Evidence map›Paper›PMID 19805520›Full record

ArticleMolecular and cellular biology2009

Human SNF5/INI1, a component of the human SWI/SNF chromatin remodeling complex, promotes nucleotide excision repair by influencing ATM recruitment and downstream H2AX phosphorylation.

Alo Ray, Safita N Mir, Gulzar Wani, Qun Zhao, Aruna Battu, Qianzheng Zhu, Qi-En Wang, Altaf A Wani

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

46 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Epigenetic Regulation of Nucleotide Excision Repair.Frontiers in cell and developmental biology · 2022
    Review
  7. Review
  8. Review
  9. Xeroderma Pigmentosum: A Model for Human Premature Aging.The Journal of investigative dermatology · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Alo RayDepartment of Radiology, The Ohio State University, Columbus, OH 43210, USA.
Safita N Mir
Gulzar Wani
Qun Zhao
Aruna Battu
Qianzheng Zhu
Qi-En Wang
Altaf A Wani
The Ohio State University · US

Funding

Cross-talking pre-incision events of eukaryotic NERR01ES012991 · NIEHS · OHIO STATE UNIVERSITY · PI WANI, ALTAF A, ZHU, QIANZHENG · 2004 to 2020
$6.2M
DNA DAMAGE RESPONSES FOLLOWING GENOTOXIN EXPOSURER01ES002388 · NIEHS · OHIO STATE UNIVERSITY · PI WANI, ALTAF A · 1985 to 2016
$4.9M
Repair of Genotoxic Damage in ChromatinR01CA093413 · NCI · OHIO STATE UNIVERSITY · PI WANI, ALTAF A · 2002 to 2011
$3.0M
NCI NIH HHS CA93413NCI NIH HHS R01 CA093413NIEHS NIH HHS ES12991NIEHS NIH HHS ES2388NIEHS NIH HHS R01 ES002388NIEHS NIH HHS R01 ES012991
6 · The paper itself

Abstract

Recent studies have implicated the role of the SWI/SNF ATP-dependent chromatin remodeling complex in nuclear excision repair (NER), but the mechanism of its function has remained elusive. Here, we show that the human SWI/SNF component human SNF5 (hSNF5) interacts with UV damage recognition factor XPC and colocalizes with XPC at the damage site. Inactivation of hSNF5 did not affect the recruitment of XPC but affected the recruitment of ATM checkpoint kinase to the damage site and ATM activation by phosphorylation. Consequently, hSNF5 deficiency resulted in a defect in H2AX and BRCA1 phosphorylation at the damage site. However, recruitment of ATR checkpoint kinase to the damage site was not affected by hSNF5 deficiency, supporting that hSNF5 functions downstream of ATR. Additionally, ATM/ATR-mediated Chk2/Chk1 phosphorylation was not affected in hSNF5-depleted cells in response to UV irradiation, suggesting that the cell cycle checkpoint is intact in these cells. Taken together, the results indicate that the SWI/SNF complex associates with XPC at the damage site and thereby facilitates the access of ATM, which in turn promotes H2AX and BRCA1 phosphorylation. We propose that the SWI/SNF chromatin remodeling function is utilized to increase the DNA accessibility of NER machinery and checkpoint factors at the damage site, which influences NER and ensures genomic integrity.

Indexed as

DNA RepairAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCell CycleCell Cycle ProteinsCell LineCheckpoint Kinase 1Checkpoint Kinase 2Chromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneDNADNA-Binding ProteinsGene DeletionHistonesHumansPhosphorylationAtaxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanBRCA1 ProteinBRCA1 protein, humanCell Cycle ProteinsCheckpoint Kinase 1Checkpoint Kinase 2CHEK1 protein, humanCHEK2 protein, humanChromosomal Proteins, Non-HistoneDNADNA-Binding ProteinsH2AX protein, humanHistonesProtein KinasesProtein Serine-Threonine KinasesSMARCB1 ProteinSMARCB1 protein, humanTranscription FactorsTumor Suppressor ProteinsXPC protein, human

Identifiers

PMID19805520
PMCPMC2786693
OpenAlexW2107747328

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.