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Is ZFP57 binding to H19/IGF2:IG-DMR affected in Silver-Russell syndrome?

Overview of attention for article published in Clinical Epigenetics, February 2018
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Is ZFP57 binding to H19/IGF2:IG-DMR affected in Silver-Russell syndrome?
Published in
Clinical Epigenetics, February 2018
DOI 10.1186/s13148-018-0454-7
Pubmed ID

Angela Sparago, Flavia Cerrato, Andrea Riccio


Loss of paternal methylation (LOM) of theH19/IGF2intergenic differentially methylated region (H19/IGF2:IG-DMR) causes alteration ofH19/IGF2imprinting and Silver-Russell syndrome (SRS). Recently, internal deletions of theH19/IGF2:IG-DMR have been associated with LOM and SRS when present on the paternal chromosome. In contrast, previously described deletions, most of which cause gain of methylation (GOM) and Beckwith-Wiedemann syndrome (BWS) on maternal transmission, were consistently associated with normal methylation and phenotype if paternally inherited. The presence of several target sites (ZTSs) and three demonstrated binding regions (BRs) for the imprinting factor ZFP57 in theH19/IGF2:IG-DMR suggest the involvement of this factor in the maintenance of methylation of this locus. By comparing the extension of theH19/IGF2:IG-DMR deletions with the binding profile of ZFP57, we propose that the effect of the deletions on DNA methylation and clinical phenotype is dependent on their interference with ZFP57 binding. Indeed, deletions strongly affecting a ZFP57 BR result in LOM and SRS, while deletions preserving a significant number of ZFPs in each BR do not alter methylation and are associated with normal phenotype. The generation of transgenic mouse lines in which the endogenousH19/IGF2:IG-DMR is replaced by the human orthologous locus including the three ZFP57 BRs or their mutant versions will allow to test the role of ZFP57 binding in imprinted methylation and growth phenotype. Similarly to what is proposed for maternally inherited BWS mutations and CTCF and OCT4/SOX2 binding, we suggest that deletions of theH19/IGF2:IG-DMR result in SRS with LOM if ZFP57 binding on the paternal chromosome is affected.

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Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 5 29%
Student > Ph. D. Student 4 24%
Student > Bachelor 2 12%
Professor > Associate Professor 2 12%
Student > Master 2 12%
Other 2 12%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 41%
Agricultural and Biological Sciences 3 18%
Pharmacology, Toxicology and Pharmaceutical Science 1 6%
Nursing and Health Professions 1 6%
Computer Science 1 6%
Other 2 12%
Unknown 2 12%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 04 March 2018.
All research outputs
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Outputs from Clinical Epigenetics
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Outputs of similar age
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Outputs of similar age from Clinical Epigenetics
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Altmetric has tracked 13,789,144 research outputs across all sources so far. This one is in the 37th percentile – i.e., 37% of other outputs scored the same or lower than it.
So far Altmetric has tracked 686 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.8. This one is in the 27th percentile – i.e., 27% of its peers scored the same or lower than it.
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