Evidence map›Paper›PMID 40940201›Full record

ReviewTrends in biochemical sciences2025

E3 ubiquitin ligases in signaling, disease, and therapeutics.

Pirouz Ebadi, Caleb M Stratton, Shaun K Olsen

Abstract readReview
In one paragraph

Review in Trends in biochemical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
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

40 citing papers in PubMed.

  1. E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  2. Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Article
  4. Article
  5. E3 Ubiquitin Ligase MDM2 Promotes Growth and CD8Journal of gastroenterology and hepatology · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Ubiquitination and NOncology letters · 2026
    Review
  14. [Ubiquitination-mediated regulation of T cell homeostasis and autoimmune diseases].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Review
  15. Review
  16. Review
  17. Article
  18. Review
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  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

3 authors.

Pirouz EbadiDepartment of Biochemistry & Structural Biology, and Greehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Caleb M StrattonDepartment of Biochemistry & Structural Biology, and Greehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Shaun K OlsenDepartment of Biochemistry & Structural Biology, and Greehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. Electronic address: olsens@uthscsa.edu.

Funding

Structural Biology of the Ubiquitin Conjugation SystemR01GM115568 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI OLSEN, SHAUN · 2015 to 2023
$2.7M
Structure and Function of the Essential Cell Cycle Regulator Cdc34R01GM128731 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Shaun Olsen · 2019 to 2026
$2.5M
A high performance computing cluster to support structural biologyS10OD036251 · OD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI OLSEN, SHAUN · 2024 to 2024
$572k
NIGMS NIH HHS R01 GM115568NIGMS NIH HHS R01 GM128731NIH HHS S10 OD036251
6 · The paper itself

Abstract

The ubiquitin-proteasome system (UPS) is a central regulator of protein turnover and signaling, with E3 ubiquitin ligases conferring substrate specificity and chain-type control. Recent advances have revealed new mechanistic classes of E3 ligases and expanded our understanding of their roles in disease, including cancer, neurodegeneration, and immune dysfunction. These insights have fueled the development of targeted protein degradation strategies that harness the UPS to eliminate disease-associated proteins. Approaches such as proteolysis-targeting chimeras (PROTACs), molecular glues, and antibody-based degraders are broadening the druggable proteome. Despite this progress, key challenges remain, including limited E3 ligase diversity, difficulties in degrader delivery, and resistance mechanisms. This review outlines recent advances in E3 ligase biology and therapeutic degradation, emphasizing opportunities to expand and refine UPS-targeted interventions.

Indexed as

NeoplasmsNeurodegenerative DiseasesSignal TransductionUbiquitin-Protein LigasesAnimalsHumansProteasome Endopeptidase ComplexProteolysisUbiquitinUbiquitinationProteasome Endopeptidase ComplexUbiquitinUbiquitin-Protein LigasesE3 ubiquitin ligasemolecular gluesPROTACtargeted protein degradationubiquitinubiquitin–proteasome system

Identifiers

PMID40940201
PMCPMC12435903

What OpenQuestion holds

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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.