| 标识符 | CSTR:16397.09.0H01000663 |
|---|---|
| 资源中文名称 | APP基因敲除小鼠 |
| 资源英文名称 | C57BL/6J-App(tm) |
| 疾病概述 | 痴呆症相关模型 |
| 实验动物背景信息 | C57BL/6 |
| 模型制作方法 | 胚胎干细胞打靶 |
| 模型表型数据 | 类淀粉样前体蛋白（AMYLOID BETA A4 PRECURSOR PROTEIN; APP）属于I型跨膜蛋白家族成员。哺乳动物APP蛋白家族大部分在脑内表达，但在其他组织中也有表达。APP主要以APP695, APP751, APP770三种形式存在，而在神经元内APP695显著性表达。APP在机体内具有多种生物学功能，尤其在神经系统发育过程中发挥重要功能。 |
| 动物模型的评价与验证 | APP基因敲除小鼠是研究APP基因功能、老年斑形成、痴呆症、帕金森症等的工具小鼠。 |
| 保存方式 | 冷冻 |
| 合作方式 | 仅限合作研究 |
| 相关文章 |
1 Calhoun ME, Wiederhold K-H, Abramowski, et al. Neuron loss in APP transgenic mice. Nature 395: 755-756, 1998. 2 Cao X, Sudhof TC, A transcriptionally active complex of APP with Fe65 and histone acetyltransferase Tip60. Science 293: 115-120, 2001. 3 Carter DA, Desmarais E, Bellis,et al. More missense in amyloid gene. (Letter) Nature Genet. 2: 255-256, 1992. 4 Chen AC, Selkoe DJ. Response, et al., 'Presenilin-dependent transcriptional control of the A-beta-degrading enzyme neprilysin by intracellular domains of beta-APP and APLP. Neuron 46, 541-554. Neuron 53: 479-483, 2007. 5 Cheng IH, Palop JJ, Esposito, et al. Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutation. Nature Med. 10: 1190-1192, 2004. 6 Colton CA, Vitek MP, Wink D, et al. NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease. Proc. Nat. Acad. Sci. 103: 12867-12872, 2006. Note: Erratum: Proc. Nat. Acad. Sci 103: 15273 only, 2006. l 7 Khoury J, Toft M,Hickman SE, et al. Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease. Nature Med. 13: 432-438, 2007. |
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