Evidence map›Paper›PMID 20022886›Full record

ArticleHuman molecular genetics2010

FANCC suppresses short telomere-initiated telomere sister chromatid exchange.

David B Rhee, Yisong Wang, Melissa Mizesko, Fang Zhou, Laura Haneline, Yie Liu

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  7. FANCM, BRCA1, and BLM cooperatively resolve the replication stress at the ALT telomeres.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  8. Review
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  13. Short telomeres: from dyskeratosis congenita to sporadic aplastic anemia and malignancy.Translational research : the journal of laboratory and clinical medicine · 2013
    Review
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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

6 authors at 3 institutions in 1 country.

David B RheeLaboratory of Molecular Gerontology, NIH Biomedical Research Center, National Institute on Aging, Baltimore, MD 21224-6825, USA.
Yisong Wang
Melissa Mizesko
Fang Zhou
Laura Haneline
Yie Liu
National Institute on Aging · USIndiana University School of MedicineOak Ridge National Laboratory · US

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Jun Wan · 1999 to 2026
$59.3M
REGULATION OF HEMATOPOIETIC CELL PRODUCTIONT32DK007519 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 1986 to 2020
$7.1M
Role of ASK1 and PKR in Fancc hematopoiesisR01HL077175 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI HANELINE, LAURA S · 2005 to 2009
$1.5M
Telomere attrition in premature aging syndromesZIAAG000748 · NIA · NATIONAL INSTITUTE ON AGING · PI LIU, YIE · 2009 to 2011
$815k
Intramural NIH HHSNCI NIH HHS P30 CA82709NHLBI NIH HHS R01 HL077175NIDDK NIH HHS T32 DK07519
6 · The paper itself

Abstract

Telomere shortening has been linked to rare human disorders that present with bone marrow failure including Fanconi anemia (FA). FANCC is one of the most commonly mutated FA genes in FA patients and the FANCC subtype tends to have a relatively early onset of bone marrow failure and hematologic malignancies. Here, we studied the role of Fancc in telomere length regulation in mice. Deletion of Fancc (Fancc(-/-)) did not affect telomerase activity, telomere length or telomeric end-capping in a mouse strain possessing intrinsically long telomeres. However, ablation of Fancc did exacerbate telomere attrition when murine bone marrow cells experienced high cell turnover after serial transplantation. When Fancc(-/-) mice were crossed into a telomerase reverse transcriptase heterozygous or null background (Tert(+/-) or Tert(-/-)) with short telomeres, Fancc deficiency led to an increase in the incidence of telomere sister chromatid exchange. In contrast, these phenotypes were not observed in Tert mutant mice with long telomeres. Our data indicate that Fancc deficiency accelerates telomere shortening during high turnover of hematopoietic cells and promotes telomere recombination initiated by short telomeres.

Indexed as

AnimalsBone Marrow CellsFanconi AnemiaFanconi Anemia Complementation Group C ProteinMiceMice, KnockoutSister Chromatid ExchangeTelomeraseTelomereFancc protein, mouseFanconi Anemia Complementation Group C ProteinTelomeraseTert protein, mouse

Identifiers

PMID20022886
PMCPMC2816614
OpenAlexW2143005627

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.