Evidence map›Paper›PMID 19016755›Full record

ArticleCancer science2008

Interaction between DNMT1 and DNA replication reactions in the SV40 in vitro replication system.

Shintaro Shimamura, Fuyuki Ishikawa

Abstract read
In one paragraph

Article in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. The applications of single-cell genomics.Human molecular genetics · 2013
    Review
  4. Article
  5. 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.

Shintaro ShimamuraDepartment of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
Fuyuki Ishikawa

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In contrast to normal cells, cancer cells exhibit both genetic and epigenetic instability. These unique properties give rise to genetic and epigenetic heterogeneity in a given population of cancer cells and provide a means for the population to undergo phenotypic progression by clonal selection. DNA methylation at CpG dinucleotides is one of the epigenetic marks that are frequently disturbed in cancer cells. To understand how the CpG methylation pattern is changeable in cancer cells, it is necessary to know how it is faithfully maintained in normal cell proliferation. Toward this goal, we have developed a novel in vitro system that is based on the well-established SV40 in vitro replication system and functions to reconstitute concurrent DNA replication and DNA maintenance methylation reactions. We found that DNA methylation was maintained only when exogenous DNA methyltransferase 1 (DNMT1) and S-adenosyl methionine (SAM) were added to the reaction. We demonstrated that DNMT1 associates with replicating and/or replicated chromatin irrespective of the DNA methylation status of template DNA. Moreover, the PCNA-binding domain (PBD) of DNMT1 is not required for the association. Taken together, we suggest that DNMT1 is recruited to replicating and/or replicated chromatin in a constitutive manner independent of the DNA methylation reaction. The in vitro system described in this report is very useful for analyzing the molecular mechanism underlying the DNA maintenance methylation reaction.

Indexed as

DNA MethylationChromatinCpG IslandsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA ReplicationHumansS-AdenosylmethionineSimian virus 40ChromatinDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanS-Adenosylmethionine

Identifiers

PMID19016755
PMCPMC11158606

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Registered trials

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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.