《Table 1.Bone diseases or dysfunctions caused by glutamate GPCR mutation or deletion》

《Table 1.Bone diseases or dysfunctions caused by glutamate GPCR mutation or deletion》   提示：宽带有限、当前游客访问压缩模式
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《The role of GPCRs in bone diseases and dysfunctions》


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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XD0061573000    严禁用于非法目的
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
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