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在小鼠子宫腔上皮中,c-rasH和鸟氨酸脱羧酶可由17β-雌二醇诱导产生,且与细胞的增殖状态无关。

c-rasH and ornithine decarboxylase are induced by oestradiol-17 beta in the mouse uterine luminal epithelium independently of the proliferative status of the cell.

作者信息

Cheng S V, Pollard J W

出版信息

FEBS Lett. 1986 Feb 17;196(2):309-14. doi: 10.1016/0014-5793(86)80269-1.

DOI:10.1016/0014-5793(86)80269-1
PMID:3949003
Abstract

Oestradiol-17 beta (E2) treatment of the ovariectomized mouse results in a synchronised wave of cell proliferation in the uterine luminal epithelium. At the peak of DNA synthesis the mRNA level of the c-rasH proto-oncogene and ornithine decarboxylase were significantly increased. Progesterone treatment completely inhibits the E2 induced wave of DNA synthesis but does not greatly influence the level of these 2 mRNAs. Thus in the uterine luminal epithelium E2 regulates the level of ornithine decarboxylase and c-rasH independently of cell proliferation.

摘要

用17β-雌二醇(E2)处理去卵巢小鼠,可导致子宫腔上皮细胞增殖同步化。在DNA合成高峰期,原癌基因c-rasH和鸟氨酸脱羧酶的mRNA水平显著升高。孕酮处理可完全抑制E2诱导的DNA合成波,但对这两种mRNA的水平影响不大。因此,在子宫腔上皮中,E2独立于细胞增殖调节鸟氨酸脱羧酶和c-rasH的水平。

相似文献

1
c-rasH and ornithine decarboxylase are induced by oestradiol-17 beta in the mouse uterine luminal epithelium independently of the proliferative status of the cell.在小鼠子宫腔上皮中,c-rasH和鸟氨酸脱羧酶可由17β-雌二醇诱导产生,且与细胞的增殖状态无关。
FEBS Lett. 1986 Feb 17;196(2):309-14. doi: 10.1016/0014-5793(86)80269-1.
2
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引用本文的文献

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Progesterone inhibits estrogen-induced cyclin D1 and cdk4 nuclear translocation, cyclin E- and cyclin A-cdk2 kinase activation, and cell proliferation in uterine epithelial cells in mice.
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