【摘要】 目的探讨P57kip2、CDK5在神经管发育缺陷(NTD)发生过程中与正常组织的差异表达,为研究正常神经胚形成的分子机制提供线索。方法用含有1 100余个已知基因的中密度芯片比较胚胎(embryonic,E)9.5、10.5d正常与同期维甲酸(RA)诱导致NTD小鼠神经管组织的P57kip2、CDK5基因表达差异,并对芯片结果进行Northern杂交验证。结果通过比较P57kip2、CDK5基因在正常E9.5d与E10.5d、E9.5d-NTD、E10.5d-NTD的表达差异,发现在正常神经胚形成前后P57kip2、CDK5表达显著上调,在RA诱导致NTD(包括E9.5d与E10.5d两个时相)P57kip2、CDK5在RA作用后呈现下调趋势。结论P57kip2、CDK5参与了神经管发育缺陷的发生过程,为研究正常神经胚形成的分子机制提供了有益线索。更多还原

【Abstract】 Objective To investigate the differential expression of P57kip2and CDK5in neural tube defects t(NTD)from the normal,and provide the clue for the research of the molecular mechanism of the normal neurula formation.Methods A cDNA microarray containing 1 100known genes was used to compare differences in P57kip2and CDK5gene expression between the normal control group and the retinoic acid(RA)-induced NTD group on embryonic(E)day 9.5and 10.5.Two differentially expressed genes were randomly selected from the two groups for Northern blotting to verify the results of the cDNA microarray.Results Compared the differences of between P57kip2and CDK5in normal and E9.5d,E10.5d,E9.5d-NTD,E10.5d-NTD,P57kip2and CDK5expression was significantly up-regulated in the before and after the formation of the normal neurulation,but them showed a downward trend in retinoic acid(RA)-induced NTD(including two phase E9.5dand E10.5d).Conclusion P57kip2and CDK5involved in the physiological process of NTD,and provide the useful clue for the research of the molecular mechanism of the normal neurula formation.更多还原