Evidence map›Paper›PMID 30705092›Full record

ArticleThe Journal of biological chemistry2019

Endonuclease and redox activities of human apurinic/apyrimidinic endonuclease 1 have distinctive and essential functions in IgA class switch recombination.

Barbara Frossi, Giulia Antoniali, Kefei Yu, Nahid Akhtar, Mark H Kaplan, Mark R Kelley, Gianluca Tell, Carlo E M Pucillo

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Nanoscale Interaction of Endonuclease APE1 with DNA.International journal of molecular sciences · 2024
    Article
  4. The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024
    Review
  5. A Novel HypomorphicAntioxidants & redox signaling · 2023
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Endogenous oxidized DNA bases and APE1 regulate the formation of G-quadruplex structures in the genome.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Article
  14. Review
  15. Article
  16. 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

8 authors.

Barbara FrossiFrom the Laboratory of Immunology, Department of Medicine, University of Udine, 33100 Udine, Italy.
Giulia Antonialithe Laboratory of Molecular Biology and DNA Repair, Department of Medicine, University of Udine, 33100 Udine, Italy.
Kefei Yuthe Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan 48824, and.ORCID 0000-0002-3870-2812
Nahid Akhtarthe Herman B. Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Mark H Kaplanthe Herman B. Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana 46202.ORCID 0000-0002-2923-8245
Mark R Kelleythe Herman B. Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Gianluca Tellthe Laboratory of Molecular Biology and DNA Repair, Department of Medicine, University of Udine, 33100 Udine, Italy, gianluca.tell@uniud.it.ORCID 0000-0001-8845-6448
Carlo E M PucilloFrom the Laboratory of Immunology, Department of Medicine, University of Udine, 33100 Udine, Italy, carlo.pucillo@uniud.it.

Funding

Novel Role of Ref-1 in Pancreatic Cancer Etiology and ProgressionR01CA167291 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI FISHEL, MELISSA L., KELLEY, MARK R. · 2013 to 2022
$5.2M
(PQ9)Mechanistic Role of APE1 and BER in chemotherapy-induced peripheral neuropathyR01CA205166 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI FEHRENBACHER, JILL C, KELLEY, MARK R. · 2017 to 2021
$2.7M
NCI NIH HHS R01 CA167291NCI NIH HHS R01 CA205166
6 · The paper itself

Abstract

The base excision repair (BER) pathway is an important DNA repair pathway and is essential for immune responses. In fact, it regulates both the antigen-stimulated somatic hypermutation (SHM) process and plays a central function in the process of class switch recombination (CSR). For both processes, a central role for apurinic/apyrimidinic endonuclease 1 (APE1) has been demonstrated. APE1 acts also as a master regulator of gene expression through its redox activity. APE1's redox activity stimulates the DNA-binding activity of several transcription factors, including NF-κB and a few others involved in inflammation and in immune responses. Therefore, it is possible that APE1 has a role in regulating the CSR through its function as a redox coactivator. The present study was undertaken to address this question. Using the CSR-competent mouse B-cell line CH12F3 and a combination of specific inhibitors of APE1's redox (APX3330) and repair (compound 3) activities, APE1-deficient or -reconstituted cell lines expressing redox-deficient or endonuclease-deficient proteins, and APX3330-treated mice, we determined the contributions of both endonuclease and redox functions of APE1 in CSR. We found that APE1's endonuclease activity is essential for IgA-class switch recombination. We provide evidence that the redox function of APE1 appears to play a role in regulating CSR through the interleukin-6 signaling pathway and in proper IgA expression. Our results shed light on APE1's redox function in the control of cancer growth through modulation of the IgA CSR process.

Indexed as

Immunoglobulin Class SwitchingAnimalsB-LymphocytesCell LineDNA-(Apurinic or Apyrimidinic Site) LyaseDNA RepairHumansImmunoglobulin AInterleukin-6MiceMice, Inbred C57BLOxidation-ReductionSignal TransductionAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseImmunoglobulin AInterleukin-6apurinic/apyrimidinic endonuclease 1 (APE1)base excision repair (BER)class switch recombinationDNA endonucleaseDNA transcriptionimmunoglobulin A (IgA)immunologyredox-inhibitor

Identifiers

PMID30705092
PMCPMC6442068

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Registered trials

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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.