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Updated: Jun 2, 2026

Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models
Published on: January 12, 2015
PNAS4 knockout does not induce obviously neurocytes apoptosis and abnormal development in mice brain
Peiling Cai1, Xiaoqiang Xia, Fanghua Li
1State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Chengdu, 610041, China.
Abstract:
Apoptosis is one kind of programmed cell death and contributes to development of a variety of organs such as brain. PNAS4 has been reported to be a novel apoptosis-related gene. Overexpression and knocking down of PNAS4 would cause zebrafish and Xenopus lavis developmental abnormalities. But its function and apoptotic mechanism in mammals are still unknown. Here, we first reported that established PNAS4 CKO (conditional knock out) mice using recombineering technology. We prepared its polyclonal antibodies which recognized both myc-PNAS4 overexpression protein and WT and CKO mice brain tissue and MEFS cells with high titre and specificity. Further we detected that PNAS4 was highly expressed in the embryonic period. However, we observed neither neural structural abnormality nor apoptosis signal in PNAS4 CKO mice brain. Our data suggested that PNAS4 was not involved in mice brain development and apoptosis.

