Using two different transgenic mice we provide evidence that Rac1 is important in thymic epithelial cell homeostasis.
Specifically, using genetically modified mice we provide evidence for the involvement of EC JAM-C in the growth and aggressiveness of peritoneal malignant tumors.
By profiling the histone methylation patterns of QSCs from young and aged mice, we provide here direct evidence for the epigenetic aspect of the aging of SCs.
Given the rather unique appearance of the amyloid pathology in the tet.MoAβ(GFP) mice, we provide here a comparison to two strains of mice that deposit HuAβ, using tet-regulated vectors and CamKII-tTA drivers to expressed humanized APP.
By administering PMA to IRAK-4 and IL-18 knockout mice we provide additional evidence that disruption of inflammatory pathways is sufficient to protect the developing brain from PMA induced injury.
By mining gateway genes related to hippocampal aging from networks made from gene expression in young and middle-aged mice, we provide a proof-of-concept of existence and importance of gateway nodes.
Although WT SOD1 is present in insoluble aggregates found in symptomatic double-transgenic mice, we provide the first evidence that dissociates WT SOD1 co-aggregation from the earlier development of paralysis.
Using this novel notochord-specific Cre mouse, we provide evidence that all cells present within the NP, from tissue formation through to skeletal maturity, are of notochord origin.
By using the FGF21KO mouse model, we provided the first experimental evidence to show that FGF21 deletion further accelerated and aggravated diabetes-induced aortic thickening, fibrotic remodeling, inflammation, cell apoptosis and oxidative stress, and FGF21 administration can reverse the pathologic changes in FGF21KO diabetic mice.
In the current study, by using a uterine-specific deletion mouse model, we provided novel evidence that although on-time embryo implantation occurs in the absence of uterine Rbpj, the normal embryonic orientation is disrupted at the time of initial implantation and results in a progressive uterine-embryonic disorientation associated with aberrant decidual patterning.
