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本文引用的文献

1
Decidual cell polyploidization necessitates mitochondrial activity.蜕膜细胞的多倍体化需要线粒体活动。
PLoS One. 2011;6(10):e26774. doi: 10.1371/journal.pone.0026774. Epub 2011 Oct 25.
2
Death effector domain-containing protein (DEDD) is required for uterine decidualization during early pregnancy in mice.死亡效应结构域蛋白(DEDD)在小鼠妊娠早期的子宫蜕膜化过程中是必需的。
J Clin Invest. 2011 Jan;121(1):318-27. doi: 10.1172/JCI44723. Epub 2010 Dec 6.
3
Implantation failure: molecular mechanisms and clinical treatment.着床失败:分子机制与临床治疗。
Hum Reprod Update. 2011 Mar-Apr;17(2):242-53. doi: 10.1093/humupd/dmq037. Epub 2010 Aug 21.
4
Polyploidization of liver cells.肝细胞的多倍体化。
Adv Exp Med Biol. 2010;676:123-35. doi: 10.1007/978-1-4419-6199-0_8.
5
Polyploidy: mechanisms and cancer promotion in hematopoietic and other cells.多倍体:造血和其他细胞中的机制和癌症促进作用。
Adv Exp Med Biol. 2010;676:105-22. doi: 10.1007/978-1-4419-6199-0_7.
6
Understanding cytokinesis failure.理解细胞分裂失败。
Adv Exp Med Biol. 2010;676:27-55. doi: 10.1007/978-1-4419-6199-0_3.
7
Molecular mechanisms and function of the spindle checkpoint, a guardian of the chromosome stability.纺锤体检验点的分子机制与功能:染色体稳定性的守护者。
Adv Exp Med Biol. 2010;676:15-26. doi: 10.1007/978-1-4419-6199-0_2.
8
Uterine-specific p53 deficiency confers premature uterine senescence and promotes preterm birth in mice.子宫特异性 p53 缺失导致子宫早衰并促进小鼠早产。
J Clin Invest. 2010 Mar;120(3):803-15. doi: 10.1172/JCI40051.
9
The death effector domain-containing DEDD forms a complex with Akt and Hsp90, and supports their stability.死亡效应结构域(DED)含有 DEDD 形成复合物与 Akt 和 Hsp90,并支持它们的稳定性。
Biochem Biophys Res Commun. 2010 Jan 22;391(4):1708-13. doi: 10.1016/j.bbrc.2009.12.137. Epub 2009 Dec 30.
10
Regional development of uterine decidualization: molecular signaling by Hoxa-10.子宫蜕膜化的区域发展:Hoxa-10 的分子信号。
Mol Reprod Dev. 2010 May;77(5):387-96. doi: 10.1002/mrd.21133.

着床部位蜕膜细胞多倍体的发育调控。

Developmental regulation of decidual cell polyploidy at the site of implantation.

作者信息

Sroga Julie M, Ma Xinghong, Das Sanjoy K

机构信息

Division of Reproductive Sciences, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.

出版信息

Front Biosci (Schol Ed). 2012 Jun 1;4(4):1475-86. doi: 10.2741/s347.

DOI:10.2741/s347
PMID:22652887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4269479/
Abstract

Polyploidy has been reported in several animal cells, as well as within humans; however the mechanism of developmental regulation of this process remains poorly understood. Polyploidy occurs in normal biologic processes as well as in pathologic states. Decidual polyploid cells are terminally differentiated cells with a critical role in continued uterine development during embryo implantation and growth. Here we review the mechanisms involved in polyploidy cell formation in normal developmental processes, with focus on known regulatory aspects in decidual cells.

摘要

多倍体现象已在多种动物细胞以及人类细胞中被报道;然而,这一过程的发育调控机制仍知之甚少。多倍体现象既出现在正常生物学过程中,也出现在病理状态下。蜕膜多倍体细胞是终末分化细胞,在胚胎着床和生长期间子宫的持续发育中起关键作用。在此,我们综述正常发育过程中多倍体细胞形成所涉及的机制,重点关注蜕膜细胞中已知的调控方面。