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Possibly this is because Nr2f1 and Nr2f2 deficiencies in mice are fatal and only conditional knockout mice are available for analysis: Owing to the relatively low levels of Nr2f1 and Nr2f2 transcripts in resting lymphocytes [ 27, 31- 33], when compared to, e.g., ovary, kidney or brain, such conditional knockouts for the immune compartment have not yet been generated.
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The outcome in these mice is fatal and the histopathological findings are similar to EHBA children.
Over-expression of activated βIIPKC in neonatal mice is fatal and, in the case of adult mice, it induces hypertrophy and myocardial dysfunction.
The results are fatal.
Some crises are fatal.
EMCV infection in mice is a fatal disease that leads to cardiac inflammation, dilated cardiomyopathy, and heart failure [ 6– 9].
HDAC2 knockout mice are viable but present fatal multiple cardiac defects.
This underlines a report by Xu et al. who showed that TLR4 knock-out mice are protected from the fatal effects of histone infusion [ 11] and also, at least in part, is in line with results from Abrams et al. showing that TLR4 blocking results in a decrease in cytokine production but not cytotoxicity.
CYP24A1 knockout mice have severe hypercalcaemia, which is fatal in half of the animals.
TSC1−/− produces a hyperactive mTOR phenotype that is fatal in mice from gestation day 13.5 (58).
Previous reports have shown that transgenic IL6 causes various pathologies of the immune system that can be fatal to mice [ 46, 47].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com