首页> 外文期刊>Генетика: Ежемес. журн. >COMPARATIVE ANALYSIS OF THE ROLE OF JNK SIGNALING PATHWAY IN REGULATING CELL PROLIFERATION AND APOPTOSIS OF RAT LIVER REGENERATION AND RAT ACUTE HEPATIC FAILURE
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COMPARATIVE ANALYSIS OF THE ROLE OF JNK SIGNALING PATHWAY IN REGULATING CELL PROLIFERATION AND APOPTOSIS OF RAT LIVER REGENERATION AND RAT ACUTE HEPATIC FAILURE

机译:JNK信号通路在调节大鼠肝再生和大鼠急性肝功能衰竭细胞增殖和凋亡中的作用的比较分析

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摘要

To compare the role of JNK signaling pathway in rat Uver regeneration (LR) and in rat acute hepatic failure (AH F) occurrence at the gene transcription level, Rat Genome 230 2.0 array was used to detect the gene expression profiles of the two processes, and bioinformatics and systems biology methods were applied to analyze the physiological activities uncovered by their gene expression profiles in this study. The results showed that 240 genes were included in the array above, though there were 302 genes related to forty two paths of JNK signaling pathway. Array detection results demonstrated that 52 genes were significantly expressed during LR, 20 genes in AHF occurrence, and 15 genes in both of above two processes. Synergy values of these genes were calculated using a mathematical model established by our lab, which revealed the following. The cell proliferation-promoting effects of paths 1, 16 and paths 1—17 of JNK signaling pathway were stronger than the control at 6—12 h and 72 h of LR, respectively, while the cell prohferation-promoting effects of paths 1—17 and the cell proliferation-inhibiting effects of path 34—35 were weaker at 6h of AHF occurrence. The cell ap-optosis-promoting effects of paths 22—23 were much stronger at 6,12 and 72 h of LR and at 12, 24 h of AHF occurrence. In conclusion, thirty eight paths of JNK signaling pathway regulate cell proliferation and apop-tosis in both LR and AHF occurrence.
机译:为了在基因转录水平上比较JNK信号通路在大鼠Uver再生(LR)和大鼠急性肝衰竭(AH F)发生中的作用,使用Rat Genome 230 2.0阵列检测这两个过程的基因表达谱,本研究利用生物信息学和系统生物学方法来分析其基因表达谱所揭示的生理活性。结果显示,尽管有302个基因与JNK信号通路的42条通路相关,但上面的阵列中包含240个基因。阵列检测结果表明,LR过程中52个基因显着表达,AHF发生20个基因,以上两个过程均15个基因。这些基因的协同作用值是使用我们实验室建立的数学模型计算得出的,该模型揭示了以下内容。 JNK信号通路的路径1、16和路径1-17的细胞增殖促进作用分别比LR的6-12h和72h的对照强,而路径1-17的细胞增殖促进作用在AHF发生6小时后,路径34-35的细胞增殖抑制作用较弱。路径22-23的细胞促凋亡作用在LR的6,12和72h以及在发生AHF的12、24 h时要强得多。总之,JNK信号通路的三十八个路径调节LR和AHF发生中的细胞增殖和凋亡。

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