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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Interleukin-1 beta and tumour necrosis factor-alpha stimulate the mRNA expression of interleukin-1 receptors in mouse anterior pituitary AtT-20 cells.
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Interleukin-1 beta and tumour necrosis factor-alpha stimulate the mRNA expression of interleukin-1 receptors in mouse anterior pituitary AtT-20 cells.

机译:IL-1β和肿瘤坏死因子-α刺激小鼠垂体前叶AtT-20细胞中IL-1受体的mRNA表达。

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摘要

The RT-PCR technique was used to study IL-1 receptor mRNA levels in AtT-20 cells. IL-1 beta increased type I IL-1 receptor mRNA levels within 1 h, with elevated levels remaining after 24 h, whereas it induced a bell-shaped alteration of type II IL-1 receptor mRNA levels, with a peak after 6 h. Tumour necrosis factor-alpha (TNF alpha) similarly up-regulated type II IL-1 receptor mRNA levels, and type I IL-1 receptor mRNAs albeit to a lesser extent than IL-1 beta. Furthermore, IL-1 beta also induced increases in TNF alpha and c-fos mRNAs. The IL-1 receptor antagonist can fully block all the above effects of IL-1 beta. Up-regulation of type II IL-1R mRNA levels in AtT-20 cells could constitute an important way to modulate IL-1 actions, since type II IL-1R is believed to antagonize IL-1 effects.
机译:RT-PCR技术用于研究AtT-20细胞中IL-1受体mRNA的水平。 IL-1 beta在1小时内增加了I型IL-1受体mRNA的水平,并在24小时后保持了升高的水平,而它诱导了II型IL-1受体mRNA的钟形变化,在6小时后达到了峰值。肿瘤坏死因子-α(TNF alpha)类似地上调II型IL-1受体mRNA水平和I型IL-1受体mRNA水平,尽管程度低于IL-1 beta。此外,IL-1β还诱导TNFα和c-fos mRNA的增加。 IL-1受体拮抗剂可以完全阻断IL-1 beta的所有上述作用。 AtT-20细胞中II型IL-1R mRNA水平的上调可能构成调节IL-1作用的重要途径,因为II型IL-1R被认为可以拮抗IL-1的作用。

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