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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 04 Mar 2015.

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: TIF1beta, CAN, HAD, DNA methyltransferase, PAN1
Papers on ZFP57
The stem cell transcription factor ZFP57 induces IGF2 expression to promote anchorage-independent growth in cancer cells.
Koide et al., Kanazawa, Japan. In Oncogene, 05 Mar 2015
The transcription factor ZFP57 is expressed in self-renewing ES cells and its expression level decreases during ES cell differentiation.
Nanog positively regulates Zfp57 expression in mouse embryonic stem cells.
Koide et al., Kanazawa, Japan. In Biochem Biophys Res Commun, Dec 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, Oct 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), Aug 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.
Genome-wide DNA methylation profiling identifies a folate-sensitive region of differential methylation upstream of ZFP57-imprinting regulator in humans.
Prescott et al., Perth, Australia. In Faseb J, Jul 2014
By far, the biggest effect observed was hypomethylation of a 923 bp region 3 kb upstream of the ZFP57 transcript, a regulator of DNA methylation during development, observed in both cell types.
High grade glioblastoma is associated with aberrant expression of ZFP57, a protein involved in gene imprinting, and of CPT1A and CPT1C that regulate fatty acid metabolism.
Peluso et al., Napoli, Italy. In Cancer Biol Ther, Jul 2014
We measured the mRNA levels of ZFP57, TRIM28, CPT1A, CPT1B, and CPT1C in a cohort of 80 patients divided in two groups: grade II and grade IV.
A familial disorder of altered DNA-methylation.
Siebert et al., Kiel, Germany. In J Med Genet, Jun 2014
Sanger sequencing and RT-PCR of imprinting-associated genes (NLRP2, NLRP7, ZFP57, KHDC3L, DNMT1o), exome sequencing and locus-specific, array-based and genome-wide technologies to determine DNA-methylation were performed.
Fine mapping genetic determinants of the highly variably expressed MHC gene ZFP57.
Knight et al., Oxford, United Kingdom. In Eur J Hum Genet, Apr 2014
ZFP57 is an important transcriptional regulator involved in DNA methylation and genomic imprinting during development.
DNA recognition of 5-carboxylcytosine by a Zfp57 mutant at an atomic resolution of 0.97 Å.
Cheng et al., Atlanta, United States. In Biochemistry, 2014
The Zfp57 gene encodes a KRAB (Krüppel-associated box) domain-containing C2H2 zinc finger transcription factor that is expressed in early development.
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).
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.
Genomic imprinting is a parental effect established in mammalian germ cells.
Li, New York City, United States. In Curr Top Dev Biol, 2012
Maintenance of the DNA methylation imprint is dependent on two distinct maternal effect genes (Zfp57 and PGC7/Stella).
Proteins involved in establishment and maintenance of imprinted methylation marks.
Ferguson-Smith et al., Cambridge, United Kingdom. In Brief Funct Genomics, 2012
Specifically, we discuss the recent findings of a critical role played by a KRAB zinc-finger protein ZFP57 and its co-factor KAP1/TRIM28 in mediating both processes.
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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