Evidence map›Paper›PMID 18958525›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society

An epigenetic aberration increased in intergenic regions of cloned mice.

Hiromi Nishida, Shinji Kondo, Takahiro Suzuki, Yuki Tsujimura, Shunsuke Komatsu, Teruhiko Wakayama, Yoshihide Hayashizaki

Abstract read
PubMed Publisher
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

7 authors at 3 institutions in 1 country.

Hiromi NishidaGenome Exploration Research Group, RIKEN Genomic Sciences Center (GSC), Yokohama, Japan. hnishida@iu.a.u-tokyo.ac.jp
Shinji Kondo
Takahiro Suzuki
Yuki Tsujimura
Shunsuke Komatsu
Teruhiko Wakayama
Yoshihide Hayashizaki
RIKEN Center for Integrative Medical Sciences · JPThe University of Tokyo · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The causes of frequent abnormal phenotypes and low success rate in mammalian cloning are poorly understood. Although epigenetic aberration is suspected to be a cause, its connection to the phenotypes has yet to be investigated. To measure the level of reprogramming of an epigenetic mark, acetylation at lysine 9 of histone H3 (H3K9Ac), in cloned mice, we examined its conservation between two cloned mice derived from distinct cell nuclei and their natural donors by utilizing whole-genome tiling arrays and quantitative PCR. Pairwise comparison of the H3K9Ac enrichment profile between the four mice revealed that H3K9Ac is less conserved in intergenic regions than in promoter regions of protein-coding genes. Intriguingly, the variation of H3K9Ac enrichment in intergenic regions is the most prominent in comparison of the two clones, possibly reflecting an additive effect of aberrant reprogramming of this epigenetic information occurring specifically in each of the two clones.

Indexed as

Epigenesis, GeneticAcetylationAnimalsCloning, OrganismDNA, IntergenicFemaleGenomeHistonesLysineMaleMiceMice, Inbred C57BLPromoter Regions, GeneticDNA, IntergenicHistonesLysine

Identifiers

PMID18958525
OpenAlexW2049427939

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.