| First Author | Liu MJ | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 362 |
| Issue | 2 | Pages | 295-300 |
| PubMed ID | 17707776 | Mgi Jnum | J:145246 |
| Mgi Id | MGI:3834033 | Doi | 10.1016/j.bbrc.2007.07.118 |
| Citation | Liu MJ, et al. (2007) Transgenic mice with neuron-specific overexpression of HtrA2/Omi suggest a neuroprotective role for HtrA2/Omi. Biochem Biophys Res Commun 362(2):295-300 |
| abstractText | 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. |
