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).
Because this mouse models included a genetic modification, the clinical features differ from the human conditions (CF−).
The mouse models included are: 1) aged mice; 2) App-Ps1 mice; 3) rTg4510, a mouse line expressing P301L mutant human tau [ 13, 14]; 4) an ME7 model of murine prion disease, associated with neuronal loss and microglial activation [ 15, 16] (for an overview of mouse models and data sets used, see Additional file 1: Table S1).
One set of mouse models included, in the 3′ untranslated region of Hras, an internal ribosome entry site followed by a β-Gal-neomycin resistance reporter, whereas the other set of mouse models effectively inserted the G12V mutation into the endogenous locus.
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−/−).
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).
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.
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.
We used our primary cell culture models as well as mouse models including knockout mice to identify the signaling proteins that may regulate AM function and by identifying the cytokine products derived from AECII.
Therefore we used a systematic approach to investigate the specific role of NPY signalling on bone homeostasis employing several NPY mutant mouse models including specific re-introduction of NPY into the hypothalamus of otherwise NPY deficient adult mice.
