Evidence map›Paper›PMID 29907570›Full record

ArticleThe Journal of biological chemistry2018

The endoplasmic reticulum-resident E3 ubiquitin ligase Hrd1 controls a critical checkpoint in B cell development in mice.

Yi Yang, Sinyi Kong, Yana Zhang, Johanna Melo-Cardenas, Beixue Gao, Yusi Zhang, Donna D Zhang, Bin Zhang, Jianxun Song, Edward Thorp and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
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  7. SEL1L-HRD1-mediated ERAD in mammals.Nature cell biology · 2025
    Review
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  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
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  15. Article
  16. Review
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  18. ATXN3 deubiquitinates YAP1 to promote tumor growth.American journal of cancer research · 2023
    Article
  19. Endoplasmic Reticulum-Associated Protein Degradation.Cold Spring Harbor perspectives in biology · 2022
    Review
  20. Article
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 5 institutions in 2 countries.

Yi YangInstitutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, China; Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Sinyi KongDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Yana ZhangDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Otolaryngology, Head and Neck Surgery of Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, China.
Johanna Melo-CardenasDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Beixue GaoDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Yusi ZhangDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Donna D ZhangDepartment of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona 85721.
Bin ZhangDepartment of Medicine, Division of Hematology/Oncology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Jianxun SongDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 16801.
Edward ThorpDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Kezhong ZhangDepartment of Immunology and Microbiology, Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Michigan 48201.
Jinping ZhangInstitutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, China. Electronic address: j_pzhang@suda.edu.cn.
Deyu FangDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611. Electronic address: fangd@northwestern.edu.
Northwestern University · USPennsylvania State University · USSoochow University · CNUniversity of Arizona · USWayne State University · US

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
Efferocytosis-Directed Inflammation Resolution and Repair in the Hypoxic HeartR01HL122309 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI THORP, EDWARD BENJAMIN · 2014 to 2024
$5.0M
The roles of Sirt1, a deacetylase, in immune tolerance and autoimmunityR01AI079056 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI FANG, DEYU · 2008 to 2017
$3.3M
TAM-Kinases in TransplantR01HL139812 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LUO, XUNRONG, THORP, EDWARD BENJAMIN · 2018 to 2021
$2.4M
The roles of Synoviolin in immune tolerance and autoimmunityR01AI108634 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI FANG, DEYU · 2014 to 2017
$1.5M
Arsenic, Nrf2 and Autophagy Dysfunction in Type II DiabetesR01DK109555 · NIDDK · UNIVERSITY OF ARIZONA · PI ZHANG, DONNA D · 2016 to 2019
$1.4M
Nrf2, autophagy, and arsenic carcinogenesisR01ES026845 · NIEHS · UNIVERSITY OF ARIZONA · PI ZHANG, DONNA D · 2016 to 2019
$1.4M
The roles of Sirt1, a deacetylase, in immune tolerance and autoimmunityR56AI079056 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI FANG, DEYU · 2012 to 2012
$386k
NHLBI NIH HHS R01 HL139812NIAID NIH HHS R01 AI079056NIAID NIH HHS R01 AI108634NIAID NIH HHS R56 AI079056NIDDK NIH HHS R01 DK109555NIEHS NIH HHS P30 ES006694NIEHS NIH HHS R01 ES026845
6 · The paper itself

Abstract

Humoral immunity involves multiple checkpoints that occur in B cell development, maturation, and activation. The pre-B-cell receptor (pre-BCR) is expressed following the productive recombination of the immunoglobulin heavy-chain gene, and sSignalsing through the pre-BCR are required for the differentiation of pre-B cells into immature B cells. However, the molecular mechanisms controlling the pre-BCR expression and signaling strength remain undefined. Herein, we probed the role of the endoplasmic reticulum-associated, stress-activated E3 ubiquitin ligase HMG-CoA reductase degradation 1 (Hrd1) in B cell differentiation. Using mice with a specific Hrd1 deletion in pro-B cells and subsequent B cell developmental stages, we showed that the E3 ubiquitin ligase Hrd1 governs a critical checkpoint during B cell development. We observed that Hrd1 is required for degradation of the pre-BCR complex during the early stage of B cell development. As a consequence, loss of Hrd1 in the B cell lineage resulted in increased pre-BCR expression levels and a developmental defect in the transition from large to small pre-B cells. This defect, in turn, resulted in reduced fewer mature B cells in bone marrow and peripheral lymphoid organs. Our results revealed a novel critical role of Hrd1 in controlling a critical checkpoint in B cell-mediated immunity and suggest that Hrd1 may functioning as an E3 ubiquitin ligase of the pre-BCR complex.

Indexed as

AnimalsBone Marrow CellsCell DifferentiationCell LineEndoplasmic ReticulumMiceMice, TransgenicPrecursor Cells, B-LymphoidReceptors, Antigen, B-CellUbiquitin-Protein LigasesReceptors, Antigen, B-CellSyvn1 protein, mouseUbiquitin-Protein Ligaseslymphocytepre-BCRprotein turnoverubiquitinubiquitin ligaseunfolded protein response (UPR)

Identifiers

PMID29907570
PMCPMC6102136
OpenAlexW2808840706

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.