Evidence map›Paper›PMID 31231659›Full record

ReviewFrontiers in molecular biosciences2019

Dynamic Regulation of the 26S Proteasome: From Synthesis to Degradation.

Richard S Marshall, Richard D Vierstra

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular biosciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed, 4 pooled it
11.3field-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

137 citing papers in PubMed, 4 syntheses or guidelines pooled it, 238 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Pooled it
  4. Pooled it
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  16. The 19S proteasome as a therapeutic target in hematologic malignancies.Frontiers in cell and developmental biology · 2026
    Review
  17. Combined Transcriptomic and Metabolomic Analyses of the Response ofJournal of fungi (Basel, Switzerland) · 2025
    Article
  18. Article
  19. More 26S and 30S proteasomes are beneficial in proteinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Article

77 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.

Richard S MarshallDepartment of Biology, Washington University in St. Louis, St. Louis, MO, United States.
Richard D VierstraDepartment of Biology, Washington University in St. Louis, St. Louis, MO, United States.
Washington University in St. Louis · US

Funding

Autophagic Clearance of Proteasomes and CDC48 as Models for Amyloidogenic Protein Quality Control.R01GM124452 · NIGMS · WASHINGTON UNIVERSITY · PI JEZ, JOSEPH MARTIN · 2018 to 2025
$2.4M
NIGMS NIH HHS R01 GM124452
6 · The paper itself

Abstract

All eukaryotes rely on selective proteolysis to control the abundance of key regulatory proteins and maintain a healthy and properly functioning proteome. Most of this turnover is catalyzed by the 26S proteasome, an intricate, multi-subunit proteolytic machine. Proteasomes recognize and degrade proteins first marked with one or more chains of poly-ubiquitin, the addition of which is actuated by hundreds of ligases that individually identify appropriate substrates for ubiquitylation. Subsequent proteasomal digestion is essential and influences a myriad of cellular processes in species as diverse as plants, fungi and humans. Importantly, dysfunction of 26S proteasomes is associated with numerous human pathologies and profoundly impacts crop performance, thus making an understanding of proteasome dynamics critically relevant to almost all facets of human health and nutrition. Given this widespread significance, it is not surprising that sophisticated mechanisms have evolved to tightly regulate 26S proteasome assembly, abundance and activity in response to demand, organismal development and stress. These include controls on transcription and chaperone-mediated assembly, influences on proteasome localization and activity by an assortment of binding proteins and post-translational modifications, and ultimately the removal of excess or damaged particles via autophagy. Intriguingly, the autophagic clearance of damaged 26S proteasomes first involves their modification with ubiquitin, thus connecting ubiquitylation and autophagy as key regulatory events in proteasome quality control. This turnover is also influenced by two distinct biomolecular condensates that coalesce in the cytoplasm, one attracting damaged proteasomes for autophagy, and the other reversibly storing proteasomes during carbon starvation to protect them from autophagic clearance. In this review, we describe the current state of knowledge regarding the dynamic regulation of 26S proteasomes at all stages of their life cycle, illustrating how protein degradation through this proteolytic machine is tightly controlled to ensure optimal growth, development and longevity.

Indexed as

assemblyautophagydegradationproteaphagyproteasomeproteolysisproteostasisubiquitin

Identifiers

PMID31231659
PMCPMC6568242
OpenAlexW2954094168

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.