Evidence map›Paper›PMID 16135795›Full record

ArticleMolecular and cellular biology2005

Function of AP-1 in transcription of the telomerase reverse transcriptase gene (TERT) in human and mouse cells.

Masahiro Takakura, Satoru Kyo, Masaki Inoue, Woodring E Wright, Jerry W Shay

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Review
  6. Cancer-specific loss ofProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Article
  8. Telomerase and Telomeres Biology in Thyroid Cancer.International journal of molecular sciences · 2019
    Review
  9. Diverse regulatory manners of human telomerase reverse transcriptase.Cell communication and signaling : CCS · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
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  19. Article
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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

5 authors at 2 institutions in 2 countries.

Masahiro TakakuraDepartment of Cell Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9039, USA.
Satoru Kyo
Masaki Inoue
Woodring E Wright
Jerry W Shay
Kanazawa University · JPThe University of Texas Southwestern Medical Center · US

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
MECHANISMS OF CELLULAR IMMORTALIZATIONR01AG007992 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI WRIGHT, WOODRING ERIK · 1989 to 2010
$3.3M
CONSEQUENCES OF INHIBITION OF CELLULAR TELOMERASER01CA085363 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI COREY, DAVID R. · 2001 to 2004
$1.4M
NCI NIH HHS CA70907NCI NIH HHS CA85363NCI NIH HHS P50 CA070907NCI NIH HHS R01 CA085363NIA NIH HHS AG07992NIA NIH HHS R01 AG007992
6 · The paper itself

Abstract

The transcriptional regulation of the human telomerase catalytic subunit (hTERT) plays a critical role in telomerase activity. Approximately 200 bp of the proximal core promoter is responsible for basic hTERT expression; however, the function of the distal regulatory elements remains unclear. The transcription factor activator protein 1 (AP-1) is involved in cellular proliferation, differentiation, carcinogenesis, and apoptosis and is expressed broadly in both cancer and normal cells. There are several putative AP-1 sites in the hTERT promoter, but their functions are unknown. The present study examined the regulatory role of AP-1 in hTERT gene transcription. Overexpression of AP-1 leads to transcriptional suppression of hTERT in cancer cells. The combination of c-Fos and c-Jun or c-Fos and JunD strongly suppresses hTERT promoter activity in transient-expression analyses. The hTERT promoter region between -2000 and -378 is responsible for this function. Gel shift and supershift analyses, as well as ChIP, show binding of JunD and c-Jun on two putative AP-1 sites within this region. Mutations in the AP-1 binding sites rescued suppressions caused by AP-1, suggesting this is a direct regulation of the hTERT promoter. In contrast, there was no effect on mTERT expression or mTERT promoter activity by AP-1 overexpression in mouse fibroblasts. The species-specific function of AP-1 in TERT expression may in part help explain the difference in telomerase activity between normal human and mouse cells.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsBase SequenceBinding SitesDNA-Binding ProteinsHeLa CellsHumansMiceMolecular Sequence DataMutationNIH 3T3 CellsPromoter Regions, GeneticProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTelomeraseTranscriptional ActivationDNA-Binding ProteinsProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTelomeraseTERT protein, humanTert protein, mouseTranscription Factor AP-1

Identifiers

PMID16135795
PMCPMC1234330
OpenAlexW2114840351

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.