Evidence map›Paper›PMID 30487218›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

SUMOylation of PCNA by PIAS1 and PIAS4 promotes template switch in the chicken and human B cell lines.

Mohiuddin Mohiuddin, Terry John Evans, Md Maminur Rahman, Islam Shamima Keka, Masataka Tsuda, Hiroyuki Sasanuma, Shunichi Takeda

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. The aflatoxin BNAR cancer · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. SUMO and the DNA damage response.Biochemical Society transactions · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Fast friends - Ubiquitin-like modifiers as engineered fusion partners.Seminars in cell & developmental biology · 2022
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 1 institution in 1 country.

Mohiuddin MohiuddinDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, 606-8501 Kyoto, Japan.
Terry John EvansDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, 606-8501 Kyoto, Japan.
Md Maminur RahmanDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, 606-8501 Kyoto, Japan.
Islam Shamima KekaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, 606-8501 Kyoto, Japan.
Masataka TsudaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, 606-8501 Kyoto, Japan.
Hiroyuki SasanumaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, 606-8501 Kyoto, Japan.
Shunichi TakedaDepartment of Radiation Genetics, Graduate School of Medicine, Kyoto University, 606-8501 Kyoto, Japan stakeda@rg.med.kyoto-u.ac.jp.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage tolerance (DDT) releases replication blockage caused by damaged nucleotides on template strands employing two alternative pathways, error-prone translesion DNA synthesis (TLS) and error-free template switch (TS). Lys164 of proliferating cell nuclear antigen (PCNA) is SUMOylated during the physiological cell cycle. To explore the role for SUMOylation of PCNA in DDT, we characterized chicken DT40 and human TK6 B cells deficient in the PIAS1 and PIAS4 small ubiquitin-like modifier (SUMO) E3 ligases. DT40 cells have a unique advantage in the phenotypic analysis of DDT as they continuously diversify their immunoglobulin (Ig) variable genes by TLS and TS [Ig gene conversion (GC)], both relieving replication blocks at abasic sites without accompanying by DNA breakage. Remarkably,

Indexed as

AnimalsB-LymphocytesCell CycleCell LineChickensDNA DamageDNA RepairDNA ReplicationGene ConversionGenes, ImmunoglobulinHumansImmunoglobulin Variable RegionPoly-ADP-Ribose Binding ProteinsProliferating Cell Nuclear AntigenProtein Inhibitors of Activated STATSumoylationImmunoglobulin Variable RegionPoly-ADP-Ribose Binding ProteinsProliferating Cell Nuclear AntigenProtein Inhibitors of Activated STATUbiquitin-Protein LigasesPCNAPIAS1PIAS4SUMOylationtemplate switching (TS)

Identifiers

PMID30487218
PMCPMC6294928
OpenAlexW2902299815

What OpenQuestion holds

Textmetadata
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.