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SOX10基因在人类发育过程中的表达。

Expression of the SOX10 gene during human development.

作者信息

Bondurand N, Kobetz A, Pingault V, Lemort N, Encha-Razavi F, Couly G, Goerich D E, Wegner M, Abitbol M, Goossens M

机构信息

Laboratoire de Génétique Moléculaire et Physiopathologie, Institut National de la Santé et de la Recherche Médicale, U.468, Hôpital Henri Mondor, Créteil, France.

出版信息

FEBS Lett. 1998 Aug 7;432(3):168-72. doi: 10.1016/s0014-5793(98)00843-6.

DOI:10.1016/s0014-5793(98)00843-6
PMID:9720918
Abstract

SOX10, a new member of the SOX gene family, is a transcription factor defective in the Dom (Dominant megacolon) mouse and in the human Shah-Waardenburg syndrome. To help unravel its physiological role during human development, we studied SOX10 gene expression in embryonic, fetal, and adult human tissues by Northern blot and in situ hybridization. As in mice, the human SOX10 gene was essentially expressed in the neural crest derivatives that contribute to the formation of the peripheral nervous system, and in the adult central nervous system. Nevertheless, it was more widely expressed in humans than in rodents. The spatial and temporal pattern of SOX10 expression supports an important function in neural crest development.

摘要

SOX10是SOX基因家族的一个新成员,是一种在Dom(显性巨结肠)小鼠和人类沙-瓦登伯格综合征中存在缺陷的转录因子。为了有助于阐明其在人类发育过程中的生理作用,我们通过Northern印迹法和原位杂交技术研究了SOX10基因在人类胚胎、胎儿及成人组织中的表达情况。与小鼠一样,人类SOX10基因主要在有助于外周神经系统形成的神经嵴衍生物以及成人中枢神经系统中表达。然而,它在人类中的表达比在啮齿动物中更为广泛。SOX10表达的时空模式支持其在神经嵴发育中具有重要功能。

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Expression of the SOX10 gene during human development.SOX10基因在人类发育过程中的表达。
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Sox10 mutation disrupts neural crest development in Dom Hirschsprung mouse model.Sox10突变破坏了Dom Hirschsprung小鼠模型中的神经嵴发育。
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Mutation of the Sry-related Sox10 gene in Dominant megacolon, a mouse model for human Hirschsprung disease.在显性巨结肠(一种人类先天性巨结肠病的小鼠模型)中,与性别决定基因Sry相关的Sox10基因发生突变。
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Survival and glial fate acquisition of neural crest cells are regulated by an interplay between the transcription factor Sox10 and extrinsic combinatorial signaling.神经嵴细胞的存活和神经胶质命运获得受转录因子Sox10和外在组合信号之间相互作用的调控。
Development. 2001 Oct;128(20):3949-61. doi: 10.1242/dev.128.20.3949.

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