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ras p21蛋白参与白细胞介素2、白细胞介素3和粒细胞/巨噬细胞集落刺激因子的信号转导途径,但不参与白细胞介素4的信号转导途径。

Involvement of ras p21 protein in signal-transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4.

作者信息

Satoh T, Nakafuku M, Miyajima A, Kaziro Y

机构信息

DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304-1104.

出版信息

Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3314-8. doi: 10.1073/pnas.88.8.3314.

DOI:10.1073/pnas.88.8.3314
PMID:1826565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC51437/
Abstract

The protooncogene ras acts as a component of signal-transduction networks in many kinds of cells. The ras gene product (p21) is a GTP-binding protein, and the activity of the protein is regulated by bound GDP/GTP. Recent studies have shown that a certain class of growth factors stimulates the formation of active p21-GTP complexes in fibroblasts and that oncogene products with enhanced tyrosine kinase activities have a similar effect on ras p21. We have measured the ratio of active GTP-bound p21 to total p21 in several lymphoid and myeloid cell lines in order to understand the role of ras in the proliferation of these cells. Interleukin 2 (IL-2), IL-3, and granulocyte/macrophage colony-stimulating factor (GM-CSF) enhance the formation of the active p21.GTP, whereas IL-4 has no effect on p21-bound GDP/GTP. These results strongly suggest that ras p21 acts as a transducer of signals from IL-2, IL-3, and GM-CSF, but not from IL-4.

摘要

原癌基因ras在多种细胞中作为信号转导网络的一个组成部分发挥作用。ras基因产物(p21)是一种GTP结合蛋白,该蛋白的活性受结合的GDP/GTP调节。最近的研究表明,某一类生长因子可刺激成纤维细胞中活性p21-GTP复合物的形成,并且具有增强酪氨酸激酶活性的癌基因产物对ras p21也有类似作用。为了了解ras在这些细胞增殖中的作用,我们测定了几种淋巴细胞和髓细胞系中活性GTP结合的p21与总p21的比例。白细胞介素2(IL-2)、IL-3和粒细胞/巨噬细胞集落刺激因子(GM-CSF)可增强活性p21.GTP的形成,而IL-4对结合p21的GDP/GTP没有影响。这些结果强烈表明,ras p21作为来自IL-2、IL-3和GM-CSF的信号转导分子,但不是来自IL-4的信号转导分子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/4a34f60ce0d0/pnas01058-0358-c.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/db794c5c603b/pnas01058-0357-c.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/b3283a38f781/pnas01058-0358-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/4a34f60ce0d0/pnas01058-0358-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/54539afdf8f0/pnas01058-0357-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/ea3594ce99e3/pnas01058-0357-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/db794c5c603b/pnas01058-0357-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/23a5b637bf33/pnas01058-0358-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/b3283a38f781/pnas01058-0358-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0976/51437/4a34f60ce0d0/pnas01058-0358-c.jpg

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