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.
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−/−).
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].
The regulation of TH on the expression of miRs-1, 206, 133a and 133b was confirmed in various mouse models including: chronic hypothyroid, short-term hyperthyroid and short-term hypothyroid followed by TH supplementation.
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].
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−).
Notable exceptions to the over-expressing mouse models include the senescence accelerated mouse model (SAMP8) [ 140] and the anti-NGF mouse [ 141].
To date, the major examination in studies of CIA mouse models includes clinical symptoms as well as radiographic and histological assessments of arthritis.
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).
