NSSR1促进小鼠胚胎癌P19细胞的神经元分化。

NSSR1 promotes neuronal differentiation of mouse embryonic carcinoma P19 cells.

作者信息

Liu Lei, Chen Xian-hua, Huang Jia, Lin Jun-ji, Lin Wan-min, Xu Ping

机构信息

Laboratory of Genomic Physiology, Center for Brain Research; National Key Laboratory of Medical Neuroscience, School of Life Sciences, Fudan University, Shanghai 200433, People's Republic of China.

出版信息

Neuroreport. 2004 Apr 9;15(5):823-8. doi: 10.1097/00001756-200404090-00017.

DOI:10.1097/00001756-200404090-00017

PMID:15073523

Abstract

We generated the small interference RNAs to specifically silence the expression of neural salient serine/arginine rich protein 1 (NSSR1) and showed that the inhibition of NSSR1 expression in mouse embryonic carcinoma cells (P19) reduces neuronal differentiation. By contrast, its over-expression promotes the differentiation. Neither inhibition nor over-expression shows distinct effect on cell proliferation. The over-expression increases the inclusion of NCAM L1 exon2 while the inhibition reduces the inclusion. The splicing of kinase insert free isoform of TrkC (TrkC-K1) is increased by the over-expression. The results demonstrate that NSSR1 promotes neuronal differentiation and the splicing of NCAML1 exon2 and TrkC-K1.

摘要

我们生成了小干扰RNA以特异性沉默神经突出丝氨酸/精氨酸丰富蛋白1（NSSR1）的表达，并表明在小鼠胚胎癌细胞（P19）中抑制NSSR1表达会降低神经元分化。相比之下，其过表达则促进分化。抑制或过表达对细胞增殖均无明显影响。过表达增加了神经细胞黏附分子L1（NCAM L1）外显子2的包含，而抑制则减少了包含。TrkC的无激酶插入异构体（TrkC-K1）的剪接通过过表达而增加。结果表明，NSSR1促进神经元分化以及NCAML1外显子2和TrkC-K1的剪接。