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Publication : Early embryonic lethality caused by targeted disruption of the mouse PHGPx gene.

First Author  Imai H Year  2003
Journal  Biochem Biophys Res Commun Volume  305
Issue  2 Pages  278-86
PubMed ID  12745070 Mgi Jnum  J:83472
Mgi Id  MGI:2662069 Doi  10.1016/s0006-291x(03)00734-4
Citation  Imai H, et al. (2003) Early embryonic lethality caused by targeted disruption of the mouse PHGPx gene. Biochem Biophys Res Commun 305(2):278-86
abstractText  Phospholipid hydroperoxide glutathione peroxidase (PHGPx) is the only known intracellular antioxidant enzyme that can directly reduce lipid hydroperoxide in membrane. Mitochondrial and non-mitochondrial PHGPx and sperm nuclei GPx are transcribed from one gene by alternative transcription using different first exons Ia and Ib, respectively. To examine the role of PHGPx in development, we generated mice deficient in PHGPx by a targeted disruption of all exons of the PHGPx gene. Heterozygotes are viable, fertile, and appear normal, despite having decreased levels of three types of PHGPx mRNA and protein. Embryos homozygous for PHGPx-null die between 7.5 and 8.5 days post coitum (dpc), probably developing distal apoptosis. We examined the expression of PHGPx in mouse embryos using immunohistochemical analysis with anti-PHGPx mAb. The expression of PHGPx was detected in the embryonic ectoderm and the yolk sac membrane at 7.5dpc. The results demonstrated that PHGPx is expressed in early gastrulation stage at 7.5dpc and that the expression of PHGPx was essential for normal mouse development.
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