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In the mouse, deletion of the MYO Va gene results in the so called "dilute lethal" mutant mice that die soon after birth (28).
In the MRL/lpr mouse, deletion of the fas gene leads spontaneously to the development of autoantibodies to DNA and snRNPs (Sm), and associated nephritis and dermatitis.
In the Cyp46a1−/− mouse deletion of the Cyp46a1 gene results in a great reduction in the level of 24S-hydroxycholesterol in brain (Table 1).
In mouse, deletion of endothelial CD146 or disruption of netrin-CD146 interaction by anti-CD146 mAb AA98 impairs netrin-1-induced angiogenesis.
In the mouse, deletion of Pou5f1 causes loss of pluripotency in the inner cell mass and differentiation to trophoblast, revealing its earliest developmental role [ 1].
In the mouse, deletion of the IG-DMR imprinting control region on the maternal allele leads to loss of expression of all the maternally expressed non-coding RNAs, and to re-expression of the paternal-specific protein-coding genes (Dlk1, Rtl1 and Dio3) on the maternal chromosome This is associated with late-gestational fetal mortality.
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Finally, mouse deletions of Peg11 and several of its associated antisense microRNAs have recently been described [77].
Hence in young mice deletion of Dicer led to a reduction of the pro-myelinating phosphorylation of Akt.
In mice, deletion of Anp32a results in no detectable health deficits or defects in neuronal function [36].
In mice, deletion of Phlda2 causes placental overgrowth [ 35].
In mice, deletion of Mll4 alone causes severe defects in BAT development.
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