Evidence map›Paper›PMID 21949400›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Separation of telomerase functions by reverse genetics.

Shibani Mukherjee, Eduardo J Firpo, Yang Wang, James M Roberts

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. AST-487 Inhibits RET Kinase Driven TERT Expression in Bladder Cancer.International journal of molecular sciences · 2022
    Article
  9. Article
  10. Review
  11. Biomedicines · 2021
    Article
  12. TRIM28 is a transcriptional activator of the mutant TERT promoter in human bladder cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  13. Article
  14. Frontiers in oncology · 2021
    Article
  15. G-Quadruplexes at Telomeres: Friend or Foe?Molecules (Basel, Switzerland) · 2020
    Review
  16. TheCells · 2020
    Review
  17. Review
  18. Article
  19. Review
  20. Non-canonical Roles of Telomerase: Unraveling the Imbroglio.Frontiers in cell and developmental biology · 2019
    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.

Shibani MukherjeeDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Eduardo J Firpo
Yang Wang
James M Roberts
Fred Hutch Cancer Center · US

Funding

Telomerase-regulated gene expression in normal and tumor cellsR01CA120294 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI ROBERTS, JAMES M · 2006 to 2010
$1.3M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA120294
6 · The paper itself

Abstract

The canonical function of the human telomerase protein (hTERT) is to synthesize telomeric DNA, but it has other biological activities, including enhancing cell proliferation, decreasing apoptosis, regulating DNA damage responses, and increasing cellular proliferative lifespan. The mechanistic relationships among these activities are not understood. We previously demonstrated that ectopic hTERT expression in primary human mammary epithelial cells diminishes their requirement for exogenous mitogens, thus giving them a proliferative advantage in a mitogen-depleted environment. Here, we show that this phenotype is caused by a combination of increased cell division and decreased apoptosis. In addition, we use a panel of hTERT mutants to demonstrate that this enhanced cell proliferation can be uncoupled not only from telomere elongation, but also from other telomerase activities, including cellular lifespan extension and regulation of DNA damage responses. We also find that the proliferative function of hTERT, which requires hTERT catalytic activity, is not caused by increased Wnt signaling, but is accompanied by alterations in key cell cycle regulators and is linked to an hTERT-catalyzed decrease in the levels of the RNA component of mitochondrial RNA processing endoribonuclease. Thus, enhanced cell proliferation is an independent function of hTERT that could provide a new target for the development of anti-telomerase cancer therapeutic agents.

Indexed as

Reverse GeneticsAnimalsBiocatalysisBreastCell DivisionCell ProliferationCell SurvivalCellular SenescenceChromosomal InstabilityDNA DamageEndoribonucleasesEpithelial CellsFemaleHumansMiceMitogensEndoribonucleasesmitochondrial RNA-processing endoribonucleaseMitogensTelomeraseTERT protein, human

Identifiers

PMID21949400
PMCPMC3250197
OpenAlexW2163523630

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.