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Murine WOX1/Wwox is critical for postnatal survival, insofar as the knockout mice could survive for only one month [20], [33].
DGAT1 knockout mice could survive and displayed a reduction in the postprandial rise of plasma TG, and increased sensitivity of insulin and leptin.
Unlike the DLC1−/− mice, which died in embryonic stage, DLC2−/− mice could survive to adulthood.
Unlike the DLC1 knockout model, DLC2 was dispensable for embryonic development and DLC2-deficient mice could survive to adulthood.
In the mouse model, DLC1 depletion was embryonic lethal while our DLC2 knockout mice could survive to adulthood.
In the pancreas of our Dicer1-hypomorphic mice, the expression levels of miRNA changed slightly compared to wild-type level which is why the mice could survive.
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There was an independent line of TLS-/ mice that could survive into adulthood on an outbred background, though their CNS phenotypes were not analyzed [ 22].
The Pdx1-Cre;Vhl f/f mice were born at the anticipated Mendelian ratio; however, these mice could not survive more than 5 days postnatally (P5).
Several studies of MYC- and MYCN-knockout mice have revealed that embryos of these mice could not survive until gestation, suggesting that the MYC family genes are required for normal development at the beginning of organogenesis.
The mice with shGnT-IV could survive significantly longer than those with the sh-control (P=0.003, Figure 5B).
Dick implanted human leukemia cells into immune-paralyzed mice and found that these leukemias could survive and grow in these mice.
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