Evidence map›Paper›PMID 10773079›Full record

ArticleNucleic acids research2000

Differential mRNA expression of the human DNA methyltransferases (DNMTs) 1, 3a and 3b during the G(0)/G(1) to S phase transition in normal and tumor cells.

K D Robertson, K Keyomarsi, F A Gonzales, M Velicescu, P A Jones

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% 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

82 citing papers in PubMed, 2 syntheses or guidelines pooled it, 200 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. DNMT Enzymes and Their Impact on Cervical Cancer: A State-of-the-Art Review.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. World journal of gastrointestinal oncology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
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  19. Article
  20. Review

22 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

5 authors at 1 institution in 1 country.

K D RobertsonNorris Comprehensive Cancer Center, University of Southern California, MS 83, 1441 Eastlake Avenue, Los Angeles, CA 90033, USA.
K Keyomarsi
F A Gonzales
M Velicescu
P A Jones
USC Norris Comprehensive Cancer Center · US

Funding

MECHANISMS OF DE NOVO METHYLATION IN CANCERR01CA082422 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI JONES, PETER A · 1999 to 2016
$5.1M
DE NOVO METHYLATION AND CANCERZ01BC010420 · BC · BASIC SCIENCES · PI ROBERTSON, KEITH · 2000 to 2004
–
NCI NIH HHS R01 CA082422NCI NIH HHS R01 CA 82422
6 · The paper itself

Abstract

DNA methylation is essential for mammalian development, X-chromosome inactivation, and imprinting yet aberrant methylation patterns are one of the most common features of transformed cells. One of the proposed causes for these defects in the methylation machinery is overexpression of one or more of the three known catalytically active DNA methyltransferases (DNMTs) 1, 3a and 3b, yet there are clearly examples in which overexpression is minimal or non-existent but global methylation anomalies persist. An alternative mechanism which could give rise to global methylation errors is the improper expression of one or more of the DNMTs during the cell cycle. To begin to study the latter possibility we examined the expression of the mRNAs for DNMT1, 3a and 3b during the cell cycle of normal and transformed cells. We found that DNMT1 and 3b levels were significantly downregulated in G(0)/G(1)while DNMT3a mRNA levels were less sensitive to cell cycle alterations and were maintained at a slightly higher level in tumor lines compared to normal cell strains. Enzymatic activity assays revealed a similar decrease in the overall methylation capacity of the cells during G(0)/G(1)arrest and again revealed that a tumor cell line maintained a higher methylation capacity during arrest than a normal cell strain. These results reveal a new level of control exerted over the cellular DNA methylation machinery, the loss of which provides an alternative mechanism for the genesis of the aberrant methylation patterns observed in tumor cells.

Indexed as

Cell CycleGene Expression Regulation, EnzymologicTranscription, GeneticBase SequenceBreast NeoplasmsCell LineDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNA Methyltransferase 3BFemaleG1 PhaseHumansKineticsMolecular Sequence DataOligodeoxyribonucleotidesDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNA Methyltransferase 3BDNMT1 protein, humanDNMT3A protein, humanOligodeoxyribonucleotidesRNA, Messenger

Identifiers

PMID10773079
PMCPMC105379
OpenAlexW2141763464

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.