Evidence map›Paper›PMID 22144682›Full record

ArticleThe Journal of biological chemistry2012

Zinc finger protein ZFP57 requires its co-factor to recruit DNA methyltransferases and maintains DNA methylation imprint in embryonic stem cells via its transcriptional repression domain.

Xiaopan Zuo, Jipo Sheng, Ho-Tak Lau, Carol M McDonald, Monica Andrade, Dana E Cullen, Fong T Bell, Michelina Iacovino, Michael Kyba, Guoliang Xu and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 176 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Morc1 reestablishes H3K9me3 heterochromatin on piRNA-targeted transposons in gonocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. ICF1-Syndrome-AssociatedBiomolecules · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

36 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

11 authors at 4 institutions in 2 countries.

Xiaopan ZuoBlack Family Stem Cell Institute, Department of Developmental and Regenerative Biology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Jipo Sheng
Ho-Tak Lau
Carol M McDonald
Monica Andrade
Dana E Cullen
Fong T Bell
Michelina Iacovino
Michael Kyba
Guoliang Xu
Xiajun Li
Icahn School of Medicine at Mount Sinai · USChinese Academy of Sciences · CNMinneapolis Heart Institute Foundation · USUniversity of Minnesota · US

Funding

Acquisition and maintenance of DNA methylation in genomic imprintingR01GM093335 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LI, XIAJUN · 2010 to 2014
$1.6M
NIGMS NIH HHS GM093335NIGMS NIH HHS R01 GM093335
6 · The paper itself

Abstract

Previously, we discovered that ZFP57 is a maternal-zygotic effect gene, and it maintains DNA methylation genomic imprint at multiple imprinted regions in mouse embryos. Despite these findings, it remains elusive how DNA methyltransferases are targeted to the imprinting control regions to initiate and maintain DNA methylation imprint. To gain insights into these essential processes in genomic imprinting, we examined how ZFP57 maintains genomic DNA methylation imprint in mouse embryonic stem (ES) cells. Here we demonstrate that the loss of ZFP57 in mouse ES cells led to a complete loss of genomic DNA methylation imprint at multiple imprinted regions, similar to its role in mouse embryos. However, reintroduction of ZFP57 into Zfp57-null ES cells did not result in reacquisition of DNA methylation imprint, suggesting that the memory for genomic imprinting had been lost or altered in Zfp57-null ES cells in culture. Interestingly, ZFP57 and DNA methyltransferases could form complexes in the presence of KAP1/TRIM28/TIF1β when co-expressed in COS cells. We also found that the wild-type exogenous ZFP57 but not the mutant ZFP57 lacking the KRAB box that interacts with its co-factor KAP1/TRIM28/TIF1β could substitute for the endogenous ZFP57 in maintaining the DNA methylation imprint in ES cells. These results suggest that ZFP57 may recruit DNA methyltransferases to its target regions to maintain DNA methylation imprint, and this interaction is likely facilitated by KAP1/TRIM28/TIF1β.

Indexed as

Zinc FingersAnimalsChlorocebus aethiopsCOS CellsDNA MethylationDNA Modification MethylasesEmbryonic Stem CellsGenomic ImprintingMiceMice, Mutant StrainsMultiprotein ComplexesMutationNuclear ProteinsRepressor ProteinsTripartite Motif-Containing Protein 28DNA Modification MethylasesMultiprotein ComplexesNuclear ProteinsRepressor ProteinsTrim28 protein, mouseTripartite Motif-Containing Protein 28Zfp-57 protein, mouse

Identifiers

PMID22144682
PMCPMC3265890
OpenAlexW2088306169

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.