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神经生长因子调节嗜铬细胞瘤PC12细胞中的微管蛋白转录水平。

Nerve growth factor modulates tubulin transcript levels in pheochromocytoma PC12 cells.

作者信息

Fernyhough P, Ishii D N

机构信息

Department of Physiology, Colorado State University, Fort Collins 80523.

出版信息

Neurochem Res. 1987 Oct;12(10):891-9. doi: 10.1007/BF00966311.

Abstract

We report that nerve growth factor (NGF) can elevate tubulin transcript levels in cultured rat pheochromocytoma PC12 cells in a manner which correlates with its capacity to enhance neurite formation. The elevation is due, at least in part, to transcript stabilization. We have previously shown that insulin and its homologs can similarly enhance neurite outgrowth and tubulin mRNA levels in human neuroblastoma cells. Insulin by itself can neither induce neurite formation nor increase tubulin transcript levels in PC12 cells. However, both responses are potentiated in cells treated with the combination of insulin and NGF. The results together support the generalization that tubulin transcript levels are specifically elevated whenever neurite elongation is initiated by polypeptide neuritogenic factors.

摘要

我们报告称,神经生长因子(NGF)能够以一种与其增强神经突形成能力相关的方式提高培养的大鼠嗜铬细胞瘤PC12细胞中的微管蛋白转录水平。这种升高至少部分是由于转录本的稳定。我们之前已经表明,胰岛素及其同系物能够类似地增强人神经母细胞瘤细胞中的神经突生长和微管蛋白mRNA水平。胰岛素本身既不能诱导PC12细胞中的神经突形成,也不能增加微管蛋白转录水平。然而,在用胰岛素和NGF联合处理的细胞中,这两种反应都得到了增强。这些结果共同支持了这样一个普遍观点,即每当多肽神经生成因子引发神经突伸长时,微管蛋白转录水平就会特异性升高。

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