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Detection of Relating Molecules for the Pathology of Amyotrophic Lateral Screlosis by the Expressed-Gene Profiling

通过表达基因谱检测肌萎缩侧索硬化病理学的相关分子

基本信息

批准号：
10670582
负责人：
DOYU Manabu
金额：
$ 1.86万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10670582/
关键词：
Amyotrophic Lateral Screlosis Molecular Indexing Expressed-Gene Profile Motor Neuron Death Novel Genes Ring Finger IBR Motif Ubiquitination 神経悪性疾患

项目摘要

The molecular mechanism of the motor neuron death in Amyotrophic lateral sclerosis (ALS) is unknown. We have demonstrated the difference in the expressed-gene profiles between the ALS and spinal anterior horns. We selected 84 clones which had drastic changes changes in their expression levels. Among them, detailed analysis of those matched to ESTs revealed two novel genes (FI39A and FI58G).FI39A cDNA was 4.4kb long and the deduced amino acid sequence should be 838 residues, of which N-terminal half region had ubiquitination-related Ring finger / IBR motif, and bipartite nuclear localization signal (NLS). Northern analysis and ISH showed the expression of FI39A transcript was ubiquitous. The intracellular localization of FI39A protein was perinuclear.FI58G cDNA was 1.8kb long and the deduced amino acid sequence should be 219 residues. The homology search revealed that FI58G protein had no significant homology to any other known molecules. FI58G had a NLS and was localized to the intranuclear region. Northern analysis demonstrated that FI58G mRNA was rich in the brain, spinal cord, heart and muscle.These two novel genes may be involved in the pathogenesis of ALS, although requiring more detailed analysis.

肌萎缩侧索硬化症（ALS）运动神经元死亡的分子机制尚不清楚。我们已经证明了ALS和脊髓前角之间的基因表达谱的差异。我们选择了84个克隆，它们的表达水平发生了剧烈的变化。其中FI 39 A和FI 58 G为新基因，FI 39 A cDNA全长4.4kb，推导的氨基酸序列为838个残基，其N端半区含有泛素化相关的Ring finger / IBR基序，并含有二分核定位信号（NLS）。北方分析和原位杂交结果显示，FI 39 A转录本在细胞内普遍表达。FI 39 A蛋白定位于细胞核周围，FI 58 G cDNA全长1.8kb，推测的氨基酸序列为219个残基。同源性搜索显示，FI 58 G蛋白与其他已知分子没有明显的同源性。FI 58 G具有NLS，定位于核内区域。北方分析表明，FI 58 G基因在脑、脊髓、心脏和肌肉中表达丰富，这两个新基因可能参与ALS的发病机制，但还需进一步研究。