Evidence map›Paper›PMID 31086255›Full record

ArticleCell research2019

Preventing abnormal NF-κB activation and autoimmunity by Otub1-mediated p100 stabilization.

Yanchuan Li, Jin-Young Yang, Xiaoping Xie, Zuliang Jie, Lingyun Zhang, Jianhong Shi, Daniel Lin, Meidi Gu, Xiaofei Zhou, Haiyan S Li and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

36 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. The NAT10/c-Myc positive feedback loop orchestrates tRNA acCellular & molecular biology letters · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. OTUB1 promotes osteoblastic bone formation through stabilizing FGFR2.Signal transduction and targeted therapy · 2023
    Article
  19. Article
  20. Review
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

16 authors at 2 institutions in 2 countries.

Yanchuan LiDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Jin-Young YangDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Xiaoping XieDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Zuliang JieDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Lingyun ZhangDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Jianhong ShiDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Daniel LinDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Meidi GuDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Xiaofei ZhouDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Haiyan S LiDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.ORCID http://orcid.org/0000-0001-5069-9735
Stephanie S WatowichDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Antrix JainVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, 77030, USA.ORCID http://orcid.org/0000-0002-2815-3645
Sung Yun JungVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, 77030, USA.ORCID http://orcid.org/0000-0003-1521-7977
Jun QinVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, 77030, USA.
Xuhong ChengDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA.
Shao-Cong SunDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston, TX, 77030, USA. ssun@mdanderson.org.ORCID http://orcid.org/0000-0001-7353-9400
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
TpI2 Kinase in Macrophage Activation by MicrobesR01AI057555 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2004 to 2021
$6.7M
Molecular Studies of Noncanonical NF-kb SignalingR01GM084459 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2008 to 2021
$4.4M
Signaling Functions of the Tumor Suppressor CYLDR01AI064639 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2006 to 2014
$3.6M
Regulation of T-cell function and autoimmune inflammation by deubiquitinases.R37AI064639 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2015 to 2021
$2.8M
NCI NIH HHS P30 CA016672NIAID NIH HHS R01 AI057555NIAID NIH HHS R01 AI064639NIAID NIH HHS R37 AI064639NIGMS NIH HHS R01 GM084459
6 · The paper itself

Abstract

NF-κB, a family of transcription factors regulating diverse biological processes including immune responses, is activated by canonical and noncanonical pathways based on degradation of IκBα and processing of the IκB-like protein p100, respectively. Although p100 responds to noncanonical NF-κB stimuli for processing, it does not undergo degradation, but rather becomes accumulated, along with canonical NF-κB activation. We show here that the stability of p100 is tightly controlled by a deubiquitinase, Otub1. Otub1 deficiency not only promotes signal-induced p100 processing and noncanonical NF-κB activation but also causes steady-state p100 degradation, leading to aberrant NF-κB activation in the canonical pathway. B-cell-conditional deletion of Otub1 results in B-cell hyperplasia, antibody hyper-production, and lupus-like autoimmunity. Otub1-deficient B cells display aberrantly activated phenotypes and overproduce the cytokine IL-6, contributing to autoimmunity induction. Thus, maintenance of p100 stability by Otub1 serves as an unusual mechanism of NF-κB regulation that prevents autoimmunity.

Indexed as

AutoimmunityAnimalsCells, CulturedCysteine EndopeptidasesDeubiquitinating EnzymesHEK293 CellsHumansI-kappa B ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNF-kappa BProtein StabilityCysteine EndopeptidasesDeubiquitinating EnzymesI-kappa B ProteinsNF-kappa BOTUB1 protein, human

Identifiers

PMID31086255
PMCPMC6796864
OpenAlexW2944987759

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.