Evidence map›Paper›PMID 24805847›Full record

ArticlePloS one2014

Characterization of ubiquitin-activating enzyme Uba1 in the nucleus by its mammalian temperature-sensitive mutant.

Kimihiko Sugaya, Yoshie Ishihara, Sonoe Inoue, Hideo Tsuji

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Cell autonomous inflammation in VEXAS is mediated by cGAS-STING.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Insights in Post-Translational Modifications: Ubiquitin and SUMO.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Quantitative proteomic analyses of mammary organoids reveals distinct signatures after exposure to environmental chemicals.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Review
  12. Review
  13. 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 1 institution in 1 country.

Kimihiko SugayaResearch Center for Radiation Protection, National Institute of Radiological Sciences, Chiba, Japan; Fukushima Project Headquarters, National Institute of Radiological Sciences, Chiba, Japan.
Yoshie IshiharaResearch Center for Radiation Protection, National Institute of Radiological Sciences, Chiba, Japan; Fukushima Project Headquarters, National Institute of Radiological Sciences, Chiba, Japan.
Sonoe InoueResearch Center for Radiation Protection, National Institute of Radiological Sciences, Chiba, Japan; Fukushima Project Headquarters, National Institute of Radiological Sciences, Chiba, Japan.
Hideo TsujiFukushima Project Headquarters, National Institute of Radiological Sciences, Chiba, Japan.
Chiba Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Temperature-sensitive (ts) CHO-K1 mutant tsTM3 exhibits chromosomal instability and cell-cycle arrest in the S to G2 phases with decreased DNA synthesis at the nonpermissive temperature, 39°C. Previously, complementation tests with other mutants showed that tsTM3 harbors a genetic defect in the ubiquitin-activating enzyme Uba1. Sequence comparison of the Uba1 gene between wild-type and mutant cells in this study revealed that the mutant phenotype is caused by a G-to-A transition that yields a Met-to-Ile substitution at position 256 in hamster Uba1. The ts defects in tsTM3 were complemented by expression of the wild-type Uba1 tagged with green fluorescent protein. Expression of the Uba1 primarily in the nucleus appeared to rescue tsTM3 cells. Incubation at 39°C resulted in a decrease of nuclear Uba1 in tsTM3 cells, suggesting that loss of Uba1 in the nucleus may lead to the ts defects. Analyses with the fluorescent ubiquitination-based cell cycle indicator revealed that loss of function of Uba1 leads to failure of the ubiquitin system in the nucleus. Incubation at 39°C caused an increase in endogenous geminin in tsTM3 cells. A ts mutation of Uba1 found in tsTM3 cells appears to be a novel mutation reflecting the important roles of Uba1 in nucleus.

Indexed as

MutationAnimalsCell NucleusCHO CellsCricetinaeCricetulusTemperatureUbiquitin-Activating EnzymesUbiquitin-Activating Enzymes

Identifiers

PMID24805847
PMCPMC4013028
OpenAlexW2076064289

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.