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作 者:田文霞[1] 刘红霞[1] 喻进[1] 卢晓晓 宁官保[1] 李宏全[1]
机构地区:[1]山西农业大学动物科技学院,山西太谷030801
出 处:《中国畜牧杂志》2014年第17期17-20,共4页Chinese Journal of Animal Science
基 金:国家自然科学基金(31072179);山西省自然科学基金(2009011043-1);山西省科技攻关项目(20130311027-3)
摘 要:本研究旨在应用cDNA芯片技术筛选福美双诱导的肉鸡胫骨软骨发育不良(TD)相关基因,提取对照组和饲喂福美双组第2、4、8、10、15、20天的AA肉鸡生长板组织总RNA,制备cRNA探针,分别与cDNA芯片杂交,重新筛选肉鸡TD差异表达克隆。结果表明:得到第2、4、8、10、15、20天2.0倍以上差异表达克隆分别为151、90、240、589、718和733个,共计1 398个。基因本体分析表明,上述差异基因分别参与调节、信号转导、转录、RNA加工与修饰、翻译、蛋白折叠和蛋白水解、运输、氧化还原、生物合成、细胞周期、增殖分化、细胞凋亡、细胞粘附、免疫应答与防御反应、应激反应、电子链传递和糖基化等生物学过程;氧化磷酸化、糖酵解与糖异生、黏着斑、细胞骨架调节、ECM-受体相互作用、MAPK、钙信号转导通路、Wnt、胰岛素信号通路、TGF-β信号通路、泛素介导的蛋白水解、神经活性的配体-受体相互作用、VEGF、GnRH、酮体的合成与分解、细胞因子与其受体的相互作用等多条代谢途径与肉鸡TD有关。为从分子水平阐明肉鸡胫骨软骨发育不良发病机制提供可靠的生物信息学依据。The aim of this study was to select the associated genes in the growth plate of broiler chickens with tibial dyschondroplasia (TD) induced by thiram with cDNA microarrays.RNA was extracted from the growth plates of control and thiram-fed Chickens on days 2,4,8,10,15 and 20.The cRNA probe was preparated,they were hybridized with cDNA chips respectively.These differential expression clones were sequenced by Shanghai Generay Biotech Co.,Ltd.And then they were analyzed with the method of bioinformatics.The results showed that the data identified 1 398 differentially expressed clones,with 151,90,240,589,713 and 733 exhibiting at least 2.0-fold changes at days 2,4,8,10,15 and 20,respectively.These differentially expressed genes participate in a variety of biological processes,including regulation,signal transduction,transcription,RNA processing and modification,translation,protein folding and proteolysis,transport,oxidation reduction,biosynthesis,cell cycle,cell proliferation division,apoptosis,cell adhesion,immune response or defense response,response to stress,electron transport chain and glycosylation process.The identified differentially expressed genes were associated with the following pathways:oxidative phosphorylation,glycolysis,focal adhesion,cystoskeleton regulation,ECM-receptor interaction,mitogen-activated protein kinase (MAPK) signaling,calcium signaling,Wnt signaling,insulin signaling,TGF-signaling,ubiquitin mediated proteolysis,neuroactive ligand-receptor interaction,VEGF,GnRH signaling pathway (GnRH),synthesis and degradation of ketone bodies and cytokine-receptor interaction.Our findings may provide reliable bioinformatics basis on understanding the molecular pathogenesis of TD.
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