中文摘要：

目的：分析S100A6蛋白分子结构和功能,预测其在肿瘤发生发展过程中可能的分子机制。方法：利用计算机软件,生物信息学工具,查询国际通用的生物信息学数据库,对S100A6氨基酸序列、二级结构域功能域、酶切位点、转录后修饰、亚细胞定位、跨膜结构域、分子功能、蛋白质相互作用等进行分析,并对其生物学功能进行分析和预测。结果：S100A6蛋白为酸性、小分子、稳定性蛋白质、亲水性评估-0.289;该蛋白的二级结构显示为非球状蛋白质,存在两个结构域及两个钙结合区域,没有跨膜区域;该蛋白为非信号肽类型的分泌蛋白,有16个酶切位点,亚细胞定位于核膜、胞质和细胞膜;有10个蛋白质与S100A6蛋白质存在直接的相互作用关系,存在3个磷酸化位点、可能存在2个赖氨酸糖化作用位点、可能存在乙酰化作用,没有糖基化位点。该蛋白质的功能区域存在4个自然突变位点。该蛋白存在钙传感器、介导细胞内钙信号释放,并与其它蛋白相互作用,间接的重组肌动蛋白细胞骨架及在细胞能动性上发挥作用,S100A6蛋白可能调控细胞周期及细胞分化,同时可能刺激Ca2＋依赖的胰岛素释放,刺激催乳素分泌及胞外分泌。结论：S100A6蛋白是钙周期蛋白,很可能在肿瘤发生发展过程中对诱导细胞分化及信号转导方面发挥十分重要的作用。

英文摘要：

Objective：To analyze the structure and function of S100A6 protein and the possible molecular mechanism of S100A6 in tumor genesis and progression.Methods： The amino acid sequence,secondary structure domain and functure domain,enzyme cutting site,posttranscription modification,subcelluar location,transmembrane structure domain,molecular function,protein interaction were analyzed and molecular function further predicted using coputer softwares,bioinformation tools and international bioinformatics database.Results： S100A6 was an acid,small molecular and stable protein,and with grand average of hydropathicity（GRAVY）-0.289.The protein had two structue domains and two calcium binding domains and no transmembrane domain.Its subcellular location was in nucleus envelope,nuclear membrane and cytoplasma.There was 16 enzmy cleage sites,10 interaction sites,3 phosphorylation sites,2 lysine saccharification sites.There was possible acetylation site and no glycosylation site.The function domain had 4 nature mutuant sites.The protein had calcium sensor that mediated cells release calcium signal and interacted with other protein,which indirectly reconbinated actin cytoskeleton and played roles in cell action.S100A6 could regulate cell cycle and cell differentiation,stimulate calcium dependant insulin release,prolactin secretion and extracellular secretion.Conclusion： S100A6 belonged to calcyclin protein,and may play an important role in inducing cell differention and signal transactoin of tumor genesis and progression.