Mice lacking Dad1, the defender against apoptotic death-1, express abnormal N-linked glycoproteins and undergo increased embryonic apoptosis.

摘要

The Dad1 gene has been shown to play a role in preventing apoptotic cell death. Embryos homozygous for a null allele of Dad1 expressed abnormal N-glycosylated proteins, and showed delayed development by day 7.5 of embryonic life. These mutants weremorphologically abnormal, had impaired mesoderm, and increased levels of apoptosis in specific tissues. The embryos died by day 10.5.