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内容编辑hTnfsf11小鼠
分类: 代谢性疾病鼠
发布时间: 2019-09-16 11:00
应用：骨质疏松症
级别：SPF
类型：TG
背景：C57BL/6
名称：hTnfsf11
编号：LM000166
级别：SPF
类型：TG
背景：C57BL/6
名称：hTnfsf11
编号：LM000166
RANKL
RANKL转基因小鼠模型可自发严重的骨质疏松症，表现为骨小梁减少、骨小梁间连接性差。人类骨质疏松症治疗药物Denosumab的治疗可显著逆转骨质疏松症状。RANKL（TNFSF11）是TNF超家族成员，参与免疫调节及骨代谢（形成/吸收），是破骨细胞分化及成熟的重要激活因子。RANKL通过与OPG竞争结合受体RANK，激活破骨细胞分化，促进骨吸收。RANKL过表达会导致破骨细胞过度活化而出现骨质疏松症。
| 疾病造模 | 代养代繁 | 药效评估 | 生化分析 | 行为分析 | 影像检测 | 病理检测 |
RANKL转基因小鼠模型可自发严重的骨质疏松症，表现为骨小梁减少、骨小梁间连接性差。人类骨质疏松症治疗药物Denosumab的治疗可显著逆转骨质疏松症状。RANKL（TNFSF11）是TNF超家族成员，参与免疫调节及骨代谢（形成/吸收），是破骨细胞分化及成熟的重要激活因子。RANKL通过与OPG竞争结合受体RANK，激活破骨细胞分化，促进骨吸收。RANKL过表达会导致破骨细胞过度活化而出现骨质疏松症。
| 疾病造模 | 代养代繁 | 药效评估 | 生化分析 | 行为分析 | 影像检测 | 病理检测 |