ライフサイエンスコーパス: paternally-expressed gene

1 ene, rather than from absent expression of a paternally expressed gene.

2 r-Willi syndrome results from the absence of paternally expressed genes.

3 y expressed genes and repression of silenced paternally expressed genes.

4 for bidirectional activation of a number of paternally expressed genes.

5 cal crosses, resembling either maternally or paternally expressed genes.

6 idespread relaxation of imprinting of mostly paternally expressed genes.

7 olute carrier family 38 member 4), and Peg1 (paternally expressed gene 1)--both MBD1 and H3K9me3 bind

8 actor receptor-bound protein 10), Peg1/Mest (paternally expressed gene 1/mesoderm-specific transcript

9 The product of the imprinted gene paternally expressed gene-10 (PEG10) has been reported t

10 -/- cells showed aberrant methylation of the paternally expressed gene 3 (Peg3) tumor suppressor gene

11 Notably, allelic imbalance in paternally expressed gene 3 (PEG3) was associated with i

12 tment of breast carcinoma xenografts induces paternally expressed gene 3 (Peg3), an imprinted gene en

13 We found that decorin induced paternally expressed gene 3 (Peg3), an imprinted tumor s

14 hin 3 maternally methylated imprinted genes: paternally expressed gene 3 (PEG3), insulin-like growth

15 receptor 2 (VEGFR2) signaling that requires paternally expressed gene 3 (PEG3).

16 ICR (Imprinting Control Region) of the Peg3 (Paternally Expressed Gene 3) domain contains an unusual

17 ation status of the CpG islands of the PEG3 (Paternally expressed gene 3) imprinted domain in the mou

18 Peg3 (paternally expressed gene 3) is an imprinted gene locali

19 Peg3 (paternally expressed gene 3) is the first imprinted gene

20 (H19 fetal liver mRNA), p57(Kip2), Peg3/Pw1 (paternally expressed gene 3), and Zac1 (zinc finger-bind

21 d domain), located 25 kb downstream of PEG3 (paternally expressed gene 3).

22 ithin 30 kb of a known imprinted gene, Peg3 (paternally expressed gene 3).

23 ssed genes, activated expression of silenced paternally expressed genes and resulted in methylation o

24 er-Willi syndrome (PWS) is caused by loss of paternally expressed genes at an imprinted locus on chro

25 oter regions and transcriptional termini and paternally expressed genes at promoters and gene bodies,

26 IPW, a paternally expressed gene cloned from this region, is no

27 ernally expressed genes (Igf2r, H19) and two paternally expressed genes (Igf2, U2af1-rs1) in ES cells

28 Mash2, Kvlqt1, and p57(Kip2), as well as two paternally expressed genes, Igf2 and Ins2, and assess th

29 e previously identified Peg1/Mest as a novel paternally expressed gene in the developing mouse embryo

30 sults from loss of function of 10 clustered, paternally expressed genes in a 1.5-Mb region of chromos

31 -Willi syndrome (PWS) is caused by a loss of paternally expressed genes in an imprinted region of chr

32 y the inactivation or deletion of imprinted, paternally expressed genes in chromosome band 15q11.2.

33 nomic alterations that inactivate imprinted, paternally expressed genes in human chromosome region 15

34 the two parental alleles of SNRPN and other paternally expressed genes in the region by using a chro

35 Transcription of paternally expressed genes in the region depends upon an

36 portant for regulation of SNRPN and of other paternally expressed genes in the region.

37 e required for the genomic imprinting of two paternally expressed genes, Ins-2 (encodes insulin-2) an

38 The paternally expressed gene insulin-like growth-factor 2 (

39 The paternally expressed genes NDN, IPW, PWCR1 and MAGEL2 we

40 determined that Pw1 is identical to Peg3, a paternally expressed gene of unknown function (and will

41 Surprisingly, paternally-expressed genes of the non-classical gene imp

42 PWS is caused by the loss of one or more paternally expressed genes on chromosome 15q11-q13, whic

43 osome 6q, believed to contain an exclusively paternally expressed gene or genes that cause transient

44 d the expression and methylation status of a paternally expressed gene Peg3, in germ cells from sex-r

45 stigate the role of the maternally imprinted/paternally expressed gene, Peg3, in several aspects of b

46 wn (CypA-KD) P19 cells, we observed a silent paternally expressed gene, Peg3.

47 mplete abolition of the transcription of two paternally expressed genes, Peg3 and Usp29, causing the

48 ressed genes (MEGs) and approximately 29% of paternally expressed genes (PEGs) in C. rubella were com

49 the mechanism by which PWS-IC activates the paternally expressed genes (PEGs) using transgenes that

50 ic crosses, whereas approximately 90% of 272 paternally expressed genes (PEGs) were found only in one

51 162 maternally expressed genes (MEGs) and 95 paternally expressed genes (PEGs), which were associated

52 and H3K36me3 peaks mostly co-localized with paternally expressed genes (PEGs), while endosperm-speci

53 54 maternally expressed genes (MEGs) and 46 paternally expressed genes (PEGs).

54 mprinting disorder caused by a deficiency of paternally expressed gene(s) in the 15q11-q13 chromosoma

55 ched for coexpressed pairs of maternally and paternally expressed genes, showed accelerated expressio

56 LK1 (delta, Drosophila, homolog-like 1) is a paternally expressed gene that encodes for a transmembra

57 located adjacent to a cluster of imprinted, paternally expressed genes that are known to be positive

58 The largest proportion of paternally expressed genes was at 7 DAP, mainly due to t

59 PWS involves loss of function of multiple paternally expressed genes, while mutations in a single