Evidence map›Paper›PMID 22645362›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Homologous chromosomes make contact at the sites of double-strand breaks in genes in somatic G0/G1-phase human cells.

Manoj Gandhi, Viktoria N Evdokimova, Karen T Cuenco, Marina N Nikiforova, Lindsey M Kelly, James R Stringer, Christopher J Bakkenist, Yuri E Nikiforov

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Mitotic Antipairing of Homologous Chromosomes.Results and problems in cell differentiation · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Mitotic antipairing of homologous and sex chromosomes via spatial restriction of two haploid sets.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Article
  14. The Nucleolus: In Genome Maintenance and Repair.International journal of molecular sciences · 2017
    Review
  15. Article
  16. Article
  17. Article
  18. Pairing and anti-pairing: a balancing act in the diploid genome.Current opinion in genetics & development · 2016
    Review
  19. Review
  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

8 authors at 3 institutions in 2 countries.

Manoj GandhiDepartment of Pathology and Laboratory Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Viktoria N Evdokimova
Karen T Cuenco
Marina N Nikiforova
Lindsey M Kelly
James R Stringer
Christopher J Bakkenist
Yuri E Nikiforov
University of Pittsburgh · USUniversity of Cincinnati · USUniversity of Dental Medicine · MM

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
Mechanisms of RET/PTC rearrangements in thyroid cancerR01CA088041 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NIKIFOROV, YURI E · 2001 to 2017
$3.8M
Regulation of DNA replication fork progression by ATM kinase activityR01CA148644 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAKKENIST, CHRISTOPHER J. · 2011 to 2015
$1.3M
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA088041NCI NIH HHS R01 CA148644NCI NIH HHS R01 CA88041
6 · The paper itself

Abstract

Double-strand DNA breaks (DSBs) are continuously induced in cells by endogenously generated free radicals and exogenous genotoxic agents such as ionizing radiation. DSBs activate the kinase activity in sensor proteins such as ATM and DNA-PK, initiating a complex DNA damage response that coordinates various DNA repair pathways to restore genomic integrity. In this study, we report the unexpected finding that homologous chromosomes contact each other at the sites of DSBs induced by either radiation or the endonuclease I-PpoI in human somatic cells. Contact involves short segments of homologous chromosomes and is centered on a DSB in active genes but does not occur at I-PpoI sites in intergenic DNA. I-PpoI-induced contact between homologous genes is abrogated by the transcriptional inhibitors actinomycin D and α-amanitin and requires the kinase activity of ATM but not DNA-PK. Our findings provide documentation of a common transcription-related and ATM kinase-dependent mechanism that induces contact between allelic regions of homologous chromosomes at sites of DSBs in human somatic cells.

Indexed as

Chromosomes, HumanDNA DamageG1 PhaseResting Phase, Cell CycleAlpha-AmanitinAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCells, CulturedDactinomycinDNA-Activated Protein KinaseDNA-Binding ProteinsHumansIn Situ Hybridization, FluorescenceProtein Serine-Threonine KinasesRadiation, IonizingTranscription, GeneticAlpha-AmanitinAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDactinomycinDNA-Activated Protein KinaseDNA-Binding ProteinsProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID22645362
PMCPMC3386068
OpenAlexW2092128195

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.