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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
8 ethylation of Igf2DMR1 region on the primary methylation imprint about 90 kilobases away.
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
12 hrony may thus be regulated differently from methylation imprints and have a separate function.
13 erases to its target regions to maintain DNA methylation imprint, and this interaction is likely faci
14  for both the acquisition and maintenance of methylation imprinting are diverging rapidly.
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
17                                          The methylation imprints are established in male and female
18                                              Methylation imprints are mostly lost, however.
19                                Intriguingly, methylation imprints are reacquired specifically at the
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
22 s required for the establishment of maternal methylation imprints at imprinting centers (ICs).
23 ization maintenance of maternal and paternal methylation imprints at multiple imprinted domains.
24 nal silencing of Ube3a, exhibit maternal DNA methylation imprints at Ndn and Mkrn3 and suffer failure
25 ration and functional necessity of secondary methylation imprints at the Igf2/H19 locus.
26 p57 results in failure to establish maternal methylation imprints at the Snrpn imprinted region.
27 hermore, we have found that differential DNA methylation imprints at the SNRPN promoter and at a CpG
28                The fact that a paternal type methylation imprint can also be established in the mater
29 somy (UPD) of this region or, rarely, from a methylation imprinting defect.
30                                     Maternal methylation imprints determine parent of origin expressi
31 of H3K4 is critical for establishing the DNA methylation imprints during oogenesis.
32 ents with AS and PWS show no evidence of DNA methylation imprint erasure at the cis-acting PSW imprin
33 he molecular mechanism that targets paternal methylation imprint establishment to the imprinting cont
34  the endogenous ZFP57 in maintaining the DNA methylation imprint in ES cells.
35  we examined how ZFP57 maintains genomic DNA methylation imprint in mouse embryonic stem (ES) cells.
36 tance, the human PWS-IC is able to acquire a methylation imprint in mouse oocytes, suggesting that ac
37 gf2 ICR in the establishment of its paternal methylation imprint in the male germ line, with implicat
38 (Mnt) the Igf2-H19 locus acquires a paternal methylation imprint in the maternal germline.
39 ate in the establishment of differential ICR methylation imprinting in the germ line.
40 of their development, and germ-line-specific methylation imprints in DMRs are reestablished around th
41                             Lack of maternal methylation imprints in heterozygous embryos derived fro
42 chanisms responsible for maintaining genomic methylation imprints in mouse embryos are not understood
43  oocytes, suggesting that acquisition of the methylation imprint is conserved.
44 aNesp55(m)) showed loss of all maternal Gnas methylation imprints, leading in kidney to increased 1A
45                                          The methylation imprint mark that we identified may be impor
46                  Therefore, this region is a methylation imprint mark.
47 aintained despite the altered expression and methylation imprint of Igf2 and H19.
48                                      Loss of methylation imprinting of H19 is linked to hypomethylati
49 th a methylation change and identify a novel methylation imprint on chromosome 6 associated with TNDM
50  maternal SMCHD1 does not alter germline DNA methylation imprints pre-implantation or later in gestat
51 rf1 is located about 30 kb downstream of the methylation imprinted site, identified by RLGS-M, and sh
52 ylation analyses in embryos lacking maternal methylation imprints suggest that the primary imprinting
53 cells did not result in reacquisition of DNA methylation imprint, suggesting that the memory for geno
54 he DMD's hypothesized role of setting up the methylation imprint, the mutation also perturbs allele-s
55    This model describes (1) the evolution of methylation imprints toward stable, yet noisy equilibria
56 erm and fetal oocytes demonstrates a gametic methylation imprint with unmethylated paternal germ cell