转基因
转基因小鼠
生物
烯醇化酶
神经保护
基因剔除小鼠
程序性细胞死亡
细胞生物学
细胞凋亡
神经元
免疫学
遗传学
基因
神经科学
免疫组织化学
作者
Ming-Jie Liu,Meng-Lu Liu,Yan Shen,Jin‐Man Kim,Byung Ho Lee,Youn Sik Lee,Seong‐Tshool Hong
标识
DOI:10.1016/j.bbrc.2007.07.118
摘要
Mammalian serine protease HtrA2/Omi has been known as an apoptosis inducer involved inactivation of caspase-dependent as well as caspase-independent cell death. Recent studies with the HtrA2/Omi mutant and knockout mouse models, however, suggested that HtrA2/Omi might play a protective role in neurons. It is important to establish a transgenic mouse model with neuron-specific overexpression of HtrA2/Omi to clarify the physiological function of mammalian HtrA2/Omi in neurons. In the present study, a transgene containing HtrA2/Omi cDNA downstream of a rat neuron-specific enolase promoter was constructed and microinjected into the pronuclei of fertilized zygotes to establish transgenic mice. Transgenic mice successfully overexpressed HtrA2/Omi in brain tissue. As expected, HtrA2/Omi-overexpressing transgenic mice showed normal development without any sign of apoptotic cell death. Our results suggest that the primary function of neuronal HtrA2/Omi might be to protect neurons against stress in contrast to its role in the somatic system.
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