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The PS1 knockout mouse is embryonic and neonatal lethal with severe developmental defects.
The LIFR−/− mouse is embryonic lethal and shows impaired placental formation, decreased bone volume associated with increased osteoclast number and size, decreased sensory neuron survival, decreased numbers of spinal and brainstem astrocytes and elevated liver glycogen [22].
Interestingly, a global knockout of UXT in mouse is embryonic lethal (Y.Z., unpublished data), suggesting that UXT might play an important role during development.
The PP2Acα knockout mouse is embryonic lethal and results in degeneration of the embryo and lack of formation of the mesoderm.
It has been previously shown that PDCD2 knockout in the mouse is embryonic lethal at 3.5 d pc (Mu et al., 2010).
Knockout of γ1 and μ1A subunits in mouse is embryonic lethal, indicating the crucial role of AP-1 in embryonic development [ 56, 57].
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Homozygous deletion of Ptc in the mouse was embryonic lethal.
Complete Pten inactivation in mice is embryonic lethal.
It is well-established that complete Pten inactivation in Pten−/− mice is embryonic lethal.
Also, germline deletion of XBP1 [ 76] or IRE1α [ 128] in mice is embryonic lethal.
Interestingly, like VEGF, haploinsufficiency for the endothelial-specific Notch ligand Delta-like 4 in mice is embryonic lethal.
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