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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.

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In our study, using Arrb1 and Arrb2 knockout mice, we provided the first evidence that genetic deletion of Arrb1, but not Arrb2, aggravated the cerebral ischemia-induced neuronal damage.

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.

Our findings suggest that the FokI-dCas9-mediated approach is a highly reliable strategy for creating GEM, including double knockout mice, and we provide accessible platforms for the CRISPR/Cas9-based generation of GEM.

Curiously, despite normal estrogen levels, large prolactinomas developed in these mice, and we provide here several lines of evidence that the elevated P4 levels are involved in the growth of these estrogen-dependent tumors.

Through expression of AtCRT1a and CRT3 in CRT-deficient mouse fibroblasts we provide evidence that the two CRT sub-groups have retained certain, but not all, CRT functions.

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