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.
复制标题
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:
影响因子:
--
通讯作者:
Lee,CH
中科院分区:
文献类型:
--
作者:
Wei,LN;Lee,CH
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.