Evidence map›Paper›PMID 10022128›Full record

ArticleOncogene1999

Telomerase reverse transcriptase gene is a direct target of c-Myc but is not functionally equivalent in cellular transformation.

R A Greenberg, R C O'Hagan, H Deng, Q Xiao, S R Hann, R R Adams, S Lichtsteiner, L Chin, G B Morin, R A DePinho

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed
18.2field-weighted citation impact, top 1% 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

134 citing papers in PubMed, 418 citations in OpenAlex.

  1. Article
  2. Telomere Reprogramming and Cellular Metabolism: Is There a Link?International journal of molecular sciences · 2024
    Review
  3. Article
  4. Observational
  5. Review
  6. Article
  7. Article
  8. InTERTwined: howCurrent opinion in endocrine and metabolic research · 2023
    Article
  9. Telomerase reactivation induces progression of mouse BrafbioRxiv : the preprint server for biology · 2023
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Regulation of human telomerase in homeostasis and disease.Nature reviews. Molecular cell biology · 2020
    Review
  20. Review

74 more citing papers are in PubMed but not listed here.

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

10 authors at 6 institutions in 1 country.

R A GreenbergDepartment of Microbiology & Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
R C O'Hagan
H Deng
Q Xiao
S R Hann
R R Adams
S Lichtsteiner
L Chin
G B Morin
R A DePinho
Albert Einstein College of Medicine · USHarvard University · USMenlo School · USVanderbilt University · USDana-Farber Cancer Institute · USGeron (United States) · US

Funding

TRAINING PROGRAM IN CELLULAR &MOLEC. BIOLOGY &GENETICST32GM007491 · NIGMS · YESHIVA UNIVERSITY · PI QUERY, CHARLES C · 1985 to 2021
$17.0M
MOLECULAR GENETICS OF LENS AND CATARACT DEVELOPMENTR01EY009300 · NEI · YESHIVA UNIVERSITY · PI DEPINHO, RONALD ANTHONY · 1991 to 2000
$320k
REGULATION OF MYC NETWORK FUNCTION IN DEVELOPMENTR01HD028317 · NICHD · YESHIVA UNIVERSITY · PI DEPINHO, RONALD ANTHONY · 1991 to 1999
–
NEI NIH HHS R01EY09300NICHD NIH HHS R01HD28317NIGMS NIH HHS 5T32GM07491
6 · The paper itself

Abstract

The telomerase reverse transcriptase component (TERT) is not expressed in most primary somatic human cells and tissues, but is upregulated in the majority of immortalized cell lines and tumors. Here, we identify the c-Myc transcription factor as a direct mediator of telomerase activation in primary human fibroblasts through its ability to specifically induce TERT gene expression. Through the use of a hormone inducible form of c-Myc (c-Myc-ER), we demonstrate that Myc-induced activation of the hTERT promoter requires an evolutionarily conserved E-box and that c-Myc-ER-induced accumulation of hTERT mRNA takes place in the absence of de novo protein synthesis. These findings demonstrate that the TERT gene is a direct transcriptional target of c-Myc. Since telomerase activation frequently correlates with immortalization and telomerase functions to stabilize telomers in cycling cells, we tested whether Myc-induced activation of TERT gene expression represents an important mechanism through which c-Myc acts to immortalize cells. Employing the rat embryo fibroblast cooperation assay, we show that TERT is unable to substitute for c-Myc in the transformation of primary rodent fibroblasts, suggesting that the transforming activities of Myc extend beyond its ability to activate TERT gene expression and hence telomerase activity.

Indexed as

Cell Transformation, NeoplasticPeptidylprolyl IsomeraseProtein BiosynthesisRNAAnimalsBacterial ProteinsBase SequenceConserved SequenceDNA-Binding ProteinsGene Expression RegulationHumansMiceMolecular Sequence DataPromoter Regions, GeneticProteinsProto-Oncogene Proteins c-mycBacterial ProteinsDNA-Binding ProteinsILPA protein, Aeromonas hydrophilaPeptidylprolyl IsomeraseProteinsProto-Oncogene Proteins c-mycRNARNA-Directed DNA PolymeraseTelomerasetelomerase RNATERT protein, humanTert protein, mouse

Identifiers

PMID10022128
OpenAlexW2002761352

What OpenQuestion holds

Texttitle and abstract
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.