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孕酮在正常及肿瘤性哺乳动物卵巢中的非基因组作用

Non-genomic actions of progesterone in the normal and neoplastic mammalian ovary.

作者信息

Peluso John J

机构信息

Department of Cell Biology, University of Connecticut School of Medicine, Farmington, Connecticut 06030, USA.

出版信息

Semin Reprod Med. 2007 May;25(3):198-207. doi: 10.1055/s-2007-973432.

DOI:10.1055/s-2007-973432
PMID:17447209
Abstract

This review summarizes recent findings on the non-genomic or membrane-initiated actions of progesterone that regulate the function of the normal and neoplastic mammalian ovary. This review focuses on three receptors: the classic progesterone receptor, the membrane progesterone receptors (MPRalpha, beta, and gamma) that were initially cloned from seatrout ovaries, and a progesterone binding protein referred to as progesterone receptor membrane component-1 (PGRMC1). Specifically, the structure of each of these receptors is compared and related to their capacity to activate various signal transduction pathways. Then the biological effects of P4 on the function of granulosa cells, luteal cells, ovarian surface epithelial cells, and ovarian cancers that are derived from the ovarian surface epithelial cells are discussed in relationship to the expression of each of these receptors. Whenever possible, studies involving human cells and tissues are presented, although data from other mammalian species are used to supplement the human studies to provide a more complete picture of this complex and rapidly developing area of membrane-initiated actions of progesterone.

摘要

本综述总结了孕酮的非基因组或膜启动作用的最新研究结果,这些作用调节正常和肿瘤性哺乳动物卵巢的功能。本综述聚焦于三种受体:经典孕酮受体、最初从海鲈卵巢克隆的膜孕酮受体(MPRα、β和γ),以及一种称为孕酮受体膜成分-1(PGRMC1)的孕酮结合蛋白。具体而言,对这些受体的结构进行了比较,并探讨了它们激活各种信号转导途径的能力。然后,结合这些受体各自的表达情况,讨论了孕酮(P4)对颗粒细胞、黄体细胞、卵巢表面上皮细胞以及源自卵巢表面上皮细胞的卵巢癌功能的生物学影响。只要有可能,就会展示涉及人类细胞和组织的研究,不过也会使用其他哺乳动物物种的数据来补充人类研究,以便更全面地了解孕酮膜启动作用这一复杂且快速发展的领域。

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Classical and Non-Classical Progesterone Signaling in Breast Cancers.乳腺癌中的经典和非经典孕酮信号传导
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Membrane progesterone receptor beta (mPRβ/Paqr8) promotes progesterone-dependent neurite outgrowth in PC12 neuronal cells via non-G protein-coupled receptor (GPCR) signaling.膜孕激素受体β(mPRβ/Paqr8)通过非 G 蛋白偶联受体(GPCR)信号促进 PC12 神经元细胞中孕激素依赖性轴突生长。
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