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Microtubules regulate expression of ICAM-1 in epidermoid cells (KB cells).

机译:微管调节表皮样细胞(KB细胞)中ICAM-1的表达。

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The intercellular adhesion molecule-1/CD54 (ICAM-1) functions as a counterreceptor for other adhesion molecules (e.g. the lymphocyte function-associated antigen-1/CD11a/CD18) required for the interaction of a large variety of cells with leucocytes. Constitutive expression of ICAM-1 in human epidermoid cells (KB cells) is low, but inducible by interferon-gamma (IFN-gamma). Treatment of KB cells with microtubule-disrupting agents, like colchicine, nocodazole and vinblastine, potentiated the constitutive and cytokine-induced ICAM-1 expression on the cell surface. Actinomycin D inhibited microtubule-disrupting agent-induced ICAM-1 surface expression. Increased steady-state levels of ICAM-1 transcripts were found after treatment of KB cells with microtubule-disrupting agents. However, microtubule-disrupting agents neither altered the glyceraldehyde-3-phosphate dehydrogenase mRNA levels nor the amount of expressed alpha(2)-, alpha(3)-and beta(1)-integrins at the cell surface. In addition, they did not changethe ICAM-1 mRNA half-life. These studies indicate a control function of the microtubule network on the expression of ICAM-1.
机译:细胞间粘附分子-1 / CD54(ICAM-1)用作其他粘附分子(例如,与淋巴细胞功能相关的抗原-1 / CD11a / CD18)的反受体,这些粘附分子是多种细胞与白细胞相互作用所需的。 ICAM-1在人表皮细胞(KB细胞)中的组成型表达较低,但可被干扰素-γ(IFN-γ)诱导。用微管破坏剂(例如秋水仙碱,诺考达唑和长春碱)处理KB细胞,可增强组成型和细胞因子诱导的ICAM-1在细胞表面的表达。放线菌素D抑制微管破坏剂诱导的ICAM-1表面表达。用微管干扰剂处理KB细胞后,发现ICAM-1转录本的稳态水平增加。但是,微管破坏剂既没有改变甘油醛-3-磷酸脱氢酶mRNA水平,也没有改变细胞表面表达的α(2)-,α(3)-和β(1)-整合素的数量。另外,它们没有改变ICAM-1 mRNA的半衰期。这些研究表明微管网络对ICAM-1表达的控制功能。

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