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作 者:董子明[1,2] 杨洪艳 张义国[1,2] 赵明耀 郑智敏[1,2]
机构地区:[1]河南医科大学病理生理学教研室 [2]耶鲁大学医学院皮肤系
出 处:《河南医科大学学报》1999年第1期14-18,共5页Journal of Henan Medical University
摘 要:目的:IL7可刺激一些良性和恶性淋巴细胞增生,其中包括来自皮肤样T细胞瘤(CTCL)病人的肿瘤细胞。Janus激酶家族(JAKs)与许多细胞因子受体的信号传导系统有关。JAK3是JAKs激酶家族的新成员,其在自然杀伤细胞(NK)和活化的T细胞上表达,并在这些细胞中从功能上和物理上与白细胞介素2受体(IL2R)结合起来。为此,本研究进一步探讨白细胞介素7(IL7)引起皮肤样T细胞瘤肿瘤细胞JAK3的磷酸化和活化。方法:CTCL外周血中分离的肿瘤细胞,用IL7分别处理1、5、10、20min,蛋白裂解物用抗JAK3抗体,抗p59fyn抗体进行免疫沉淀,用抗JAK3和抗磷酸化酪氨酸作Western印迹检测。结果:IL7能引起CTCL肿瘤细胞的JAK3酪氨酸磷酸化,抗p59fyn抗体能结合JAK3,未发现IL12能诱导CTCL细胞的JAK3磷酸化。结论:提示IL7可能在CTCL的病理生理学上起一定的作用,且证实在CTCL细胞中IL7受体介导了酪氨酸磷酸化的信号传导途径。Aim: To study induced phosphorylation and activation of JAK 3 in cutaneous T cell lymphoma (CTCL) by interleukin 7 (IL 7).IL 7 stimulates proliferation of several benign and malignant lymphocyte populations including tumor cells from patients with CTCL.The Janus family of kinases (JAKs) has been shown to be involved in the signal transduction of a number of cytokine receptors.A novel JAK family member JAK 3,which is expressed in natural killer (NK) and activated T cells,is coupled functionally and physically with the interleukin 2 (IL 2) receptor (IL 2R) in those cells.Methods:Cells isolated from peripheral blood of CTCL patients were treated with IL 7 in vitro for 1,5,10,15 and 20 min,respectively.Immunoprecipitating the lysates was performed with anti JAK 3 andanti p59fyn antibodies and Western blotting with anti phosphorylated tyrosine and anti JAK 3 antibodies.Results:IL 7 induced tyrosine phosphorylation of JAK 3 in CTCL cells.Anti p59fyn antibody co immunoprecipitated with JAK 3.But it was not found that IL 12 could induce phosphorylation of JAK 3.Conclusion: These results suggest that lL 7 may play a role in pathophysiology of CTCL,and indicate that the IL 7 receptor (IL 7R) mediates the activation of the tyrosine phosphorylation signal transduction pathway.
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