ライフサイエンスコーパス: zeta-globin

1 beta1- and beta2-globins, and down-regulate zeta-globin.

2 an erythroid cell line that does not express zeta-globin.

3 an embryonic-stage erythroid line expressing zeta-globin.

4 embly assays demonstrate that the alpha- and zeta-globin 3'UTRs assemble a previously described mRNP

5 Constructs containing 67, 84 and 556 bp of zeta-globin 5' flanking region linked to a beta-galactos

6 hanging its normal alpha-globin subunits for zeta-globin, an endogenous, developmentally silenced, no

7 he notion that there is an absolute need for zeta-globin and indicating that alpha-globin alone can s

8 factor is present in K562 cells that express zeta-globin, but is absent in the OCIM1 cell line, a hum

9 (used to create the null mutation) into the zeta-globin gene appears to influence the expression of

10 n gene cluster is selective silencing of the zeta-globin gene as erythropoiesis shifts from primitive

11 A mouse strain carrying an embryonic zeta-globin gene disrupted by the insertion of a PGK-Neo

12 ine embryonic Ey- and beta h1-globin but not zeta-globin gene expression in the E10.5 yolk sac, compa

13 ndividually, the silencing activities of the zeta-globin gene promoter and 3'-flanking region were mi

14 criptional regulation of the human embryonic zeta-globin gene promoter.

15 y to current models, however, the alpha- and zeta-globin gene promoters were not sufficient to establ

16 Instead, full silencing of the zeta-globin gene required the combined activities of thi

17 s, full developmental silencing of the human zeta-globin gene requires elements encoded within the tr

18 sac to the fetal liver is parallaled by the zeta-globin gene silencing and enhanced expression of th

19 ased upon these data, we propose a model for zeta-globin gene silencing in fetal and adult erythroid

20 ssibility, we created a null mutation of the zeta-globin gene using homologous recombination in embry

21 l cis determinants of this switch, the human zeta-globin gene, the alpha-globin gene, and chimeric re

22 to a 108 bp segment located 1.2 kb 3' to the zeta-globin gene.

23 -globin locus, located 40 kb upstream of the zeta-globin gene.

24 or full developmental silencing of the human zeta-globin gene.

25 ssay, co-expression of GATA-1 and endogenous zeta-globin genes is detected in hematopoietic tissues o

26 tract contained by both the human alpha- and zeta-globin mRNA 3'UTRs.

27 A potential pathway for accelerated zeta-globin mRNA decay is suggested by the observation t

28 ouse model system, we demonstrate that human zeta-globin mRNA is unstable in adult erythroid cells re

29 rminant of the difference between alpha- and zeta-globin mRNA stability is mapped by in vivo expressi

30 -1/-2-globin genes in parental B6SUtA cells; zeta-globin mRNA was not detected in SB- and TSA-treated

31 onally by reducing the relative stability of zeta-globin mRNA.

32 Extravascular zeta-globin(+) primitive erythroid cells were found in p

33 This finding raises the possibility that zeta-globin production might be wholly or partially redu

34 res the cellular and molecular regulation of zeta-globin promoted transgene expression.

35 tream sites causes a progressive decrease in zeta-globin promoter activity.

36 v-Ha-ras coding region flanked 5' by a mouse zeta-globin promoter and 3' by an SV-40 polyadenylation

37 The human zeta-globin promoter contains a strong positive regulato

38 ted v-Ha-ras oncogene fused to the embryonic zeta-globin promoter develops an array of spontaneous ep

39 r start site, supporting the belief that the zeta-globin promoter directs v-Ha-ras expression in eryt

40 These results show that zeta-globin promoter function is highly dependent on a 6

41 t embryonic-specific activation of the human zeta-globin promoter is conferred by a 67 bp zeta-promot

42 transgene mRNA is initiated from the natural zeta-globin promoter start site, supporting the belief t

43 onsisting of v-Ha-Ras driven by an embryonic zeta-globin promoter) would not ordinarily be expected t

44 ssion from all constructs, including a 67 bp zeta-globin promoter, was erythroid-specific and most ac

45 the effect that deletion of sequences 5' to zeta-globin's CCAAT box have on zeta-promoter activity i

46 The zeta-globin transcribed region appeared to contribute to

47 le by providing for accelerated clearance of zeta-globin transcripts.

48 ies, expression of the individual alpha- and zeta-globin transgenes was found to be developmentally a

49 nt in the 5' flanking region, designated the zeta-globin upstream regulatory element (URE).