Demethylation in the 5'-flanking region of mouse cellular retinoic acid binding protein-I gene is associated with its high level of expression in mouse embryos and facilitates its induction by retinoic acid in P19 embryonal carcinoma cells.

Demethylation in the 5'-flanking region of mouse cellular retinoic acid binding protein-I gene is associated with its high level of expression in mouse embryos and facilitates its induction by retinoic acid in P19 embryonal carcinoma cells.
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小鼠细胞视黄酸结合蛋白-I 基因 5 侧翼区域的去甲基化与其在小鼠胚胎中的高水平表达相关,并促进其在 P19 胚胎癌细胞中被视黄酸诱导。

DOI:
10.1002/aja.1002010102
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发表时间:
1994
期刊:
Developmental dynamics : an official publication of the American Association of Anatomists
影响因子:
--
通讯作者:
Lee,CH
Lee,CH
中科院分区:
--
文献类型:
--
作者:
Wei,LN;Lee,CH

文献摘要

相似文献

小鼠细胞视黄酸结合蛋白-I(CRABP-I)基因在P19小鼠胚胎癌细胞中被视黄酸(RA)特异性上调,其在动物中的表达在空间和时间上局限于胚胎发育期间的RA敏感组织。本研究表明,在CRABP-I基础水平表达的成年小鼠组织和P19细胞中,CRABP-I基因的5′-侧翼区在所有Hpa II位点的C残基处均高度甲基化。相反,在小鼠胚胎发育的早期阶段,当检测到CRABP-I基因的表达水平高得多时,该区域在这些HpaII位点发生去甲基化。在P19中,在5-氮杂胞苷(5-AzaC)与RA联合处理的细胞中可以观察到RA诱导的CRABP-I上调的增强,其中观察到CRABP-I基因5′侧翼区域的部分去甲基化。核运行实验表明,P19细胞中CRABP-I的信息水平增加可以至少部分地通过其转录速率的增加来解释。5-AzaC也可增强RA对维甲酸受体(RAR)β的诱导,但程度要小得多。相反,结构基因部分中的所有Hpa II位点,至少在前两个外显子中,在C残基处完全去甲基化。© 1994 Wiley利斯公司
The mouse cellular retinoic acid binding protein‐I (CRABP‐I) gene is specifically up‐regulated by retinoic acid (RA) in P19 mouse embryonal carcinoma cells, and its expression in animals is spatially and temporally restricted to RA‐sensitive tissues during embryonic development. This study demonstrates that, in adult mouse tissues and P19 cells where the expression of CRABP‐I is detected at the basal level, the 5′‐ flanking region of the CRABP‐I gene is hypermethylated at the C residues of all theHpaII sites. Conversely, in mouse embryos during early stages of development when the expression of CRABP‐I gene is detected at a much higher level, this region is demethylated at theseHpaII sites. In P19, enhancement on the RA‐induced up‐regulation of CRABP‐I can be observed in cells treated with 5‐azacytidine (5‐AzaC) in conjunction with RA, where partial demethylation in the 5′‐flanking region of CRABP‐I gene is observed. Nuclear run‐on experiments indicate that increased message levels of CRABP‐I in P19 cells can be accounted for, at least partially, by increases in its transcription rates. The induction of retinoic acid receptor (RAR) β by RA can also be enhanced by 5‐AzaC, but to a much lesser degree. In contrast, all theHpaII sites in the structural gene portion, at least in the first two exons, are fully demethylated at the C residues. © 1994 Wiley‐Liss, Inc.