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These mice have elevated levels of functional Db on the surface of their CNS neurons.
Specifically, we show that Vav2/Vav3-deficient mice have elevated IOP, which eventually manifests as buphthalmos.
Knockout Scarb1−/− mice have elevated HDL cholesterol levels, reduced selective HDL-cholesterol clearance, decreased bile cholesterol concentration and secretion, and thus reduced reverse cholesterol transport (RCT) [6] [10].
This is consistent with previous studies demonstrating that CD36-deficient mice have elevated plasma triglyceride levels [34], [35], further supporting the role of CD36 in ApoE−/− Nrf2−/− mice.
MUFAs are also important for cellular cholesterol ester synthesis [11] and SKO mice have elevated levels of skin free cholesterol [18].
These mice have elevated levels of class II MHC as compared to I-A-β-EGFP mice, and immature bone marrow-derived dendritic cells show redistribution of class II MHC to the cell surface.
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In addition, it has been shown that R6/2 mice had elevated levels of NFκB pathways that may be involved in muscle atrophy [15].
These Tg mice had elevated caspase activation and cardiomyocyte apoptosis, which contributed to ventricular wall thinning and a decline in cardiac function.
Myocardium and pulmonary arteries from genetically engineered mice having elevated plasma levels of EETs (Ephx2−/−) exhibited protection from H/R-induced injury over that of wild type controls, suggesting that endogenously produced EETs may have pro-survival effects.
H/K-IFN-γ mice had elevated levels of mRNA for IFN-γ target genes and the pro-inflammatory cytokines IL-6, IL-1β, and tumor necrosis factor-α.
Furthermore, while Ing1−/− mice had elevated incidence of B-cell lymphomas [51], [52], Ing2−/− mice had elevated incidence of histiocytic sarcoma (Table 3,S3).
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