Evidence map›Paper›PMID 25320237›Full record

ArticleBlood2014

An antiapoptotic role for telomerase RNA in human immune cells independent of telomere integrity or telomerase enzymatic activity.

Francesca S Gazzaniga, Elizabeth H Blackburn

Abstract read
In one paragraph

Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
–field-weighted citation impact
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

54 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Observational
  8. Article
  9. Article
  10. Telomere Reprogramming and Cellular Metabolism: Is There a Link?International journal of molecular sciences · 2024
    Review
  11. Article
  12. Global Gene Expression of Post-Senescent Telomerase-NegativeJournal of fungi (Basel, Switzerland) · 2023
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

2 authors.

Francesca S GazzanigaDepartment of Biophysics and Biochemistry, University of California, San Francisco, San Francisco, CA.ORCID http://orcid.org/0000-0002-5434-9991
Elizabeth H BlackburnDepartment of Biophysics and Biochemistry, University of California, San Francisco, San Francisco, CA.ORCID http://orcid.org/0000-0002-4885-0544

Funding

Synergism of telomere maintenance and telomerase with cancer-promoting signalingR01CA096840 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BLACKBURN, ELIZABETH H · 2002 to 2016
$4.8M
Chronic and Acute Psychosocial Stress and Impaired Cell AgingR01AG030424 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EPEL, ELISSA S. · 2010 to 2014
$3.5M
Chronic and Acute Psychosocial Stress and Impaired Cell AgingR56AG030424 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EPEL, ELISSA S. · 2008 to 2009
$260k
NCI NIH HHS CA096840NCI NIH HHS R01 CA096840NIA NIH HHS AG030424NIA NIH HHS R01 AG030424NIA NIH HHS R56 AG030424
6 · The paper itself

Abstract

Telomerase is a ribonucleoprotein complex that adds telomeric DNA to the ends of linear chromosomes. It contains two core canonical components: the essential RNA component, hTR, which provides the template for DNA synthesis, and the reverse transcriptase protein component, hTERT. Low telomerase activity in circulating peripheral blood mononuclear cells has been associated with a variety of diseases. It is unknown, however, whether telomerase, in addition to its long-term requirement for telomere maintenance, is also necessary for short-term immune cell proliferation and survival. We report that overexpression of enzymatically inactive hTR mutants protected against dexamethasone-induced apoptosis in stimulated CD4 T cells. Furthermore, hTR knockdown reproducibly induced apoptosis in the absence of any detectable telomere shortening or DNA damage response. In contrast, hTERT knockdown did not induce apoptosis. Strikingly, overexpression of hTERT protein caused apoptosis that was rescued by overexpression of enzymatically inactive hTR mutants. Hence, we propose that hTR can function as a noncoding RNA that protects from apoptosis independent of its function in telomerase enzymatic activity and long-term telomere maintenance in normal human immune cells. These results imply that genetic or environmental factors that alter hTR levels can directly affect immune cell function to influence health and disease.

Indexed as

AdolescentAdultAnti-Inflammatory AgentsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11Blotting, WesternCD4-Positive T-LymphocytesCells, CulturedDexamethasoneGene ExpressionHumansMembrane ProteinsMutationProto-Oncogene ProteinsReverse Transcriptase Polymerase Chain ReactionAnti-Inflammatory AgentsApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl-2-Like Protein 11DexamethasoneMembrane ProteinsProto-Oncogene ProteinsRNATelomerasetelomerase RNA

Identifiers

PMID25320237
PMCPMC4263978

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.