Evidence map›Paper›PMID 20479226›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Telomere length is inherited with resetting of the telomere set-point.

Y Jeffrey Chiang, Rodrigo T Calado, Karen S Hathcock, Peter M Lansdorp, Neal S Young, Richard J Hodes

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Article
  6. Humanization of the mouseResearch square · 2024
    Article
  7. Review
  8. Review
  9. Article
  10. Transient induction of telomerase expression mediates senescence and reduces tumorigenesis in primary fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  11. Telomeres in Interstitial Lung Disease: The Short and the Long of It.Annals of the American Thoracic Society · 2019
    Review
  12. Article
  13. Article
  14. Premature Physiologic Aging as a Paradigm for Understanding Increased Risk of Adverse Health Across the Lifespan of Survivors of Childhood Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018
    Review
  15. Article
  16. Article
  17. Review
  18. Article
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  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

6 authors at 4 institutions in 3 countries.

Y Jeffrey ChiangExperimental Immunology Branch, National Cancer Institute, Hematology Branch, National Heart, Lung and Blood Institute, and National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA. chiangj@mail.nih.gov
Rodrigo T Calado
Karen S Hathcock
Peter M Lansdorp
Neal S Young
Richard J Hodes
National Cancer Institute · MYNational Heart Lung and Blood Institute · USNational Institute on Aging · USRockefeller University · US

Funding

Telomeres DiseasesZIAHL006089 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI YOUNG, NEAL S · 2010 to 2025
$26.2M
Regulation of Lymphocyte Proliferation and Replicative CapacityZIABC009405 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HODES, RICHARD J. · 2009 to 2023
$6.4M
Intramural NIH HHS
6 · The paper itself

Abstract

We have studied models of telomerase haploinsufficiency in humans and mice to analyze regulation of telomere length and the significance of "set points" in inheritance of telomere length. In three families with clinical syndromes associated with short telomeres resulting from haploinsufficient mutations in TERT, the gene encoding telomerase reverse transcriptase, we asked whether restoration of normal genotypes in offspring of affected individuals would elongate inherited short telomeres. Telomeres were shorter than normal in some but not all genotypically normal offspring of telomerase-mutant parents or grandparents. Analysis of these findings was complicated by heterogeneity of telomere length among individuals, as well as by the admixing of telomeres inherited from affected parents with those inherited from unaffected ("wild-type" TERT) parents. To understand further the inheritance of telomere length, we established a shortened-telomere mouse model. When Tert(+/-) heterozygous mice were successively cross-bred through 17 generations, telomere length shortened progressively. The late-generation Tert(+/-) mice were intercrossed to produce genotypically wild-type Tert(+/+) mice, for which telomere length was characterized. Strikingly, telomere length in these Tert(+/+) mice was not longer than that of their Tert(+/-) parents. Moreover, when successive crosses were carried out among these short-telomere Tert(+/+) offspring mice, telomere length was stable, with no elongation up to six generations. This breeding strategy therefore has established a mouse strain, B6.ST (short telomeres), with C57BL/6 genotype and stable short telomeres. These findings suggest that the set point of telomere lengths of offspring is determined by the telomere lengths of their parents in the presence of normal expression of telomerase.

Indexed as

Anemia, AplasticAnimalsCrosses, GeneticFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsModels, GeneticMutationPedigreePhenotypeTelomeraseTelomereTelomeraseTERT protein, humanTert protein, mouse

Identifiers

PMID20479226
PMCPMC2890496
OpenAlexW2103634044

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.