Notable exceptions to the over-expressing mouse models include the senescence accelerated mouse model (SAMP8) [ 140] and the anti-NGF mouse [ 141].
The existing mouse models include induction of diabetes by streptozotocin [ 24], naturally mutated mouse lines like db/db [ 25] and Akita mice [ 26], and more recent genetically engineered models, for example, Ove26 mice [ 27] and endothelial nitric oxide synthase deficient diabetic mice [ 28].
Key factors that have been shown to affect the severity of kidney disease in mouse models include the complement receptors [ 70], cytokines such as macrophage colony-stimulating factor and macrophage migration inhibitory factor [ 71], and chemokines such as monocyte chemoattractant protein-1 [ 72].
All quantified experiments for in vivo mouse models included both biological (n = 4 mice) and technical replicates (3 4 histological sections each at least).
Here we quantitatively examine the composition of the nuclear envelope, as well as the architecture and functions of the cytoskeleton in cells derived from two laminopathic mouse models, including Hutchinson-Gilford progeria syndrome (LmnaL530P/L530P) and Emery-Dreifuss muscular dystrophy (Lmna−/−).
Here, we employed several engineered mouse models, including B cell-specific overexpression of Lin28a or the let-7a-1/let-7d/let-7f-1 cluster (let-7adf) and knockout of individual let-7 clusters to show that let-7adf specifically inhibits T cell-independent (TI) antigen-induced immunoglobulin (Ig)M antibody production.
We present a consolidated view of the complexity and challenges of designing studies for measurement of energy metabolism in mouse models, including a practical guide to the assessment of energy expenditure, energy intake and body composition and statistical analysis thereof.
Hence, to enhance treatment efficacy and minimize drug resistance, the HER2-directed CAR approach has been developed and validated in diverse tumor-bearing mouse models, including those of osteosarcoma (Rainusso et al., 2012), breast cancer (Sun et al., 2014), renal cancer (Schonfeld et al., 2015), and glioblastoma (Zhang et al., 2016).
The use of genetically modified mouse models including the Pax3eGFP/+ and Myf5Cre/+ targeted alleles has raised the possibility that the satellite cell population may be heterogeneous [16], [19].
Here, we investigated the effect of the thyromimetic T-0681 on reverse cholesterol transport (RCT) and atherosclerosis, and studied the underlying mechanisms using different mouse models, including mice lacking LDLr, SR-BI, and apoE, as well as CETP transgenic mice.
The mouse models included a polyglutamine expanded (polyQ) AR knock-in model (AR113Q), a polyQ AR transgenic model (AR97Q), and a transgenic mouse that overexpresses wild type AR solely in skeletal muscle (HSA-AR).
