Evidence map›Paper›PMID 27568564›Full record

ArticleCell reports2016

The Sel1L-Hrd1 Endoplasmic Reticulum-Associated Degradation Complex Manages a Key Checkpoint in B Cell Development.

Yewei Ji, Hana Kim, Liu Yang, Haibo Sha, Christopher A Roman, Qiaoming Long, Ling Qi

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

55 citing papers in PubMed, 71 citations in OpenAlex.

  1. Cell autonomous inflammation in VEXAS is mediated by cGAS-STING.bioRxiv : the preprint server for biology · 2026
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  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
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  11. SEL1L-HRD1-mediated ERAD in mammals.Nature cell biology · 2025
    Review
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  15. Article
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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

7 authors at 3 institutions in 2 countries.

Yewei JiDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Hana KimGraduate Field of Immunology and Infectious Disease, Cornell University, Ithaca, NY 14853, USA.
Liu YangDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Haibo ShaDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Christopher A RomanDepartment of Cell Biology, College of Medicine and Program in Molecular and Cellular Biology, The School of Graduate Studies, State University of New York, Downstate Medical Center at Brooklyn, New York, NY 11203, USA.
Qiaoming LongLaboratory Animal Research Center, Medical College of Soochow University, Suzhou 215006, Jiangsu, China.
Ling QiDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA; Graduate Field of Immunology and Infectious Disease, Cornell University, Ithaca, NY 14853, USA. Electronic address: lingq@med.umich.edu.
Cornell University · USSoochow University · CNState University of New York · US

Funding

Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
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
Intracellular Signaling by the Precursor B Cell ReceptorR03AI074801 · NIAID · SUNY DOWNSTATE MEDICAL CENTER · PI ROMAN, CHRISTOPHER AJ · 2007 to 2008
$155k
NIAID NIH HHS R03 AI074801NIDDK NIH HHS P30 DK020541NIDDK NIH HHS R01 DK105393NIGMS NIH HHS R01 GM113188
6 · The paper itself

Abstract

Endoplasmic reticulum (ER)-associated degradation (ERAD) is a principal mechanism that targets ER-associated proteins for cytosolic proteasomal degradation. Here, our data demonstrate a critical role for the Sel1L-Hrd1 complex, the most conserved branch of ERAD, in early B cell development. Loss of Sel1L-Hrd1 ERAD in B cell precursors leads to a severe developmental block at the transition from large to small pre-B cells. Mechanistically, we show that Sel1L-Hrd1 ERAD selectively recognizes and targets the pre-B cell receptor (pre-BCR) for proteasomal degradation in a BiP-dependent manner. The pre-BCR complex accumulates both intracellularly and at the cell surface in Sel1L-deficient pre-B cells, leading to persistent pre-BCR signaling and pre-B cell proliferation. This study thus implicates ERAD mediated by Sel1L-Hrd1 as a key regulator of B cell development and reveals the molecular mechanism underpinning the transient nature of pre-BCR signaling.

Indexed as

Cell Cycle CheckpointsEndoplasmic Reticulum-Associated DegradationAnimalsAntigens, CD19B-LymphocytesCell CycleCell SizeIntracellular Signaling Peptides and ProteinsMice, Inbred C57BLPrecursor Cells, B-LymphoidProteinsReceptors, Antigen, B-CellSubstrate SpecificityTranscription Factor CHOPUbiquitin-Protein LigasesAntigens, CD19Intracellular Signaling Peptides and ProteinsProteinsReceptors, Antigen, B-CellSel1h protein, mouseSyvn1 protein, mouseTranscription Factor CHOPUbiquitin-Protein LigasesB cell developmentendoplasmic reticulum-associated degradationHrd1large pre-B cellspre-B cell receptorSel1L

Identifiers

PMID27568564
PMCPMC5014582
OpenAlexW2514806077

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.