Integrin avb3 also controls dynamic

Integrin avb3 also controls dynamic changes in the OC cyto￾skeleton associated with the bone resorptive process [19]. Deletion
of b3 in mice leads to a progressive increase in bone mass due to
failure of resorption [25]. When differentiated in vitro, b3/ OCs
do not spread or form a podosome belt upon plating in physio￾logical amounts of receptor activator of NF-kB (RANKL) and
macrophage colony-stimulating factor (M-CSF) [26]. Confirming
their attenuated resorptive activity, b3/ OCs generate fewer and
shallower resorptive lacunae on dentine slices than their wild-type
counterparts. Furthermore, the absence of b3 integrin impairs
motility toward M-CSF [19]. Several lines of evidence show that a
number of signaling molecules, including c-Src, Pyk2, c-Cbl, and
p130Cas are involved in the avb3 integrin-dependent signaling
pathway [27e30]. Integrin signaling first activates c-Src kinase,
which phosphorylates the tyrosine residues of Pyk2, p130Cas,
paxillin, and PLC-g, leading to osteoclast activation. PLC-g is a cross￾talk molecule that acts between avb3 integrin-mediated and M￾CSF-induced signaling in OCs [31,32]. Because integrin avb3 plays a
rate-limiting role in OC-mediated bone resorption, its inhibitors
m

結果 (中文) 1:

整合素 avb3 还控制与骨吸收过程 [19] 有关的业主立案法团细胞骨架的动态变化。删除b3 在小鼠导致的骨质量会逐步增加的失败的吸收 [25]。在体外，b3 加以区分时 / 业主立案法团不传播或形成一条 podosome 带后镀在生理逻辑大量的核转录因子-kB (RANKL) 受体激活剂和巨噬细胞集落刺激因子 (CSF) [26]。确认他们吸收活性减毒、 b3 / 业主立案法团生成少和浅吸收陷窝上牙片比其野生型同行。此外，b3 整合素没有损害运动对 M-CSF [19]。几行的证据表明，数字的信号分子，包括 c-Src，Pyk2，c-Cbl，和p130Cas 参与了 avb3 整合素依赖信号路径 [27e30]。整合素信号首先激活 c Src 激酶其中磷酸化酪氨酸残基的 Pyk2，p130Cas，蛋白和 PLC-g，导致破骨细胞活化。PLC-g 是相声分子，avb3 整合素介导和 M CSF 诱导信号在业主立案法团 [31,32] 之间的行为。因为整合素 avb3 起速率限制在 OC 介导的骨吸收，其抑制剂中的作用m

結果 (中文) 3:

整合素avb3也控制在OC细胞￾骨骼与骨吸收过程[ 19 ]相关的动态变化。删除小鼠B3导致由于骨量逐渐增加吸收失败[ 25 ]。当在体外分化，B3 / OCS不传播或在镀在生理￾逻辑量的NF-κB受体激活剂形成伪足小体带（RANKL）和巨噬细胞集落刺激因子（M-CSF）[ 26 ]。确认他们的衰减吸收活性，B3 / OCS产生少较浅的骨吸收陷窝牙本质片比野生型相对应的人.此外，B3整合素缺失损害对M-CSF [ 19 ]运动。几行的证据表明，一个许多信号分子，包括c-Src，Pyk2，c-Cbl、和p130cas参与avb3整合素依赖的信号路径[ 27e30 ]。整合素信号首先激活c-Src激酶，磷酸化PYK2的酪氨酸残基，p130Cas，桩和plc-g，导致破骨细胞激活。plc-g是跨￾谈分子整合素介导的和M之间avb3行为￾CSF诱导OCS [31,32]信号。由于整合素avb3起限制作用在OC率介导的骨吸收，其抑制剂M