Evidence map›Paper›PMID 20662484›Full record

ArticleACS chemical biology2010

Identification of novel small molecule inhibitors of the XPA protein using in silico based screening.

Tracy M Neher, Sarah C Shuck, Jing-Yuan Liu, Jian-Ting Zhang, John J Turchi

Abstract read
In one paragraph

Article in ACS chemical biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Frontiers in oncology · 2022
    Article
  6. Review
  7. Role of Nucleotide Excision Repair in Cisplatin Resistance.International journal of molecular sciences · 2020
    Review
  8. Review
  9. XPA: DNA Repair Protein of Significant Clinical Importance.International journal of molecular sciences · 2020
    Review
  10. Article
  11. Drugging the Cancers Addicted to DNA Repair.Journal of the National Cancer Institute · 2017
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. 14-3-3σ confers cisplatin resistance in esophageal squamous cell carcinoma cells via regulating DNA repair molecules.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  17. Article
  18. Redefining the DNA-binding domain of human XPA.Journal of the American Chemical Society · 2014
    Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Tracy M NeherDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Sarah C Shuck
Jing-Yuan Liu
Jian-Ting Zhang
John J Turchi
Indiana University – Purdue University Indianapolis · US

Funding

Validation of RPA as a Target for Cancer ChemotherapyR01CA082741 · NCI · WRIGHT STATE UNIVERSITY · PI TURCHI, JOHN J. · 2000 to 2011
$2.3M
Role of p170 in lung tumorigenesisR01CA094961 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI ZHANG, JIAN-TING · 2003 to 2007
$1.5M
Development of methodologies for the analysis of DNA repair capacity to predict tR21CA128628 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI TURCHI, JOHN J. · 2008 to 2009
$374k
NCI NIH HHS CA082741NCI NIH HHS CA94961NCI NIH HHS R01 CA082741NCI NIH HHS R01 CA094961NCI NIH HHS R21 CA128628
6 · The paper itself

Abstract

The nucleotide excision repair pathway catalyzes the removal of bulky adduct damage from DNA and requires the activity of more than 30 individual proteins and complexes. A diverse array of damage can be recognized and removed by the NER pathway including UV-induced adducts and intrastrand adducts induced by the chemotherapeutic compound cisplatin. The recognition of DNA damage is complex and involves a series of proteins including the xeroderma pigmentosum group A and C proteins and the UV-damage DNA binding protein. The xeroderma pigmentosum group A protein is unique in the sense that it is required for both transcription coupled and global genomic nucleotide excision repair. In addition, xeroderma pigmentosum group A protein is required for the removal of all types of DNA lesions repaired by nucleotide excision repair. Considering its importance in the damage recognition process, the minimal information available on the mechanism of DNA binding, and the potential that inhibition of xeroderma pigmentosum group A protein could enhance the therapeutic efficacy of platinum based anticancer drugs, we sought to identify and characterize small molecule inhibitors of the DNA binding activity of the xeroderma pigmentosum group A protein. In silico screening of a virtual small molecule library resulted in the identification of a class of molecules confirmed to inhibit the xeroderma pigmentosum group A protein-DNA interaction. Biochemical analysis of inhibition with varying DNA substrates revealed a common mechanism of xeroderma pigmentosum group A protein DNA binding to single-stranded DNA and cisplatin-damaged DNA.

Indexed as

Drug DesignDNADNA RepairFluorescence PolarizationModels, MolecularProtein BindingProtein Structure, TertiarySmall Molecule LibrariesXeroderma Pigmentosum Group A ProteinDNASmall Molecule LibrariesXeroderma Pigmentosum Group A Protein

Identifiers

PMID20662484
PMCPMC2955790
OpenAlexW2011120012

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.