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目的 探讨人类粒巨噬细胞集落刺激因子(GMCSF) 受体(GMR) 在NIH3T3 细胞中表达的功能特性。方法 将编码人GMRα和β亚单位的cDNA 转染到无人GMR表达的小鼠NIH3T3 细胞中,并检测其阳性转染子在配体刺激后的增殖信号传导与酪氨酸磷酸化。结果 重建的功能性GMRα/β可以介导细胞增殖与细胞集落形成,并诱导βc、Jak2、Shc 及Shc 相关蛋白P145(SHIP) 酪氨酸磷酸化,然而,人GMCSF并不能激活仅含GMRα的NIH3T3 细胞出现有丝分裂信号表达。结论 人GMRα与β亚单位同时转染入NIH3T3 细胞后,可通过βc 磷酸化,激活Jak2 、Shc 和SHIP信号传导途径,而导致配体依赖性细胞生长与集落形成
Objective To investigate the functional characteristics of human GM-CSF receptor (GMR) expressed in NIH3T3 cells. Methods The cDNA encoding human GMRα and β subunits was transfected into mouse NIH3T3 cells without human GMR and the proliferation signal transduction of the positive transfectants after ligand stimulation was tested. The Results The reconstructed functional GMRα / β could mediate cell proliferation and colony formation, and induced tyrosine phosphorylation of βc, Jak2, Shc and Shc-associated protein P145 (SHIP). However, human GMCSF did not activate NIH3T3 cells containing only GM Rα appear mitotic signal expression. Conclusions Simultaneous transfection of human GMRα and β subunits into NIH3T3 cells activates Jak2, Shc and SHIP signaling pathways through βc phosphorylation, leading to ligand-dependent cell growth and colony formation