Minor expression of fascin-1 gene (FSCN1) in NTera2 cells depleted of CREB-binding protein
Minor expression of fascin-1 gene (FSCN1) in NTera2 cells depleted of CREB-binding protein
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DOI：
10.1016/j.neulet.2005.02.027
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发表时间：
2005-06-10
影响因子：
2.5
通讯作者：
Mazzilli, MC
中科院分区：
文献类型：
--
作者：
Megiorni, F;Indovina, P;Mazzilli, MC
creb结合蛋白（CBP）是一种转录辅激活因子，其突变可引起基因表达的普遍扰动。采用RNA干扰法对NT2神经前体细胞的CBP基因进行了沉默。在1.2 K人cDNA微阵列上的杂交实验表明，编码fasin -1蛋白的FSCN1基因在cbp缺失的细胞中的表达明显低于对照组。Real Time PCR和Western blotting检测证实了这种减少。我们还分析了视黄酸（RA）诱导的NT2神经元分化过程中FSCN1的表达谱，显示FSCNI在神经发生过程中上调。这种mRNA的增加表明，根据其动作蛋白捆绑功能及其在神经突和神经元生长锥中的定位，筋膜蛋白-1在成熟神经元形成中的重要性。在没有CBP因子的情况下，在ra处理的细胞中也建立了较低的FSCNI转录量。总之，本研究支持FSCN1作为NT2神经元分化的新标记物，以及CBP在其调控中的可能作用。2005爱思唯尔爱尔兰有限公司版权所有。
CREB-binding protein (CBP) is a transcriptional coactivator whose mutations may cause a generalized perturbation of gene expression. We silenced the CBP gene in NT2 neuronal precursor cells by RNA interference. Hybridization experiments on 1.2 K human cDNA microarrays showed that the FSCN1 gene, encoding for fascin-1 protein, was clearly less expressed in CBP-depleted cells than in controls. This reduction was confirmed by Real Time PCR and Western blotting assays. We also analyzed FSCN1 expression profile during NT2 neuronal differentiation induced by retinoic acid (RA), showing that FSCNI was up-regulated during neurogenesis. This mRNA increasing suggests the importance of fascin-1 in the formation of mature neurons, in accordance with its actin-bundling function and its localization in neurites and neuronal growth cones. The lower amount of FSCNI transcript in the absence of the CBP factor was also established in RA-treated cells. In conclusion, this research supports FSCN1 as a novel marker of NT2 neuronal differentiation and the possible role of CBP in its regulation. (c) 2005 Elsevier Ireland Ltd. All rights reserved.