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1 pect to H19, but without loss of the gametic methylation imprint.
2 control regions to initiate and maintain DNA methylation imprint.
3 s, but they all fail to restore the maternal methylation imprints.
4 b(+/-)] mice also fail to establish maternal methylation imprints.
5 stance associated with loss of maternal GNAS methylation imprints.
6 tion UBE3A mutations, uniparental disomy, or methylation imprint abnormalities in AS are associated w
7 ns (class I), uniparental disomy (class II), methylation imprinting abnormalities (class III), and mu
9 unction on the maternal chromosome through a methylation imprint acquired during female gametogenesis
10 essential for the establishment of maternal methylation imprints and appropriate expression of mater
11 associated with erasure of all maternal GNAS methylation imprints and autosomal-dominant pseudohypopa
13 erases to its target regions to maintain DNA methylation imprint, and this interaction is likely faci
15 We first demonstrated that the H19 secondary methylation imprints are entirely stable through multipl
16 tation embryonic germ cells, suggesting that methylation imprints are erased in the germ cells prior
20 sult that genes normally carrying a maternal methylation imprint assume a paternal epigenetic pattern
21 cells led to a complete loss of genomic DNA methylation imprint at multiple imprinted regions, simil
24 nal silencing of Ube3a, exhibit maternal DNA methylation imprints at Ndn and Mkrn3 and suffer failure
27 hermore, we have found that differential DNA methylation imprints at the SNRPN promoter and at a CpG
32 ents with AS and PWS show no evidence of DNA methylation imprint erasure at the cis-acting PSW imprin
34 we examined how ZFP57 maintains genomic DNA methylation imprint in mouse embryonic stem (ES) cells.
35 tance, the human PWS-IC is able to acquire a methylation imprint in mouse oocytes, suggesting that ac
38 of their development, and germ-line-specific methylation imprints in DMRs are reestablished around th
40 chanisms responsible for maintaining genomic methylation imprints in mouse embryos are not understood
42 aNesp55(m)) showed loss of all maternal Gnas methylation imprints, leading in kidney to increased 1A
47 th a methylation change and identify a novel methylation imprint on chromosome 6 associated with TNDM
48 rf1 is located about 30 kb downstream of the methylation imprinted site, identified by RLGS-M, and sh
49 ylation analyses in embryos lacking maternal methylation imprints suggest that the primary imprinting
50 cells did not result in reacquisition of DNA methylation imprint, suggesting that the memory for geno
51 he DMD's hypothesized role of setting up the methylation imprint, the mutation also perturbs allele-s
52 This model describes (1) the evolution of methylation imprints toward stable, yet noisy equilibria
53 erm and fetal oocytes demonstrates a gametic methylation imprint with unmethylated paternal germ cell
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