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Nodal null mutant mouse embryos do not gastrulate, and hypomorphic mutants form abnormal hearts [16], [17].
Methods developed to activate mouse embryos do not translate well to rat embryos.
Geminin-deficient Xenopus and mouse embryos do not develop past the blastula stage because of defects in DNA replication.
STAT3-null mouse embryos do not develop beyond embryonic day 7 [ 47].
No phenotype has been reported in Kif22+/− mice; however, ∼50% of Kif22− /− mouse embryos do not survive past the morula stage (Ohsugi et al., 2008).
It should be noted that early mouse embryos do not tolerate the overexpression of TBP2 [ 57], whereas in Xenopus embryos, which in contrast to mouse embryos require TBP2, this factor can partially rescue a knockdown of TBP.
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However, genetic inactivation of p19Arf in RPS6-deficient mouse embryos does not rescue the embryos and these embryos do not activate ATM suggesting other pathways mediate p53 upregulation in this model [25].
Genetic inactivation of one Bmp7 allele in Grem1-deficient mouse embryos does not alleviate the bilateral renal agenesis, while complete inactivation of Bmp7 restores ureteric bud outgrowth and branching.
However, removal of the node in chicken and mouse embryos does not affect axial elongation.
In contrast, the same protein concentration of brain extract derived from Nogo-A KO mouse embryos did not change the adhesion of neural precursor cells compared with the control situation.
YAP knockout mice embryos do not survive past E8.5.
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