Knockout mice as model systems for studying nm23/NDP kinase gene functions.: Application to the nm23-M1 gene
Knockout mice as model systems for studying nm23/NDP kinase gene functions.: Application to the nm23-M1 gene
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DOI：
10.1023/a:1023561821551
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发表时间：
2003-02-01
影响因子：
3
通讯作者：
Daniel, JY
中科院分区：
文献类型：
--
作者：
Arnaud-Dabernat, S;Bourbon, PM;Daniel, JY
已经产生了在nm 23-M1基因中携带纯合种系突变的小鼠，该突变消除了其蛋白质表达并通过nm 23-M1启动子驱动β-半乳糖苷酶的表达。nm 23-M1基因失活不具有致畸性，并且幼仔可以生长至成年而没有明显的健康问题。然而，他们经历了生长迟缓和敲除的女性不能养活他们的幼崽。这两种效应都依赖于背景。在胚胎发生过程中nm 23-M1启动子激活的β-半乳糖苷酶图谱显示，nm 23-M1基因主要在组织的上皮层中表达，其需要诱导的上皮-间充质相互作用来形成。因此，nm 23-M1基因失活的小鼠可以作为研究nm 23-M1基因在信号转导通路调控或肿瘤诱导和增殖中的作用的模型。
Mice carrying a homozygous germ-line mutation in the nm23-M1 gene that eliminates its protein expression and drives expression of beta-galactosidase by nm23-M1 promoter have been generated. nm23-M1 gene inactivation is not teratogenic and the pups can grow to adult age without apparent health problems. However, they undergo a growth retardation and knocked out females cannot feed their pups. Both effects are background dependent. beta-galactosidase mapping of nm23-M1 promoter activation during embryogenesis shows that the nm23-M1 gene is principally expressed in epithelial layer of tissues which require inductive epithelial-mesenchymal interactions for their formation. In conclusion, invalidated mice could be interesting models to analyze the role of nm23-M1 on signal transduction pathway regulation, or cancer induction and proliferation.