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The activation level of the TNF family receptor, Edar, determines cusp number and tooth number during tooth development

机译:TNF家族受体Edar的激活水平决定了牙齿发育过程中的齿尖数和齿数

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摘要

Mutations in members of the ectodysplasin (TNF-related) signalling pathway, EDA, EDAR, and EDARADD in mice and humans produce an ectodermal dysplasia phenotype that includes missing teeth and smaller teeth with reduced cusps. Using the keratin 14 promoter to target expression of an activated form of Edar in transgenic mice, we show that expression of this transgene is able to rescue the tooth phenotype in Tabby (Eda) and Sleek (Edar) mutant mice. High levels of expression of the transgene in wild-type mice result in molar teeth with extra cusps, and in some cases supernumerary teeth, the opposite of the mutant phenotype. The level of activation of Edar thus determines cusp number and tooth number during tooth development. (C) 2004 Elsevier Inc. All rights reserved.
机译:小鼠和人类中的外生增生素(TNF相关)信号传导途径,EDA,EDAR和EDARADD成员的突变会产生外胚层发育异常表型,包括缺失的牙齿和较小的牙齿,但牙尖减少。使用角蛋白14启动子靶向转基因小鼠中Edar激活形式的表达,我们表明该转基因的表达能够挽救Tabby(Eda)和Sleek(Edar)突变小鼠的牙齿表型。在野生型小鼠中转基因的高水平表达导致臼齿有额外的尖齿,在某些情况下是多余的牙齿,与突变表型相反。因此,Edar的激活水平决定了牙齿发育过程中的尖齿数和齿数。 (C)2004 Elsevier Inc.保留所有权利。

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