In order to investigate a putative role for Lgl1 in OPC differentiation, we used a mouse model where Lgl1 knockout is targeted to NG2 cells28.
Using the GT-tg bigenic mouse model, where brain-selective Tat expression is induced by activation of a doxycycline (Dox) promotor, we tested the effects of Tat on cocaine (10 mg/kg, s.c.) induced locomotion and conditioned place preference (CPP).
Forbes and colleagues report on a population of hepatic progenitor cells that regenerate the adult liver in a mouse model where more than 98% of all hepatocytes are irreversibly damaged.
We demonstrate that an anti-MSLN antibody diminished adhesion formation in a mouse model where adhesions were induced by surgical ligation to form ischemic buttons and subsequent surgical abrasion of the peritoneum.
One potent lead K6a inhibitor, which was highly specific for K6a, was tested in a mouse model where reporter gene constructs were injected intradermally into mouse paw and luciferase activity was used as an in vivo readout.
We now report that in a mouse model where oncogenic Kras is activated in all pancreatic cell types, two brief episodes of acute pancreatitis caused rapid PanIN progression and accelerated pancreatic cancer development.
Application of these technologies on a genetic mouse model where green fluorescent protein (GFP) is expressed in endothelial cells, controlled by the Claudin5 (Cldn5) promoter, reveals that capillaries and postcapillary venules, with no or low Cldn5 expression, respond to VEGFA with rapid changes in blood flow, vessel tone, and leakage.
This study was the first to investigate the impact of exogenous cannabinoid administration in an acutely stressed mouse model, where CD1 mice were pre-treated with HU-210, a potent CB1R agonist, prior to acute stress exposure and subsequent behavioral testing.
Human NASH livers and a high-fat (60% kcal) diet-fed chronic mouse model, where hepatotoxin bromodichloromethane was used to induce NASH, were used for this study.
Here, we present a novel mouse model where the presence of a single autoreactive B cell clone drives the TLR7-dependent activation, expansion, and differentiation of other autoreactive B cells in spontaneous GCs.
The role of GATA factors in pancreas development got verified in a mouse model where the simultaneous inactivation of both Gata4 and Gata6 perturbed the proliferation of pancreatic progenitor cells and caused faulty branching morphogenesis[42].
