Evidence map›Paper›PMID 31887540›Full record

ArticleDNA repair2020

The splicing component ISY1 regulates APE1 in base excision repair.

Aruna S Jaiswal, Elizabeth A Williamson, Gayathri Srinivasan, Kimi Kong, Carrie L Lomelino, Robert McKenna, Christi Walter, Patrick Sung, Satya Narayan, Robert Hromas

Open access · hybridAbstract read
In one paragraph

Article in DNA repair, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Nanoscale Interaction of Endonuclease APE1 with DNA.International journal of molecular sciences · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. In Vitro Reconstitutive Base Excision Repair (BER) Assay.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  12. 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

10 authors at 3 institutions in 1 country.

Aruna S JaiswalDivision of Hematology and Medical Oncology, Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229 United States. Electronic address: jaiswala@uthscsa.edu.
Elizabeth A WilliamsonDivision of Hematology and Medical Oncology, Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229 United States.
Gayathri SrinivasanDivision of Hematology and Medical Oncology, Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229 United States.
Kimi KongDivision of Hematology and Medical Oncology, Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229 United States.
Carrie L LomelinoDepartment of Biochemistry and Molecular Biology, University of Florida Health, Gainesville, FL 32610 United States.
Robert McKennaDepartment of Biochemistry and Molecular Biology, University of Florida Health, Gainesville, FL 32610 United States.
Christi WalterDepartment of Cell Systems and Anatomy, University of Texas Health Science Center, San Antonio, TX 78229 United States.
Patrick SungDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center Department of Molecular Biophysics and Biochemistry, Yale School of Medicine, New Haven, CT 06520 San Antonio, TX 78229 United States.
Satya NarayanDepartment of Anatomy and Cell Biology, University of Florida, Gainesville, FL 32610 United States.
Robert HromasDivision of Hematology and Medical Oncology, Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229 United States. Electronic address: hromas@uthscsa.edu.
The University of Texas Health Science Center at San Antonio · USUniversity of Florida Health · USUniversity of Florida · US

Funding

EEPD1 Repair of Stressed Replication ForksR01CA205224 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Robert A Hromas · 2016 to 2026
$3.3M
EPIGENETIC CONTROL OF NHEJ DNA REPAIRR01CA139429 · NCI · UNIVERSITY OF NEW MEXICO · PI HROMAS, ROBERT A · 2010 to 2014
$1.5M
Biomarkers For BRCA1-Deficient CancersR01CA279971 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Kimi Y Kong · 2024 to 2026
$1.3M
Genome Maintenance via the BRCA-PALB2 Tumor Suppressor NetworkR01CA220123 · NCI · YALE UNIVERSITY · PI SUNG, PATRICK · 2017 to 2019
$1.2M
Mechanisms for Chromosomal TranslocationsR01GM109645 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HROMAS, ROBERT A · 2015 to 2018
$1.2M
NCI NIH HHS R01 CA139429NCI NIH HHS R01 CA205224NCI NIH HHS R01 CA220123NCI NIH HHS R01 CA279971NIGMS NIH HHS R01 GM109645
6 · The paper itself

Abstract

The integrity of cellular genome is continuously challenged by endogenous and exogenous DNA damaging agents. If DNA damage is not removed in a timely fashion the replisome may stall at DNA lesions, causing fork collapse and genetic instability. Base excision DNA repair (BER) is the most important pathway for the removal of oxidized or mono-alkylated DNA. While the main components of the BER pathway are well defined, its regulatory mechanism is not yet understood. We report here that the splicing factor ISY1 enhances apurinic/apyrimidinic endonuclease 1 (APE1) activity, the multifunctional enzyme in BER, by promoting its 5'-3' endonuclease activity. ISY1 expression is induced by oxidative damage, which would provide an immediate up-regulation of APE1 activity in vivo and enhance BER of oxidized bases. We further found that APE1 and ISY1 interact, and ISY1 enhances the ability of APE1 to recognize abasic sites in DNA. Using purified recombinant proteins, we reconstituted BER and demonstrated that ISY1 markedly promoted APE1 activity in both the short- and long-patch BER pathways. Our study identified ISY1 as a regulator of the BER pathway, which would be of physiological relevance where suboptimal levels of APE1 are present. The interaction of ISY1 and APE1 also establishes a connection between DNA damage repair and pre-mRNA splicing.

Indexed as

DNA RepairA549 CellsDNA-(Apurinic or Apyrimidinic Site) LyaseHCT116 CellsHEK293 CellsHumansMCF-7 CellsOxidative StressPC-3 CellsRNA Splicing FactorsSignal TransductionAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseISY1 protein, humanRNA Splicing FactorsAP Endonuclease-1Base excision repairISY1Oxidative stressRNA splicing

Identifiers

PMID31887540
PMCPMC7185567
OpenAlexW2996545990

What OpenQuestion holds

Textmetadata
LicenceTDM
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.