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Overall, the responses in the baboon closely mimicked those observed in the mouse suggesting a conserved mechanism of immune activation by the CARDS toxin.
VU0467154 exhibited an in vitro fup of 0.022 and fubr of 0.014 in mouse, suggesting a brain-to-plasma Kp of 1.6 at unrestricted equilibrium.
The delay in their expression occurs in multiple tissues of the DN-p38αAF/+ mouse suggesting a simultaneous delay of the irreversible growth arrest and the senescence phenotype [ 24].
Structural defects in axons of the Twitcher mouse suggesting a dying-back neuropathy were previously observed by our group (Castelvetri et al., 2011).
The average dN/dS ratio is highest in humans suggesting a small effective population size, while it is smallest in mouse suggesting a larger effective population size.
In the current study, our findings suggest that either loss or gain of function of Grhl2 can cause spina bifida in the mouse, suggesting a key requirement for regulation of Grhl2 during spinal neurulation.
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This region is highly homologous between human and mouse, suggesting an evolutionarily conserved regulatory mechanism for controlling miR-146a expression.
However the Mc2r−/– mouse suggests a more directly important role.
In contrast, the GO and network analysis in mouse suggests a direct role of TGFBR1.
Importantly, the absence of PWS region sno-lncRNAs in mouse suggested a possible reason why current mouse models fail to fully recapitulate pathological features of human PWS.
Under the assumption that a compromised immune system can cause chronic fatigue, this knockout mouse suggests a potential role for FOXN1 in chronic fatigue.
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