Evidence map›Paper›PMID 31409866›Full record

ArticleScientific reports2019

Nuclear and cytoplasmic WDR-23 isoforms mediate differential effects on GEN-1 and SKN-1 substrates.

Brett N Spatola, Jacqueline Y Lo, Bin Wang, Sean P Curran

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
    Review
  2. LIN-23 AffectsbioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Food science & nutrition · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. A dicer-related helicase opposes the age-related pathology from SKN-1 activation in ASI neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

4 authors at 2 institutions in 2 countries.

Brett N SpatolaUniversity of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA.
Jacqueline Y LoUniversity of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA.
Bin WangThe University of Dundee, Centre for Gene Expression and Regulation, Dundee, Scotland.
Sean P CurranUniversity of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA. spcurran@usc.edu.
University of Southern California · USUniversity of Dundee · GB

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Characterizing WDR23 in Alzheimer's disease pathologyRF1AG063947 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CURRAN, SEAN P · 2019 to 2019
$2.9M
Age-dependent SKN-1/NRF cytoprotection at the cost of metabolic homeostasisR01AG058610 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CURRAN, SEAN P · 2019 to 2023
$2.1M
Novel roles for Maf1 as a central regulator of lipid homeostasisR01GM109028 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CURRAN, SEAN P · 2014 to 2018
$1.8M
NIA NIH HHS R01 AG058610NIA NIH HHS RF1 AG063947NIGMS NIH HHS R01 GM109028NIH HHS P40 OD010440
6 · The paper itself

Abstract

Maintaining a healthy cellular environment requires the constant control of proteostasis. E3 ubiquitin ligase complexes facilitate the post-translational addition of ubiquitin, which based on the quantity and specific lysine linkages, results in different outcomes. Our studies reveal the CUL4-DDB1 substrate receptor, WDR23, as both a positive and a negative regulator in cellular stress responses. These opposing roles are mediated by two distinct isoforms: WDR-23A in the cytoplasm and WDR-23B in the nucleus. C. elegans expressing only WDR-23A display activation of SKN-1 and enhanced survival to oxidative stress, whereas animals with restricted WDR-23B expression do not. Additionally, we identify GEN-1, a Holliday junction resolvase, as an evolutionarily conserved WDR-23 substrate and find that the nuclear and cytoplasmic isoforms of WDR-23 differentially affect double-strand break repair. Our results suggest that through differential ubiquitination, nuclear WDR-23B inhibits the activity of substrates, most likely by promoting protein turnover, while cytoplasmic WDR-23A performs a proteasome-independent role. Together, our results establish a cooperative role between two spatially distinct isoforms of WDR-23 in ensuring proper regulation of WDR-23 substrates.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell NucleusCytoplasmDNA-Binding ProteinsGene Expression RegulationOxidative StressProteolysisProteostasisRepressor ProteinsSubstrate SpecificityTranscription FactorsUbiquitinationUbiquitin-Protein LigasesCaenorhabditis elegans ProteinsDNA-Binding ProteinsRepressor Proteinsskn-1 protein, C elegansTranscription FactorsUbiquitin-Protein LigasesWDR-23 protein, C elegans

Identifiers

PMID31409866
PMCPMC6692315
OpenAlexW2967043424

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.