Expression data from RNAi SNCA treated human neuroblastoma cell line

The pre-synaptic protein α-synuclein is a key player in the pathogenesis of Parkinson's disease. Together with accumulation and missfolding of α-synuclein protofibrils serve as seed structures for the aggregation of numerous proteins in the cytoplasm of neuronal cells, the so-called Lewy bodies. Furthermore, missense mutations in the SNCA gene and gene multiplications lead to autosomal dominant forms of familiar PD. However, so far the exact biological role of α-synuclein in normal brain is elusive. To gain more insights into the biological function of this protein we monitored whole genome expression changes in dopaminergic neuroblastoma cells (SH-SY5Y) caused by a 90% reduction of α-synuclein by RNA interference. Keywords: whole genome expression changes through the loss of α-synuclein comparison of expression profil changes in cells with normal α-synuclein level (control siRNA treatment) and reduced α-synuclein level (siSNCA4 treatment), triplicatesof each condition

突触前蛋白α-突触核蛋白（α-synuclein）是帕金森病发病机制中的关键效应分子。α-突触核蛋白原纤维的聚集与错误折叠可作为种子结构，诱导神经元细胞胞质内多种蛋白质聚集形成所谓的路易小体（Lewy bodies）。此外，SNCA基因的错义突变与基因拷贝数增加会引发常染色体显性遗传的家族性帕金森病（PD）。但截至目前，α-突触核蛋白在正常大脑中的确切生物学功能仍不明确。为深入解析该蛋白的生物学功能，本研究通过RNA干扰技术将多巴胺能神经母细胞瘤细胞（SH-SY5Y）内的α-突触核蛋白表达水平下调90%，并监测了全基因组表达变化。关键词：α-突触核蛋白缺失诱导的全基因组表达变化；对比正常α-突触核蛋白水平细胞（对照siRNA处理组）与α-突触核蛋白水平下调细胞（siSNCA4处理组）的表达谱变化，每组设置三次生物学重复。