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Characterization of genetically engineered mouse models carrying Col2a1-cre-induced deletions of Lrp5 and/or Lrp6

机译:携带Col2a1-cre诱导的Lrp5和/或Lrp6缺失的基因工程小鼠模型的表征

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Mice carrying Collagen2a1-cre -mediated deletions of Lrp5 and/or Lrp6 were created and characterized. Mice lacking either gene alone were viable and fertile with normal knee morphology. Mice in which both Lrp5 and Lrp6 were conditionally ablated via Collagen2a1 -cre-mediated deletion displayed severe defects in skeletal development during embryogenesis. In addition, adult mice carrying Collagen2a1-cre -mediated deletions of Lrp5 and/or Lrp6 displayed low bone mass suggesting that the Collagen2a1-cre transgene was active in cells that subsequently differentiated into osteoblasts. In both embryonic skeletal development and establishment of adult bone mass, Lrp5 and Lrp6 carry out redundant functions.
机译:创建并表征了携带胶原2a1-cre介导的Lrp5和/或Lrp6缺失的小鼠。仅缺乏这两种基因的小鼠就具有正常膝盖形态的存活力和繁殖力。 Lrp5和Lrp6都通过Collagen2a1 -cre介导的缺失条件消融的小鼠在胚胎发生过程中显示出骨骼发育的严重缺陷。另外,携带Collagen2a1-cre介导的Lrp5和/或Lrp6缺失的成年小鼠显示出低骨量,表明Collagen2a1-cre转基因在随后分化为成骨细胞的细胞中具有活性。 Lrp5和Lrp6在胚胎骨骼发育和成年骨量建立中都具有冗余功能。

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