Evidence map›Paper›PMID 35523963›Full record

ReviewNature reviews. Rheumatology2022

Disorders of ubiquitylation: unchained inflammation.

David B Beck, Achim Werner, Daniel L Kastner, Ivona Aksentijevich

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Rheumatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 3 pooled it
9.9field-weighted citation impact, top 1% 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

73 citing papers in PubMed, 3 syntheses or guidelines pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
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  13. Cell autonomous inflammation in VEXAS is mediated by cGAS-STING.bioRxiv : the preprint server for biology · 2026
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Computational Pipelines for Protein Ubiquitylation Analysis and Prediction.Methods in molecular biology (Clifton, N.J.) · 2026
    Article

13 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

4 authors at 1 institution in 1 country.

David B BeckInflammatory Disease Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Achim WernerStem Cell Biochemistry Unit, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-1051-8447
Daniel L KastnerInflammatory Disease Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Ivona AksentijevichInflammatory Disease Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA. aksentii@mail.nih.gov.ORCID http://orcid.org/0000-0002-6564-7214
National Institutes of Health · US

Funding

Genetics, Pathophysiology, and Treatment of Recessive Autoinflammatory DiseasesZIAHG200372 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI KASTNER, DANIEL · 2011 to 2025
$27.2M
Genetics, Pathophysiology, and Treatment of Dominant Autoinflammatory DiseasesZIAHG200373 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI KASTNER, DANIEL · 2011 to 2024
$21.0M
Genetic Analysis of Complex Inflammatory DisordersZIAHG200371 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI KASTNER, DANIEL · 2011 to 2024
$18.8M
Ubiquitin-dependent cell-fate decisions during human development and diseaseZIADE000749 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI WERNER, ACHIM · 2018 to 2025
$14.1M
Understanding the Role of Somatic Mutations in Adult Inflammatory DiseasesR00AR078205 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BECK, DAVID · 2022 to 2024
$740k
NIAMS NIH HHS R00 AR078205
6 · The paper itself

Abstract

Ubiquitylation is an essential post-translational modification that regulates intracellular signalling networks by triggering proteasomal substrate degradation, changing the activity of substrates or mediating changes in proteins that interact with substrates. Hundreds of enzymes participate in reversible ubiquitylation of proteins, some acting globally and others targeting specific proteins. Ubiquitylation is essential for innate immune responses, as it facilitates rapid regulation of inflammatory pathways, thereby ensuring sufficient but not excessive responses. A growing number of inborn errors of immunity are attributed to dysregulated ubiquitylation. These genetic disorders exhibit broad clinical manifestations, ranging from susceptibility to infection to autoinflammatory and/or autoimmune features, lymphoproliferation and propensity to malignancy. Many autoinflammatory disorders result from disruption of components of the ubiquitylation machinery and lead to overactivation of innate immune cells. An understanding of the disorders of ubiquitylation in autoinflammatory diseases could enable the development of novel management strategies.

Indexed as

InflammationUbiquitinHumansImmunity, InnateProtein Processing, Post-TranslationalUbiquitinationUbiquitin

Identifiers

PMID35523963
PMCPMC9075716
OpenAlexW4229001458

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.