To overcome limitations of current animal models and to test the hypothesis that pharmacologic prenylation inhibition can prevent the production of HDV virions in vivo, we established a convenient mouse-based model of HDV infection capable of yielding viremia.
In the lab we have a mouse-based model of all forms of acute brain injury including models of stroke, subarachnoid hemorrhage, lobar hemorrhage, closed head injury, and penetrating brain injury.
Interestingly, repression of Cdo1 expression was identified to be associated with the malignant transition from mammary intraepithelial neoplasia to tumors in an engineered mouse-based model of ductal carcinoma in situ [ 26].
The mouse-based homology model predicts that the Val253 Ala259 and Gly269 Lys272 segments would be loops, whereas the C. elegans-based model predicts that these segments would be present as α-helices.
For therapeutic antibody development, a cross-reactive antibody against the human and mouse targets provides a convenient way to evaluate the antibody in mouse-based in vivo efficacy models and eliminates the need for a surrogate antibody during preclinical and animal toxicity studies.
Here we extend the open-source simulation software The Virtual Brain to whole mouse brain network modeling based on individual diffusion Magnetic Resonance Imaging (dMRI -based or tracer-basedMRI -basedmorse connectomes.
Furthermore, the cardiac glycoside, neriifolin, protects against neuronal injury in a mouse brain slide-based model and whole-animal studies.
It is also critical to understand the consequences of LRRK2 overexpression for understanding models of LRRK2 PD, as all Drosophila, mouse and cell-based models published to date have relied on overexpression.
The observation of a mixed Th2/Th17 response in susceptible mice is in contrast to our previous observation of a clearly Th2-dominant pattern of cytokines in susceptible A/J mice and a preponderance of IFNγ in C3H mice in an OVA-based model [58].
Mouse-model-based studies of Th17 cells and IL-17 have provided key insights into the role of the IL-17 pathway in the pathogenesis of severe asthma (Fig. 2).
We next set out to uncover the underlying mechanism of this temporarily enhanced insulin-induced Akt signaling, using primary mouse hepatocytes as a cell-based model.
