum StressEndoribonucleasesEnteritisEnterocytesFemaleGastrointestinal MicrobiomeHaploinsufficiencyHomeostasisIntracellular Signaling Peptides and ProteinsMaleMice, Inbred C57BLMice, TransgenicDdit3 protein, mouseEndoribonucleasesErn1 protein, mouseIntracellular Signaling Peptides and ProteinsProteinsProtein Serine-Threonine KinasesSel1h protein, mouseSyvn1 protein, mouseTranscription Factor CHOPUbiquitin-Protein Ligases

Identifiers

PMID26631554
PMCPMC4751599
OpenAlexW2282594374

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.