Evidence map›Paper›PMID 22792074›Full record

ArticlePLoS genetics2012

FANCJ/BACH1 acetylation at lysine 1249 regulates the DNA damage response.

Jenny Xie, Min Peng, Shawna Guillemette, Steven Quan, Stephanie Maniatis, Yuliang Wu, Aditya Venkatesh, Scott A Shaffer, Robert M Brosh, Sharon B Cantor

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. The repair geneOncology reviews · 2021
    Article
  6. The Role ofCancers · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. CREBBP and p300 lysine acetyl transferases in the DNA damage response.Cellular and molecular life sciences : CMLS · 2018
    Review
  17. Article
  18. Review
  19. Article
  20. Fork Protection and Therapy Resistance in Hereditary Breast Cancer.Cold Spring Harbor symposia on quantitative biology · 2017
    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 2 institutions in 1 country.

Jenny XieDepartment of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America.
Min Peng
Shawna Guillemette
Steven Quan
Stephanie Maniatis
Yuliang Wu
Aditya Venkatesh
Scott A Shaffer
Robert M Brosh
Sharon B Cantor
University of Massachusetts Chan Medical School · USNational Institutes of Health · US

Funding

Roles Of DNA Helicases In Pathways Required For Maintenance Of Genomic StabilityZIAAG000741 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$7.6M
Model Genetic Systems to Study DNA RepairZIAAG000752 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$4.8M
Fanconi Anemia PathwayZIAAG000753 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$4.3M
BACH1/FANCJ Checkpoint, Recombination, and ChemoresistanceR01CA129514 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CANTOR, SHARON B · 2007 to 2011
$1.6M
NCI NIH HHS CA129514-01A1NCI NIH HHS R01 CA129514
6 · The paper itself

Abstract

BRCA1 promotes DNA repair through interactions with multiple proteins, including CtIP and FANCJ (also known as BRIP1/BACH1). While CtIP facilitates DNA end resection when de-acetylated, the function of FANCJ in repair processing is less well defined. Here, we report that FANCJ is also acetylated. Preventing FANCJ acetylation at lysine 1249 does not interfere with the ability of cells to survive DNA interstrand crosslinks (ICLs). However, resistance is achieved with reduced reliance on recombination. Mechanistically, FANCJ acetylation facilitates DNA end processing required for repair and checkpoint signaling. This conclusion was based on the finding that FANCJ and its acetylation were required for robust RPA foci formation, RPA phosphorylation, and Rad51 foci formation in response to camptothecin (CPT). Furthermore, both preventing and mimicking FANCJ acetylation at lysine 1249 disrupts FANCJ function in checkpoint maintenance. Thus, we propose that the dynamic regulation of FANCJ acetylation is critical for robust DNA damage response, recombination-based processing, and ultimately checkpoint maintenance.

Indexed as

AcetylationBasic-Leucine Zipper Transcription FactorsDNAFanconi Anemia Complementation Group ProteinsBRCA1 ProteinDNA DamageDNA RepairG2 Phase Cell Cycle CheckpointsGene Expression RegulationHEK293 CellsHeLa CellsHistone AcetyltransferasesHomologous RecombinationHumansLysineMutationBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsBRCA1 ProteinBRCA1 protein, humanDNAFanconi Anemia Complementation Group ProteinsHistone AcetyltransferasesLysine

Identifiers

PMID22792074
PMCPMC3390368
OpenAlexW2072756686

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.