Single nucleotide polymorphisms/haplotypes associated with multiple rubella-specific immune response outcomes post-MMR immunization in healthy children.
Rochester, United States. In Immunogenetics, 31 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).
Nanog positively regulates Zfp57 expression in mouse embryonic stem cells.
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].
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.
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.
A familial disorder of altered DNA-methylation.
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.
Genes, assisted reproductive technology and trans-illumination.
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.