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Studies using a mouse model revealed that P-FU 4 can significantly inhibit tumor progression, with a tumor-inhibition rate of 60.2%.
In addition to cell autocrine effects, study results from a tetracycline-off mouse model revealed that osteopontin, an essential component of the stem cell niche, was upregulated in Bcr-Abl positive cells (Jamieson et al., 2004a, b).
Our mouse model revealed a statistically significant contribution of the hydrodynamic method itself, with or without DNA, to tumor formation.
One mouse model revealed that ribosome biogenesis is impaired after conditional deletion of one allele of Rps6 [11].
The BCL11B knockout mouse model revealed the apoptotic phenotype of Bcl11b−/− thymocytes accompanied by decreased expression of BCLxL and BCL-2 genes [14].
A septic shock mouse model revealed that the anti-phagocytic properties of LT could exacerbate the bacterial clearance and enhance mortality in mice (Fig. 5C).
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Endothelial lineage tracing analyses in this PH mouse model reveals that endothelial cells in the pulmonary neointima have detectable smooth muscle gene expression.
Our studies of a mouse model reveal that phospholipase Cγ1 (PLCγ1) is the dominant signaling effector by which excessive activation of TrkB promotes epilepsy.
However, multiple ex vivo examinations of the same KO mouse model reveals that glial function is compromised in a significant manner (Golovina et al. 2003a, b; Hartford et al. 2004).
Recently, O'Farrell et al. (2017) by using state-of-the-art technologies, including high-resolution confocal imaging in combination with myocardial ischemia/reperfusion mouse model, reveal that pericytes contribute to the no-reflow phenomenon post-ischemia in the heart.
Although the mechanism through which DHCR7 deficiency causes any of these characteristics/phenotypes is unknown, a gene expression study of a DHCR7 knockout mouse model reveals altered expression of numerous genes affecting not only cholesterol biosynthesis, but also neurodevelopment and functions such as Wnt signaling, axon guidance, neuronal cytoskeletal assembly, and neurodegeneration [77].
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