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本文引用的文献

1
Ion Channel Contributions to Wing Development in .离子通道对……翅膀发育的贡献
G3 (Bethesda). 2019 Apr 9;9(4):999-1008. doi: 10.1534/g3.119.400028.
2
Kir2.1 is important for efficient BMP signaling in mammalian face development.Kir2.1对哺乳动物面部发育中高效的骨形态发生蛋白(BMP)信号传导至关重要。
Dev Biol. 2018 Dec 1;444 Suppl 1(Suppl 1):S297-S307. doi: 10.1016/j.ydbio.2018.02.012. Epub 2018 Mar 20.
3
Inwardly rectifying potassium channels influence wing morphogenesis by regulating Dpp release.内向整流钾通道通过调节Dpp释放来影响翅形态发生。
Development. 2017 Aug 1;144(15):2771-2783. doi: 10.1242/dev.146647. Epub 2017 Jul 6.
4
Endogenous Bioelectric Signaling Networks: Exploiting Voltage Gradients for Control of Growth and Form.内源性生物电信号网络:利用电压梯度控制生长和形态。
Annu Rev Biomed Eng. 2017 Jun 21;19:353-387. doi: 10.1146/annurev-bioeng-071114-040647.
5
KCNK9 imprinting syndrome-further delineation of a possible treatable disorder.KCNK9印记综合征——对一种可能可治疗疾病的进一步描述
Am J Med Genet A. 2016 Oct;170(10):2632-7. doi: 10.1002/ajmg.a.37740. Epub 2016 May 6.
6
Bioelectric signalling via potassium channels: a mechanism for craniofacial dysmorphogenesis in KCNJ2-associated Andersen-Tawil Syndrome.通过钾通道的生物电信号传导:KCNJ2相关的安德森-陶威尔综合征中颅面畸形发生的一种机制
J Physiol. 2016 Jun 15;594(12):3245-70. doi: 10.1113/JP271930. Epub 2016 Apr 13.
7
Corrigendum: Mutations in the voltage-gated potassium channel gene KCNH1 cause Temple-Baraitser syndrome and epilepsy.勘误:电压门控钾通道基因KCNH1突变导致坦普尔-巴拉伊特瑟综合征和癫痫。
Nat Genet. 2015 Mar;47(3):304. doi: 10.1038/ng0315-304b.
8
Keppen-Lubinsky syndrome is caused by mutations in the inwardly rectifying K+ channel encoded by KCNJ6.凯彭-卢宾斯基综合征由KCNJ6编码的内向整流钾通道突变引起。
Am J Hum Genet. 2015 Feb 5;96(2):295-300. doi: 10.1016/j.ajhg.2014.12.011. Epub 2015 Jan 22.
9
Molecular bioelectricity: how endogenous voltage potentials control cell behavior and instruct pattern regulation in vivo.分子生物电:内源性电压电位如何控制细胞行为并指导体内模式调控。
Mol Biol Cell. 2014 Dec 1;25(24):3835-50. doi: 10.1091/mbc.E13-12-0708.
10
Mutations in the voltage-gated potassium channel gene KCNH1 cause Temple-Baraitser syndrome and epilepsy.电压门控钾通道基因 KCNH1 的突变导致 Temple-Baraitser 综合征和癫痫。
Nat Genet. 2015 Jan;47(1):73-7. doi: 10.1038/ng.3153. Epub 2014 Nov 24.

骨形态发生蛋白信号传导中的离子通道

Ion Channels in Bone Morphogenetic Protein Signaling.

作者信息

George Laura Faith, Isner Trevor, Bates Emily Anne

机构信息

Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado.

出版信息

Bioelectricity. 2019 Mar 1;1(1):46-48. doi: 10.1089/bioe.2019.0003. Epub 2019 Mar 18.

DOI:10.1089/bioe.2019.0003
PMID:34471808
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8370264/
Abstract

How a single fertilized egg develops into a complex multicellular organism is one of the great mysteries of life. Developmental biology textbooks describe cascades of ligands, receptors, kinases, and transcription factors that designate proliferation, migration, and ultimately fate of cells organized into a multicellular organism. Recently, it has become apparent that ion channels are integral to the process of developmental signaling. Ion channels provide bioelectric signals that must intersect with the known developmental signaling pathways. We review some evidence that bioelectric signaling contributes to bone morphogenetic protein signaling.

摘要

一个受精卵如何发育成一个复杂的多细胞生物体是生命的重大奥秘之一。发育生物学教科书描述了一系列配体、受体、激酶和转录因子,它们决定了组成多细胞生物体的细胞的增殖、迁移以及最终命运。最近,很明显离子通道是发育信号传导过程中不可或缺的一部分。离子通道提供生物电信号,这些信号必须与已知的发育信号通路相互交叉。我们回顾了一些生物电信号传导有助于骨形态发生蛋白信号传导的证据。