To determine whether their findings were relevant to atherosclerosis in vivo, Wang and colleagues used a mouse model of atherosclerosis.
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.
To address this question, the researchers used a mouse model of 16p11.2 microdeletion, created by Alea Mills at Cold Spring Harbor Laboratory.
To investigate the feasibility and efficacy of mRNA administration for the treatment of sensory nerve disorders, we used a mouse model of experimentally induced olfactory dysfunction.
We used a mouse model of disrupted VEGF isoform expression that eliminates the predominant brain isoform, VEGF164, and expresses only the diffusible form, VEGF120.
Here we used a mouse model with chronic GSH deficit induced by knockout (KO) of the key GSH-synthesizing enzyme, glutamate-cysteine ligase modulatory subunit (GCLM).
Here, we used a mouse model to investigate CD8+ T cell and humoral responses to a set of potential DENV vaccines based on recombinant modified vaccinia virus Ankara (rMVA).
We used a mouse model to experimentally test how the level and type of activity influences forelimb muscle architecture of spinodeltoideus, acromiodeltoideus, and superficial pectoralis, bone growth rate and gross morphology of their insertion sites.
Here, we used a mouse model of focal cortical stroke to test 2 hypotheses.
To explore scVEGF/177Lu in adjuvant settings, we used a mouse model with metastatic lesions but without primary tumor.
We also used a mouse model of systemic candidiasis and determined that candidemia is optimally detectable during the first few days after infection.
