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甲状旁腺素增强成骨样细胞ROS 17/2.8中酪氨酸蛋白磷酸化的研究
Parathyroid Hormone Increase the Level of Tyrosine Protein Phosphorylation in Osteoblast like ROS 17/2 8 cells
【摘要】 为了研究甲状旁腺素(parathyroidhormone,PTH)促成骨样细胞ROS17/2.8增殖分化的信号传递的机理,观察了PTH对细胞内酪氨酸蛋白激酶(tyrosineproteinkinases,TPK)活性及酪氨酸蛋白磷酸化水平的影响,并检测了PTH对c-rasmRNA表达的诱导作用.结果表明,PTH可增强细胞内TPK活性,提高细胞内酪氨酸蛋白磷酸化水平,以及促进c-rasmRNA的持续表达.这些结果提示,PTH促增殖的细胞内信息传递通路与酪氨酸蛋白激酶-ras-MAPKinase通路密切相关,而PKA/PKC通路的最终效应可能是通过与上述通路的crosstalk实现的
【Abstract】 Recent studies have shown that parathyroid hormone exerts its anabolic action on bone.The mechanism is still not clear.Since the main signal transduction pathway of PTH is via PKA or PKC,but in most cases cell proliferation is always associated with tyrosine protein phosphorylation Ras MAP Kinase pathway.This work is an attempt to demonstrate that PTH can also induce tyrosine protein phosphorylation and ras expression.The results showed that in osteoblast like ROS 17/2 8 cells,after treated with PTH(10 -9 mol/L)or IGF Ⅰ(10 -9 mol/L)(as positive control)for 60 h,tyrosine protein kinase activity was increased 71 6% and 87% respectively.Whereas tyrosine phosphorylated protein level was increased 165% and 305% respectively,the expression of c ki ras mRNA was also enhanced by 226% and 358% respectively after 6 h treatment.These results indicate that PTH can induce cell proliferation via tyrosine protein phosphorylation pathway indirectly.
- 【文献出处】 中国生物化学与分子生物学报 ,CHINESE JOURNAL OF BIOCHEMISTRY AND MOLECULAR BIOLOGY , 编辑部邮箱 ,1999年02期
- 【分类号】Q573
- 【被引频次】2
- 【下载频次】78