Early decrease of survival signal protein and DNA repair enzyme in spinal motor neuron of presymptomatic transgenic mice with a mutant SOD1 gene

机译：用突变SOD1基因早期降低生存信号蛋白和脊柱运动神经元中的脊髓运动神经元的DNA修复酶

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We examined expressions of phosphatidylinositol 3-kinase (PI3-K), Akt and redox factor-1 protein (Ref-1) in the spinal cord of transgenic mice with G93A mutant superoxide dismutase (SOD1) (Tg), a valuable model of human amyotrophic lateral sclerosis (ALS), at early and presymptomatic stage, 18 and 25 weeks of age. Significant decrease of PI3-K, and Akt in Tg/18 mice, and of PI3-K, Akt and Ref-1 in Tg/25 was observed on immunoblotting. Immunohistochem-istry revealed the significant decrease of PI3-K, Akt and Ref-l in spinal motor neurons of Tg/25 mice. No significant loss of anterior horn neurons was detected.Therefore, the decrease of survival signal or impairment of DNA repair in the spinal motor neurons precedes a subsequent death of anterior horn neurons, and may account for the mutant SODl-mediated motor neuronal death in this model.

机译：在具有G93A突变过量的超氧化物歧化酶（SOD1）（TG）的转基因小鼠的脊髓中，在转基因小鼠的脊髓中检查了磷脂酰肌醇3-激酶（PI3-K），AKT和氧化还原因子-1蛋白（REF-1）的表达，是一种有价值的人类肌营养的外侧硬化症（ALS），在早期和假期阶段，18天和25周。在免疫印迹上观察到PI3-K和TG / 18小鼠中的PI3-K，AKT，AKT，AKT和REF-1的显着降低。免疫组织中的研究显示，TG / 25小鼠的脊柱马云中PI3-K，AKT和REF-L的显着降低。未检测到前喇叭神经元的显着损失。因此，脊髓马达神经元中的存活信号或DNA修复的减少损害在后喇叭神经元的后续死亡，并且可能占突变体苏打介导的运动神经元死亡模型。

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《International Symposium on Molecular Mechanism and Epochal Therapeutics for Ischemic Stroke and Dementia》|2003年||共7页
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M. Shiote; H. Ilieva; I. Nagano; T. Murakami; T. Hayashi; M. Shoji; K. Abe;
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中图分类急性脑血管疾病（中风）;
关键词
Phosphatidylinositol 3-kinase; Akt; Redox factor; ALS; SOD1;

机译：磷脂酰肌醇3-激酶;akt;氧化还原因子;als;sod1;

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1. Early decrease of survival factors and DNA repair enzyme in spinal motor neurons of presymptomatic transgenic mice that express a mutant SOD1 gene. [J] . Nagano I, Murakami T, Manabe Y, Life sciences . 2002,第4a5期

机译：表达突变型SOD1基因的症状前转基因小鼠脊髓运动神经元中生存因子和DNA修复酶的早期下降。
2. Early decrease of mitochondrial DNA repair enzymes in spinal motor neurons of presymptomatic transgenic mice carrying a mutant SOD1 gene. [J] . Murakami T, Nagai M, Miyazaki K, Brain research . 2007,第0期

机译：携带突变SOD1基因的症状前转基因小鼠脊髓运动神经元中线粒体DNA修复酶的早期减少。
3. Early decrease of mitochondrial DNA repair enzymes in spinal motor neurons of presymptomatic transgenic mice carrying a mutant SOD1 gene. [J] . Murakami T, Nagai M, Miyazaki K, Brain research . 2007,第0期

机译：携带突变SOD1基因的症状前转基因小鼠脊髓运动神经元中线粒体DNA修复酶的早期减少。
4. Early decrease of survival signal protein and DNA repair enzyme in spinal motor neuron of presymptomatic transgenic mice with a mutant SOD1 gene [C] . M. Shiote, H. Ilieva, I. Nagano, International Symposium on Molecular Mechanism and Epochal Therapeutics for Ischemic Stroke and Dementia . 2003

机译：用突变SOD1基因早期降低生存信号蛋白和脊柱运动神经元中的脊髓运动神经元的DNA修复酶
5. Investigating the pre-mRNA splicing of the Survival Motor Neuron genes to model the Spinal Muscular Atrophy disease phenotype. [D] . Gladman, Jordan Tanin. 2010

机译：研究生存运动神经元基因的mRNA前剪接，以建模脊髓性肌萎缩症疾病表型。
6. Nuclear Localization of Human Superoxide Dismutase 1 (SOD1) and Mutant SOD1-Specific Disruption of Survival Motor Neuron Protein Complex in Transgenic Amyotrophic Lateral Sclerosis Mice [O] . Barry Gertz, Margaret Wong, Lee J. Martin -1

机译：人超氧化物歧化酶1（SOD1）和突变SOD1特定的生存运动神经元蛋白复合体在转基因肌萎缩性侧索硬化小鼠中的核定位。
7. Overexpression of survival motor neuron improves neuromuscular function and motor neuron survival in mutant SOD1 mice [O] . Turner, BJ, Alfazema, N, Sheean, RK, 2014

机译：存活运动神经元的过表达改善突变型SOD1小鼠的神经肌肉功能和运动神经元存活

Early decrease of survival signal protein and DNA repair enzyme in spinal motor neuron of presymptomatic transgenic mice with a mutant SOD1 gene

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