Evidence map›Paper›PMID 19586908›Full record

ArticleThe Journal of biological chemistry2009

Checkpoint kinase ATR promotes nucleotide excision repair of UV-induced DNA damage via physical interaction with xeroderma pigmentosum group A.

Steven M Shell, Zhengke Li, Nikolozi Shkriabai, Mamuka Kvaratskhelia, Chris Brosey, Moises A Serrano, Walter J Chazin, Phillip R Musich, Yue Zou

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

51 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. ATR prevents CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  11. XPA: DNA Repair Protein of Significant Clinical Importance.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Progerin sequestration of PCNA promotes replication fork collapse and mislocalization of XPA in laminopathy-related progeroid syndromes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  19. Article
  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

9 authors at 3 institutions in 1 country.

Steven M ShellDepartment of Biochemistry and Molecular Biology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614, USA.
Zhengke Li
Nikolozi Shkriabai
Mamuka Kvaratskhelia
Chris Brosey
Moises A Serrano
Walter J Chazin
Phillip R Musich
Yue Zou
East Tennessee State University · USThe Ohio State University · USVanderbilt University · US

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
MOLECULAR BIOPHYSICS TRAINING PROGRAM AT VANDERBILTT32GM008320 · NIGMS · VANDERBILT UNIVERSITY · PI CHAZIN, WALTER J. · 1989 to 2023
$7.9M
Structural Basis for RPA Functions in DNA ProcessingR01GM065484 · NIGMS · VANDERBILT UNIVERSITY · PI CHAZIN, WALTER J. · 2003 to 2015
$3.9M
RECOGNITION AND REPAIR OF UV DAMAGE TO HUMAN DNAR01CA086927 · NCI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ZOU, YUE · 2000 to 2011
$2.2M
HIV-1 Integrase Structure and Function as a Therapeutic TargetK02AI077341 · NIAID · OHIO STATE UNIVERSITY · PI KVARATSKHELIA, MAMUKA · 2008 to 2012
$593k
Checkpoint Signaling and Repair of UV Damage to Human DNAR56CA086927 · NCI · EAST TENNESSEE STATE UNIVERSITY · PI ZOU, YUE · 2007 to 2007
$231k
Mechanism of Nuclear Defects in Hutchinson-Gilford Progeria SyndromeR03AG031503 · NIA · EAST TENNESSEE STATE UNIVERSITY · PI ZOU, YUE · 2008 to 2009
$117k
NCI NIH HHS CA092584NCI NIH HHS CA86927NCI NIH HHS P01 CA092584NCI NIH HHS R01 CA086927NCI NIH HHS R56 CA086927NIAID NIH HHS AI077341NIAID NIH HHS K02 AI077341NIA NIH HHS AG031503NIA NIH HHS R03 AG031503NIGMS NIH HHS GM065484NIGMS NIH HHS R01 GM065484NIGMS NIH HHS T32 GM008320
6 · The paper itself

Abstract

In response to DNA damage, eukaryotic cells activate a series of DNA damage-dependent pathways that serve to arrest cell cycle progression and remove DNA damage. Coordination of cell cycle arrest and damage repair is critical for maintenance of genomic stability. However, this process is still poorly understood. Nucleotide excision repair (NER) and the ATR-dependent cell cycle checkpoint are the major pathways responsible for repair of UV-induced DNA damage. Here we show that ATR physically interacts with the NER factor Xeroderma pigmentosum group A (XPA). Using a mass spectrometry-based protein footprinting method, we found that ATR interacts with a helix-turn-helix motif in the minimal DNA-binding domain of XPA where an ATR phosphorylation site (serine 196) is located. XPA-deficient cells complemented with XPA containing a point mutation of S196A displayed a reduced repair efficiency of cyclobutane pyrimidine dimers as compared with cells complemented with wild-type XPA, although no effect was observed for repair of (6-4) photoproducts. This suggests that the ATR-dependent phosphorylation of XPA may promote NER repair of persistent DNA damage. In addition, a K188A point mutation of XPA that disrupts the ATR-XPA interaction inhibits the nuclear import of XPA after UV irradiation and, thus, significantly reduced DNA repair efficiency. By contrast, the S196A mutation has no effect on XPA nuclear translocation. Taken together, our results suggest that the ATR-XPA interaction mediated by the helix-turn-helix motif of XPA plays an important role in DNA-damage responses to promote cell survival and genomic stability after UV irradiation.

Indexed as

Ultraviolet RaysActive Transport, Cell NucleusAmino Acid MotifsAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineCell NucleusCell SurvivalDNA DamageDNA RepairHumansMass SpectrometryPhosphorylationPoint MutationProtein BindingAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsProtein Serine-Threonine KinasesXeroderma Pigmentosum Group A ProteinXPA protein, human

Identifiers

PMID19586908
PMCPMC2782015
OpenAlexW1967049460

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.