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1. 发明申请

US20060015959A1 Transgenic animals expressing transglutaminase II 审中-公开
标题翻译：表达转谷氨酰胺酶II的转基因动物
公开(公告)号：US20060015959A1
公开(公告)日：2006-01-19
申请号：US11167991
申请日：2005-06-27
申请人： Feng Bian , Rathna Iyer , Kevin Wang , Yuang Ye
发明人： Feng Bian , Rathna Iyer , Kevin Wang , Yuang Ye
IPC分类号： A01K67/027 , C07H21/04 , C12N5/06
CPC分类号： C07K14/70503 , A01K67/0275 , A01K2217/05 , A01K2227/105 , A01K2267/0393 , C12N9/1044 , C12N15/85 , C12N2830/008 , C12N2830/85
摘要： The invention provides transgenic, non-human animals and transgenic non-human mammalian cells harboring a transgene encoding a TGII (activator of the protein kinase cdk 5) polypeptide. The two neuropathological lesions associated with Alzheimer's disease (AD) are amyloid plaques and neurofibrillary tangles (NFTs), composed predominantly of amyloid β peptides and hyperphosphorylated tau, respectively. While animal models for plaque formation exist, there is no animal model that recapitulates the formation of NFTs. This invention provides transgenic mice that overexpress human TGII, an activator of cdk5, resulting in tau that is hyperphosphorylated at AD-relevant epitopes. Deposition of tau is detected in the amygdala, thalamus and cortex. Increased phosphorylated neurofilament, silver-positive neurons and neuronal death are also observed in these regions. We conclude that the overexpression of TGII, an activator of cdk5, is sufficient to produce hyperphosphorylation of tau and neuronal death. The TGII transgenic mouse represents the first model for tau pathology in AD.
摘要翻译：本发明提供具有编码TGII（蛋白激酶cdk 5的激活物）多肽的转基因的转基因非人动物和转基因非人哺乳动物细胞。与阿尔茨海默氏病（AD）相关的两个神经病理学损伤分别是淀粉样蛋白斑和主要由淀粉样β肽组成的神经原纤维缠结（NFT）。虽然存在斑块形成的动物模型，但没有重现NFT形成的动物模型。本发明提供过表达人类TGII（cdk5的激活剂）的转基因小鼠，导致在AD相关表位上过度磷酸化的tau。在杏仁核，丘脑和皮质中检测到tau的沉积。在这些区域也观察到增加的磷酸化神经丝，银阳性神经元和神经元死亡。我们得出结论，cdk5的激活剂TGII的过度表达足以产生tau和神经元死亡的过度磷酸化。 TGII转基因小鼠代表AD中第一个tau病理模型。

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