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While HIF-1α deletion results in embryonic lethality at day 9 11 [ 26, 27], with defects evident as early as 7 days, combined genetic deletion of IKKα and IKKβ results in lethality at day 12 [ 28].
Systemic deletion of Yap results in embryonic lethality at day E8.5 [145],[146].
It was observed that knockdown of the ZNF335 ortholog in mice (ZFP335) resulted in early embryonic lethality at day E7.5.
However, it has been reported that the ADAM10 knock out leads to severely affected Notch signaling and embryonic lethality at day 9.5 [ 11].
Mice heterozygous for the knockout Nrbp1 allele (Nrbp1 +/− ) were grossly normal at birth and fertile (data not shown); however, homozygosity resulted in embryonic lethality at day E7.5 (Supplementary Figure 2).
ADAM10-deficient mice have been generated [ 11], but their early lethality at day E9.5 prevents a reliable analysis of ADAM10's α-secretase function in vivo, especially in neuronal cells.
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By contrast, 100% of Fgf10 pups died within 8 days of hyperoxic injury, with lethality starting at day 5, while Fgf10 pups were all alive.
We found that targeted inactivation of Rbx1 caused embryonic lethality at embryonic day E7.5 due to proliferation failure.
Cell type-specific deletion of Dicer in committed osteoprogenitors results in embryonic lethality at embryonic day (E 14.5 [ 44].
Homozygous knockout of the Tip60 gene in mouse results in pre-implantation lethality at embryonic day 3.5 [ 13].
Deletion of murine c-myc by gene targeting results in embryonic lethality at embryonic day 9-10 [ 23].
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