Using a basonuclin-null mouse, we demonstrate for the first time the requirement of basonuclin in keratinocyte proliferation.
Using a cardiac-specific ecSOD Tg mouse, we demonstrate that ecSOD overexpression leads to both decreased ROS and ONOO− levels and increased NO bioavailability.
Thus, utilizing a direct genetic approach in the mouse, we demonstrate that PML suppresses tumourigenesis through repression of mTOR, while mTORC1 hyper-activation does not suffice to initiate tumourigenesis in the kidney.
Exemplified by human and mouse, we demonstrated that the inter-species modules may code some common or essential biological processes, despite a relatively big difference between their contents.
In mouse, we demonstrated that tissue-derived adult mesenchymal stem cells, when co-transplanted with a minimal pancreatic islet mass, facilitate restoration of normoglycemia and neovascularization of the graft [18].
In a thoroughly characterized wound healing model [16], [27], where a 20 mm full thickness incisional skin wound is inflicted along the back midline of an anaesthetized mouse, we demonstrated a phenotypic overlap between MMP-13 and uPA, defined as an additional delay in wound healing in the double-deficient mice compared to the single-deficient mice.
Importantly, using the Blg-Cre; R26 reporter mouse, we demonstrated that these basal marker-expressing cells were of luminal origin.
Using both pharmacologic and genetic approaches in mice, we demonstrate that L1 expression in the adult hippocampus enables long-term memory formation.
Using genetic intercrosses between Nf1 +/− and class I A-PI-3K-deficient mice, we demonstrate that hyperactivation of the p21ras-class IA PI-3K pathway is the mechanism for this phenotype.
Using genetically engineered tracing mice, we demonstrate that, in dystrophic muscle, specialized cells of muscular, endothelial, and hematopoietic origins gain plasticity toward a fibrogenic fate via a TGFβ-mediated pathway.
In mice, we demonstrate that microneedle-mediated delivery of ChAd63.ME-TRAP induced similar numbers of transgene-specific CD8+ T cells compared to intradermal (ID) administration with needle-and-syringe, following a single immunisation and after a ChAd63/MVA heterologous prime-boost schedule.
