CAJ | 학술논문

背景:从蛋白质组学水平研究 B6-Co 突变系小鼠浑浊角膜与正常 B6小鼠角膜组织的异同,有利于阐释人类角膜混浊的发生机制,开辟从表型驱动研究基因功能的新途径.目的:应用二维凝胶电泳分析技术比较分析 B6和 B6-Co 小鼠的角膜蛋白质组学差异.方法:分别提取 B6与 B6-Co 突变系小鼠角膜组织蛋白,将所获得的蛋白质样品进行二维凝胶电泳和凝胶染色,分析电泳图谱,比较正常角膜组织与混浊角膜组织的蛋白质异同.结果与结论:实验成功建立了对小鼠两种角膜组织蛋白的提取及二维凝胶电泳的基本方法和条件,二维凝胶电泳图谱清晰,通过比较分析发现 B6-Co 突变系小鼠混浊角膜蛋白质组中有13个蛋白质点显著下调,6个表达显著上调.B6小鼠和 B6-Co 突变系小鼠角膜蛋白质组有显著差异表达,提示由于基因的突变导致了相关信号通路的基因表达上调、下调或沉默.
배경:종단백질조학수평연구 B6-Co 돌변계소서혼탁각막여정상 B6소서각막조직적이동,유리우천석인류각막혼탁적발생궤제,개벽종표형구동연구기인공능적신도경.목적:응용이유응효전영분석기술비교분석 B6화 B6-Co 소서적각막단백질조학차이.방법:분별제취 B6여 B6-Co 돌변계소서각막조직단백,장소획득적단백질양품진행이유응효전영화응효염색,분석전영도보,비교정상각막조직여혼탁각막조직적단백질이동.결과여결론:실험성공건립료대소서량충각막조직단백적제취급이유응효전영적기본방법화조건,이유응효전영도보청석,통과비교분석발현 B6-Co 돌변계소서혼탁각막단백질조중유13개단백질점현저하조,6개표체현저상조.B6소서화 B6-Co 돌변계소서각막단백질조유현저차이표체,제시유우기인적돌변도치료상관신호통로적기인표체상조、하조혹침묵.
BACKGROUND: The similarities and differences between opaque cornea of B6-Co mutant mice and normal cornea of normal B6 mice at the proteomic level have been studied, which can help to il uminate the mechanisms of human corneal opacity and develop new ways for studying gene function using the phenotype-driven approach. OBJECTIVE: To compare and analyze the similarities and differences of cornea proteomics between B6 mice and B6-Co mutant mice using two-dimensional gel electrophoresis method. METHODS: After the corneal tissue protein of B6 mice and B6-Co mutant mice was extracted respectively, the samples acquired were performed two-dimensional gel electrophoresis and gel staining. And then, the electropherograms were analyzed for comparing the similarities and differences of the protein between normal and opaque corneal tissues. RESULTS AND CONCLUSION: The extract of the corneal tissue protein, basic method and condition of two-dimensional gel electrophoresis were established successful y. The gel electropherogram was clear and the result showed that 13 protein spots were significantly downregulated and six protein spots were significantly upregulated in opaque corneal protein of B6-Co mutant mice. There was a significant difference in cornea proteomics between B6 mice and B6-Co mutant mice. These results suggest that gene mutation can lead to the gene up-, and down-regulation or silencing in related signal pathways.