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.
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).
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.
No difference in virulence was detected when comparing two prevalent CA-MRSA strains, LAC (USA300 lineage) and MW2 (USA400 lineage), to their respective isogenic PVL knockout mutants in several mouse models, including subcutaneous abscess, sepsis and pneumonia models [10] [13].
Th17 cells are implicated in the pathogenesis of autoimmune diseases based on studies showing that neutralization or genetic deletion of IL-17 inhibits the development of autoimmune diseases in several mouse models, including the collagen-induced arthritis model [14], [45] [47].
