Evidence map›Paper›PMID 22122465›Full record

ReviewCurrent molecular pharmacology2012

Targeting DNA polymerase ß for therapeutic intervention.

Eva M Goellner, David Svilar, Karen H Almeida, Robert W Sobol

Abstract readReview
In one paragraph

Review in Current molecular pharmacology, 2012. 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
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Protein Domain Specific Covalent Inhibition of Human DNA Polymerase β.Chembiochem : a European journal of chemical biology · 2021
    Article
  7. Selective Inhibition of DNA Polymerase β by a Covalent Inhibitor.Journal of the American Chemical Society · 2021
    Article
  8. Article
  9. CREBBP and p300 lysine acetyl transferases in the DNA damage response.Cellular and molecular life sciences : CMLS · 2018
    Review
  10. Article
  11. Article
  12. 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

4 authors at 1 institution in 1 country.

Eva M GoellnerDepartment of Pharmacology & Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213-1863, USA.
David Svilar
Karen H Almeida
Robert W Sobol
University of Pittsburgh · US

Funding

UNDERGRADUATE RESEARCH AND SEMINARSP20RR016457 · NCRR · UNIVERSITY OF RHODE ISLAND · PI SHAKARIAN, ALISON M · 2001 to 2011
$35.5M
Novel approaches to enhance tumor cell cytotoxicity of alkylating agentsR01CA148629 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SOBOL, ROBERT W · 2010 to 2021
$3.4M
DNA repair deficient cells for analysisR44GM087798 · NIGMS · TREVIGEN, INC. · PI GEORGE, JAY, SOBOL, ROBERT W · 2010 to 2011
$2.5M
DNA repair deficient human cells for genomic variation analysisR43GM087798 · NIGMS · TREVIGEN, INC. · PI GEORGE, JAY, SOBOL, ROBERT W · 2009 to 2009
$200k
NCI NIH HHS CA148629NCI NIH HHS R01 CA148629NCRR NIH HHS P20 RR016457NCRR NIH HHS P20RR016457NIGMS NIH HHS GM087798NIGMS NIH HHS R43 GM087798NIGMS NIH HHS R44 GM087798
6 · The paper itself

Abstract

DNA damage plays a causal role in numerous disease processes. Hence, it is suggested that DNA repair proteins, which maintain the integrity of the nuclear and mitochondrial genomes, play a critical role in reducing the onset of multiple diseases, including cancer, diabetes and neurodegeneration. As the primary DNA polymerase involved in base excision repair, DNA polymerase ß (Polß) has been implicated in multiple cellular processes, including genome maintenance and telomere processing and is suggested to play a role in oncogenic transformation, cell viability following stress and the cellular response to radiation, chemotherapy and environmental genotoxicants. Therefore, Polß inhibitors may prove to be effective in cancer treatment. However, Polß has a complex and highly regulated role in DNA metabolism. This complicates the development of effective Polß-specific inhibitors useful for improving chemotherapy and radiation response without impacting normal cellular function. With multiple enzymatic activities, numerous binding partners and complex modes of regulation from post-translational modifications, there are many opportunities for Polß inhibition that have yet to be resolved. To shed light on the varying possibilities and approaches of targeting Polß for potential therapeutic intervention, we summarize the reported small molecule inhibitors of Polß and discuss the genetic, biochemical and chemical studies that implicate additional options for Polß inhibition. Further, we offer suggestions on possible inhibitor combinatorial approaches and the potential for tumor specificity for Polß-inhibitors.

Indexed as

Biological ProductsDNA Polymerase betaDNA RepairEnzyme InhibitorsHumansMutationNeoplasmsProtein Processing, Post-TranslationalBiological ProductsDNA Polymerase betaEnzyme Inhibitors

Identifiers

PMID22122465
PMCPMC3894524
OpenAlexW2040212747

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.