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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。
Objective To investigate the differential expression of P57kip2 and CDK5 in normal nerve tissue during the development of neural tube defects (NTD), and provide clues for studying the molecular mechanism of normal neurogenesis. Methods The gene expression of P57kip2 and CDK5 in NTD mice induced by embryonic (E) 9.5 and normal retinoic acid (RA) for 10.5 days was compared with that of embryonic (E) in medium density chips containing more than 1,100 known genes. Northern blot verification of chip results. Results By comparing the expression of P57kip2 and CDK5 gene between normal E9.5d and E10.5d, E9.5d-NTD and E10.5d-NTD, P57kip2 and CDK5 expression were significantly up-regulated before and after normal neurogenesis, NTD (including E9.5d and E10.5d two phase) P57kip2, CDK5 showed a downward trend after RA. Conclusion P57kip2 and CDK5 are involved in the development of neural tube defects and provide useful clues for studying the molecular mechanism of normal neurogenesis.