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MOF is essential for mammalian embryonic development and unlike the male-specific lethality in Drosophila, deletion of Mof in mice is lethal for both sexes (Gupta et al., 2008; Thomas et al., 2008).
Knockout of either p68 or p72 in mice is lethal (E11.5 or P2, respectively) and double knockout animals show earlier lethality without obvious specific degeneration of organogenesis [ 103].
Deletion of RagA in adult mice is lethal.
Ablated or defective Runx2 expression in mice is lethal as there is an absence of osteoblasts and bone in such animal models [27], [30], [31].
Targeted deletion of Lsd1 in mice is lethal.
Knockout of Ang-1 in mice is lethal by embryonic day E12.5.
Similar(38)
Survivin is essential in suppressing apoptosis during mouse development, Survivin null mice are lethal at early embryonic stage (Uren et al., 2000).
We demonstrate that STX-T plays an essential role in the fast recycling of transferrin receptor and STX-T-deficiency mice are lethal with iron deficiency anemia.
Administration of high-dose CpdA to mice was lethal while treatment of EAE with low to intermediate amounts of CpdA dissolved in water significantly ameliorated the disease.
CASK knockout mice are lethal but show no dramatic synaptic alterations except increased neuroligin protein levels and higher spontaneous event frequency at glutamatergic synapses [57], consistent with our data and a subtle role in synaptic protein organization.
In contrast, the Dicer-knockout mice are lethal by extensive internal hemorrhage at the later embryonic stage [ 47].
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