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Zinc finger protein 57 homolog

The protein encoded by this gene is a zinc finger protein containing a KRAB domain. Studies in mouse suggest that this protein may function as a transcriptional repressor. Mutations in this gene have been associated with transient neonatal diabetes mellitus type 1 (TNDM1).[provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: CAN, TIF1beta, HAD, DNA methyltransferase, ZFP
Papers on ZFP57
ZFP57 recognizes multiple and closely spaced sequence motif variants to maintain repressive epigenetic marks in mouse embryonic stem cells.
Riccio et al., Caserta, Italy. In Nucleic Acids Res, Nov 2015
ZFP57 and KAP1 are both required for maintaining the repressive DNA methylation and H3-lysine-9-trimethylation (H3K9me3) at ICRs.
Germline-derived DNA methylation and early embryo epigenetic reprogramming: The selected survival of imprints.
Monk, Barcelona, Spain. In Int J Biochem Cell Biol, Oct 2015
This suggests that trans-acting factors such as Zfp57 can discriminate imprinted differentially methylated regions (DMRs) from the thousands of CpG rich regions that are differentially marked in the gametes.
Single nucleotide polymorphisms/haplotypes associated with multiple rubella-specific immune response outcomes post-MMR immunization in healthy children.
Poland et al., Rochester, United States. In Immunogenetics, Oct 2015
Of these SNPs, we detected eight in the PVRL3 gene, five in the PVRL1 gene, one in the TRIM22 gene, two in the IL10RB gene, two in the TLR4 gene, and five in other genes (PVR, ADAR, ZFP57, MX1, and BTN2A1/BTN3A3).
Maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development.
Li et al., Beijing, China. In Proc Natl Acad Sci U S A, May 2015
Zfp57 is a maternal-zygotic effect gene that maintains genomic imprinting.
Intrahaplotypic Variants Differentiate Complex Linkage Disequilibrium within Human MHC Haplotypes.
Ren et al., Singapore, Singapore. In Sci Rep, 2014
We further show that the strong linkage disequilibrium structure within the human MHC that typically confounds precise identification of genetic features can be resolved using intra-CEH variants, as evidenced by rs3129063 and rs448489, which affect expression of ZFP57, a gene important in methylation and epigenetic regulation.
Identification of Genes Whose Expression Profile Is Associated with Non-Progression towards AIDS Using eQTLs.
Zagury et al., Paris, France. In Plos One, 2014
Our study also drew our attention to lesser-known functions such as mitochondrial ribosomal proteins and a zinc finger protein, ZFP57, which could be central to the effectiveness of HIV infection.
Allele-specific binding of ZFP57 in the epigenetic regulation of imprinted and non-imprinted monoallelic expression.
Ferguson-Smith et al., Cambridge, United Kingdom. In Genome Biol, 2014
The Kruppel-like zinc finger protein ZFP57 acts as a factor necessary for maintaining the DNA methylation memory at multiple imprinting control regions in early mouse embryos and embryonic stem (ES) cells.
Nanog positively regulates Zfp57 expression in mouse embryonic stem cells.
Koide et al., Kanazawa, Japan. In Biochem Biophys Res Commun, 2014
Zinc finger protein 57 (Zfp57) is specifically expressed in self-renewing ES cells and its expression level is reduced upon ES cell differentiation, suggesting that expression of this transcription factor is regulated by core transcription factors.
[The roles of maternal-effect proteins in the maintenance of genomic imprints].
Luan et al., Changchun, China. In Yi Chuan, 2014
In order to obtain a better understanding for the mechanism of maternal-effect proteins in the maintenance of genomic imprints, the recent study progress of maternal-effect proteins, such as DPPA3, ZFP57, TRIM28 and DNMT1, are summarized, and the regulation mechanism of these maternal-effect proteins for genomic imprints are discussed.
The specification of imprints in mammals.
Kelsey et al., Cambridge, United Kingdom. In Heredity (edinb), 2014
Among the factors involved in this selection, the zinc-finger protein Zfp57 can be regarded as an imprint-specific, sequence-specific DNA binding factor responsible for maintaining methylation at most ICRs.
Pre- and postovulatory aging of murine oocytes affect the transcript level and poly(A) tail length of maternal effect genes.
Grümmer et al., Essen, Germany. In Plos One, 2013
Similarly, transcripts of in vitro-grown oocytes were deadenylated after 12 h of postovulatory aging (Tet3, Trim28, Zfp57, Dnmt1, Nlrp5, Zar1).
Searching for "monogenic diabetes" in dogs using a candidate gene approach.
Ollier et al., Manchester, United Kingdom. In Canine Genet Epidemiol, 2013
Six SNP associations were found from five genes, with one gene (ZFP57) being associated in two different breeds.
Genes, assisted reproductive technology and trans-illumination.
Maher et al., Birmingham, United Kingdom. In Epigenomics, 2013
Studies of rare human imprinting disorders such as familial hydatidiform mole, Beckwith-Wiedemann syndrome and familial transient neonatal diabetes mellitus have enabled the identification of genetic (e.g., mutations in KHDC3L [C6ORF221], NLRP2 [NALP2], NLRP7 [NALP7] and ZFP57) and environmental (assisted reproductive technologies) factors that can disturb the normal trans mechanisms for imprinting establishment and/or maintenance.
On how mammalian transcription factors recognize methylated DNA.
Defossez et al., Salt Lake City, United States. In Epigenetics, 2013
The last piece of the puzzle has been recently revealed by the structural resolution of two different zinc finger proteins, Kaiso and ZFP57, in complex with methylated DNA.
No evidence for pathogenic variants or maternal effect of ZFP57 as the cause of Beckwith-Wiedemann Syndrome.
Grønskov et al., Glostrup, Denmark. In Eur J Hum Genet, 2012
no evidence for ZFP57 alterations as a major cause in sporadic Beckwith-Wiedemann Syndrome cases
Screening for genomic variants in ZFP57 in Silver-Russell syndrome patients with 11p15 epimutations.
Eggermann et al., Aachen, Germany. In Eur J Med Genet, 2009
this study does not provide evidence that ZFP57 mutations are the cause of 11p15-hypomethylation in Silver-Russell syndrome (SRS) patients and contribute to the aetiology of SRS
Hypomethylation of multiple imprinted loci in individuals with transient neonatal diabetes is associated with mutations in ZFP57.
Temple et al., Southampton, United Kingdom. In Nat Genet, 2008
Study reports mutations in ZFP57, which encodes a zinc-finger transcription factor expressed in early development, in seven pedigrees with a shared pattern of mosaic hypomethylation and a conserved range of clinical features.
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