Evidence map›Paper›PMID 30867233›Full record

ReviewPharmacological reviews2019

A Practical Review of Proteasome Pharmacology.

Tiffany A Thibaudeau, David M Smith

Open access · hybridAbstract readReview
In one paragraph

Review in Pharmacological reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 2 pooled it
15.9field-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

193 citing papers in PubMed, 2 syntheses or guidelines pooled it, 340 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Preclinical evaluation of ixazomib for high-risk pediatric brain tumors.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

133 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

2 authors at 1 institution in 1 country.

Tiffany A ThibaudeauDepartment of Biochemistry, West Virginia University School of Medicine, Morgantown, West Virginia.
David M SmithDepartment of Biochemistry, West Virginia University School of Medicine, Morgantown, West Virginia dmsmith@hsc.wvu.edu.
West Virginia University · US

Funding

Training Program In Lung SciencesT32HL076139 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAREN M RIDGE, Jacob I Sznajder · 2004 to 2026
$9.6M
Mechanisms regulating proteasomal substrate degradationR01GM107129 · NIGMS · WEST VIRGINIA UNIVERSITY · PI SMITH, DAVID MATTHEW · 2014 to 2022
$2.7M
NHLBI NIH HHS T32 HL076139NIGMS NIH HHS R01 GM107129
6 · The paper itself

Abstract

The ubiquitin proteasome system (UPS) degrades individual proteins in a highly regulated fashion and is responsible for the degradation of misfolded, damaged, or unneeded cellular proteins. During the past 20 years, investigators have established a critical role for the UPS in essentially every cellular process, including cell cycle progression, transcriptional regulation, genome integrity, apoptosis, immune responses, and neuronal plasticity. At the center of the UPS is the proteasome, a large and complex molecular machine containing a multicatalytic protease complex. When the efficiency of this proteostasis system is perturbed, misfolded and damaged protein aggregates can accumulate to toxic levels and cause neuronal dysfunction, which may underlie many neurodegenerative diseases. In addition, many cancers rely on robust proteasome activity for degrading tumor suppressors and cell cycle checkpoint inhibitors necessary for rapid cell division. Thus, proteasome inhibitors have proven clinically useful to treat some types of cancer, especially multiple myeloma. Numerous cellular processes rely on finely tuned proteasome function, making it a crucial target for future therapeutic intervention in many diseases, including neurodegenerative diseases, cystic fibrosis, atherosclerosis, autoimmune diseases, diabetes, and cancer. In this review, we discuss the structure and function of the proteasome, the mechanisms of action of different proteasome inhibitors, various techniques to evaluate proteasome function in vitro and in vivo, proteasome inhibitors in preclinical and clinical development, and the feasibility for pharmacological activation of the proteasome to potentially treat neurodegenerative disease.

Indexed as

AnimalsApoptosisDrug DevelopmentDrug Evaluation, PreclinicalHumansNeoplasmsNeurodegenerative DiseasesProteasome Endopeptidase ComplexProteasome InhibitorsProteasome Endopeptidase ComplexProteasome Inhibitors

Identifiers

PMID30867233
PMCPMC6423620
OpenAlexW2921234630

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.