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本文引用的文献

1
Inhibition of Sox2-dependent activation of Shh in the ventral diencephalon by Tbx3 is required for formation of the neurohypophysis.Tbx3 通过抑制 Sox2 依赖性 Shh 的激活,对神经垂体的形成是必需的。
Development. 2013 Jun;140(11):2299-309. doi: 10.1242/dev.094524.
2
Multiple endocrine neoplasia type 4.多发性内分泌肿瘤 4 型。
Front Horm Res. 2013;41:63-78. doi: 10.1159/000345670. Epub 2013 Mar 19.
3
Mutations in FGF17, IL17RD, DUSP6, SPRY4, and FLRT3 are identified in individuals with congenital hypogonadotropic hypogonadism.在先天性低促性腺激素性性腺功能减退症患者中鉴定出 FGF17、IL17RD、DUSP6、SPRY4 和 FLRT3 的突变。
Am J Hum Genet. 2013 May 2;92(5):725-43. doi: 10.1016/j.ajhg.2013.04.008.
4
Mammalian interphase cdks: dispensable master regulators of the cell cycle.哺乳动物间期周期蛋白依赖性激酶:细胞周期中并非必需的主要调节因子。
Genes Cancer. 2012 Nov;3(11-12):614-8. doi: 10.1177/1947601913479799.
5
The homeobox gene Otx2 in development and disease.同源盒基因 Otx2 在发育和疾病中的作用。
Exp Eye Res. 2013 Jun;111:9-16. doi: 10.1016/j.exer.2013.03.007. Epub 2013 Mar 21.
6
Signaling pathways that control cell proliferation.控制细胞增殖的信号通路。
Cold Spring Harb Perspect Biol. 2013 Mar 1;5(3):a008904. doi: 10.1101/cshperspect.a008904.
7
Mechanisms of activin-stimulated FSH synthesis: the story of a pig and a FOX.激活素刺激 FSH 合成的机制:一个猪和一个 FOX 的故事。
Biol Reprod. 2013 Mar 28;88(3):78. doi: 10.1095/biolreprod.113.107797. Print 2013 Mar.
8
Angiogenesis in the intermediate lobe of the pituitary gland alters its structure and function.垂体中间叶的血管生成改变了其结构和功能。
Gen Comp Endocrinol. 2013 May 1;185:10-8. doi: 10.1016/j.ygcen.2013.01.009. Epub 2013 Jan 30.
9
Impaired fertility and FSH synthesis in gonadotrope-specific Foxl2 knockout mice.促性腺激素细胞特异性Foxl2基因敲除小鼠的生育力受损及促卵泡激素合成障碍
Mol Endocrinol. 2013 Mar;27(3):407-21. doi: 10.1210/me.2012-1286. Epub 2013 Jan 22.
10
The forkhead transcription factor, Foxd1, is necessary for pituitary luteinizing hormone expression in mice.叉头框转录因子 Foxd1 对于小鼠垂体促黄体生成素的表达是必需的。
PLoS One. 2012;7(12):e52156. doi: 10.1371/journal.pone.0052156. Epub 2012 Dec 19.

垂体腺的发育和疾病:从干细胞到激素生成。

Pituitary gland development and disease: from stem cell to hormone production.

机构信息

Department of Biological Sciences, University of South Carolina, Columbia, South Carolina, USA.

出版信息

Curr Top Dev Biol. 2013;106:1-47. doi: 10.1016/B978-0-12-416021-7.00001-8.

DOI:10.1016/B978-0-12-416021-7.00001-8
PMID:24290346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4039019/
Abstract

Many aspects of pituitary development have become better understood in the past two decades. The signaling pathways regulating pituitary growth and shape have emerged, and the balancing interactions between the pathways are now appreciated. Markers for multipotent progenitor cells are being identified, and signature transcription factors have been discovered for most hormone-producing cell types. We now realize that pulsatile hormone secretion involves a 3D integration of cellular networks. About a dozen genes are known to cause pituitary hypoplasia when mutated due to their essential roles in pituitary development. Similarly, a few genes are known that predispose to familial endocrine neoplasia, and several genes mutated in sporadic pituitary adenomas are documented. In the next decade, we anticipate gleaning a deeper appreciation of these processes at the molecular level, insight into the development of the hypophyseal portal blood system, and evolution of better therapeutics for congenital and acquired hormone deficiencies and for common craniopharyngiomas and pituitary adenomas.

摘要

在过去的二十年中,人们对垂体发育的许多方面有了更好的理解。调节垂体生长和形态的信号通路已经出现,并且现在人们已经认识到这些通路之间的平衡相互作用。多能祖细胞的标志物正在被鉴定,并且大多数产生激素的细胞类型的特征转录因子已经被发现。我们现在意识到,脉冲式激素分泌涉及细胞网络的 3D 整合。由于在垂体发育中具有重要作用,约有十几个基因在发生突变时会导致垂体发育不全。同样,已知有一些基因易导致家族性内分泌肿瘤,并且已经记录了一些在散发的垂体腺瘤中发生突变的基因。在未来十年,我们预计将在分子水平上更深入地了解这些过程,深入了解垂体门脉血液系统的发育,以及为先天性和获得性激素缺乏症以及常见的颅咽管瘤和垂体腺瘤开发更好的治疗方法。