《Table 4.Bone diseases or dysfunctions caused by theγ-group of rhodopsin GPCR mutation or deletion》下
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《The role of GPCRs in bone diseases and dysfunctions》
Furthermore,several GPCR gene knockout mice displayed different phenotypes in different strains.The bone mass was reduced in young(4-week-old)P2y13-knockout mice via promotion of osteoblastogenesis and suppression of osteoclastogenesis,but mature(>10-week-old)P2y13-knockout mice showed the opposite bone phenotype via suppression of osteoblastogenesis.229,231P2y2 deficiency increased mouse bone mass in C57BL/6mice225,232by promoting bone reformation and suppressing bone resorption but exhibited reduced bone mass in SV129 mice233by reducing osteoblast differentiation and mineralization.P2y7knockout reduced bone mass in mixed genetic mice(129/OlaXC57BL/6XDBA/2)by reducing osteoblast number and activity234but increased cortical thickness in C57 mice235promoting osteoclast-mediated bone resorption(Table 5).
图表编号 | XD0061573900 严禁用于非法目的 |
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绘制时间 | 2019.06.01 |
作者 | Jian Luo、Peng Sun、Stefan Siwko、Mingyao Liu、Jianru Xiao |
绘制单位 | East China Normal University and Shanghai Changzheng Hospital Joint Research Center for Orthopedic Oncology,Shanghai Key Laboratory of Regulatory Biology,Institute of Biomedical Sciences and School of Life Sciences,East China Normal University、East China |
更多格式 | 高清、无水印(增值服务) |
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