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TrkA的表达赋予一种永生化下丘脑细胞系对神经生长因子具有神经元样反应性。

Expression of TrkA confers neuron-like responsiveness to nerve growth factor on an immortalized hypothalamic cell line.

作者信息

Zhou J, Holtzman D M, Weiner R I, Mobley W C

机构信息

Department of Neurology, University of California, San Francisco 94143.

出版信息

Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3824-8. doi: 10.1073/pnas.91.9.3824.

DOI:10.1073/pnas.91.9.3824
PMID:8170995
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC43674/
Abstract

The result of nerve growth factor (NGF) actions depends upon the cells in which it signals. To define how signaling is influenced by cellular context, it would be useful to examine cells committed to different fates or cells of a single type at different developmental stages. Interest in NGF actions on neurons of the central nervous system led us to examine GT1-1 cells, an immortalized hypothalamic cell line. GT1-1 cells demonstrated neuronal properties but were unresponsive to NGF and other neurotrophins. Through transfection, trkA expression conferred NGF signaling leading to enhanced neuronal differentiation, including dose-dependent induction of neurite outgrowth and a rapid transient increase in c-fos and NGFI-A mRNA. Under serum-free culture conditions, NGF also delayed cell death. These findings suggest that trkA transfection of neurons and neuronal precursors can be used to better define NGF signaling.

摘要

神经生长因子(NGF)的作用结果取决于其发出信号的细胞。为了确定细胞环境如何影响信号传导,研究致力于不同命运的细胞或处于不同发育阶段的单一类型细胞将很有帮助。对NGF作用于中枢神经系统神经元的兴趣促使我们研究GT1-1细胞,一种永生化的下丘脑细胞系。GT1-1细胞表现出神经元特性,但对NGF和其他神经营养因子无反应。通过转染,trkA的表达赋予了NGF信号传导能力,导致神经元分化增强,包括剂量依赖性诱导神经突生长以及c-fos和NGFI-A mRNA的快速短暂增加。在无血清培养条件下,NGF还能延迟细胞死亡。这些发现表明,对神经元和神经元前体进行trkA转染可用于更好地定义NGF信号传导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/6fcae7f743ed/pnas01131-0359-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/e74ceb44df6f/pnas01131-0357-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/62dcfa33dbf4/pnas01131-0358-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/97ca88b142fb/pnas01131-0358-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/6fcae7f743ed/pnas01131-0359-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/e74ceb44df6f/pnas01131-0357-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/62dcfa33dbf4/pnas01131-0358-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/97ca88b142fb/pnas01131-0358-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34af/43674/6fcae7f743ed/pnas01131-0359-a.jpg

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本文引用的文献

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Transfection with trk restores "slow" NGF binding, efficient NGF uptake, and multiple NGF responses to NGF-nonresponsive PC12 cell mutants.用trk转染可恢复“缓慢”的神经生长因子(NGF)结合、高效的NGF摄取以及对NGF无反应的PC12细胞突变体的多种NGF反应。
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