Evidence map›Paper›PMID 32591648›Full record

ReviewExperimental & molecular medicine2020

SUMO and cellular adaptive mechanisms.

Hong-Yeoul Ryu, Seong Hoon Ahn, Mark Hochstrasser

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Synthesizing Defined Ubiquitin-Modified SUMO Dimers.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  14. Review
  15. Article
  16. The SUMO Pathway.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  17. Article
  18. Review
  19. Article
  20. Biological resilience in health and disease.Disease models & mechanisms · 2024
    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

3 authors at 3 institutions in 2 countries.

Hong-Yeoul RyuSchool of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of National Sciences, Kyungpook National University, Daegu, 41566, Republic of Korea.
Seong Hoon AhnDepartment of Molecular and Life Science, College of Science and Convergence Technology, Hanyang University, Ansan, 15588, Republic of Korea.
Mark HochstrasserDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, 06520, USA. mark.hochstrasser@yale.edu.ORCID http://orcid.org/0000-0002-1131-5484
Hanyang University · KRKyungpook National University · KRYale University · US

Funding

Mechanisms of Cell Regulation and Manipulation by the Ubiquitin SystemR35GM136325 · NIGMS · YALE UNIVERSITY · PI Mark W Hochstrasser · 2020 to 2026
$6.5M
FUNCTIONS AND MECHANISMS OF DEUBIQUITINATING ENZYMESR01GM053756 · NIGMS · YALE UNIVERSITY · PI HOCHSTRASSER, MARK W · 1996 to 2019
$6.5M
National Research Foundation of Korea (NRF) 2020R1C1C1009367National Research Foundation of Korea (NRF) NRF-2016R1A2B2008217NIGMS NIH HHS R01 GM053756NIGMS NIH HHS R35 GM136325U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) GM053756
6 · The paper itself

Abstract

The ubiquitin family member SUMO is a covalent regulator of proteins that functions in response to various stresses, and defects in SUMO-protein conjugation or deconjugation have been implicated in multiple diseases. The loss of the Ulp2 SUMO protease, which reverses SUMO-protein modifications, in the model eukaryote Saccharomyces cerevisiae is severely detrimental to cell fitness and has emerged as a useful model for studying how cells adapt to SUMO system dysfunction. Both short-term and long-term adaptive mechanisms are triggered depending on the length of time cells spend without this SUMO chain-cleaving enzyme. Such short-term adaptations include a highly specific multichromosome aneuploidy and large changes in ribosomal gene transcription. While aneuploid ulp2Δ cells survive, they suffer severe defects in growth and stress resistance. Over many generations, euploidy is restored, transcriptional programs are adjusted, and specific genetic changes that compensate for the loss of the SUMO protease are observed. These long-term adapted cells grow at normal rates with no detectable defects in stress resistance. In this review, we examine the connections between SUMO and cellular adaptive mechanisms more broadly.

Indexed as

AneuploidyAnimalsHumansSUMO-1 ProteinSUMO-1 Protein

Identifiers

PMID32591648
PMCPMC7338444
OpenAlexW3037748774

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.