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The knockout mouse has also shown that TASK-2 channels expressed in retrotrapezoid nucleus neurons are important in mediating central CO2 and O2 chemosensitivity [17].
The Pept2-/ mouse has also been used to look at substrate distribution after intracerebroventricular (icv) administration.
The mouse has also been a pivotal model in obesity research.
A myeloid lineage-specific FAK null mouse has also been generated and revealed that FAK has important roles in adhesion signaling and adhesion-independent signaling in neutrophils [10].
The Pept2-/ mouse has also allowed examination of the role of Pept2 in the distribution of potential substrates between blood, CP, CSF and brain in vivo.
However, Cys287 (Cys283 in mouse) has also been reported to make a disulfide bond with Cys245 (Cys241 in mouse) in the murine MCAK crystal structure.
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The iAs-induced malformations in mouse have also been shown to be associated with systems-level changes in gene expression (Robinson et al. 2011).
Furthermore, studies with a doubly transgenic mouse have also demonstrated that the CD25+CD4+ TR cells show a high self-reactivity and differentiate on thymic epithelial cells [ 41, 42].
This prednisone-induced decrease in body weight and reduction of weight gain in mdx mice has also been noted in previous studies [8], [9].
Increased tau phosphorylation in non-transgenic mice has also been shown to be associated with decreased protein phosphatase 2A (PP2activityity [18], [19].
Recently, a syngeneic model in FVB/n mice has also been developed [21].
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