Sentence examples for mouse models demonstrated from inspiring English sources

Studies using genetically engineered mouse models demonstrated a central role of JAK2 V617F in the pathogenesis of MPNs.

Genetically engineered mouse models demonstrated that HAI-1 is critical for epidermal function, possibly through direct and indirect regulation of cell surface proteases, such as matriptase and prostasin.

In vivo implantation of NGCs with microchannels into complete sciatic nerve transections of mouse models demonstrated the effective directional guidance of regenerating sciatic nerves via branching into the microchannels and extending toward the distal end of the injury site.

First, the cross of these mouse models demonstrated that genetic deletion of NE results in a substantial reduction of neutrophils in BAL from βENaC-Tg mice confirming an important role of this protease in neutrophilic airway inflammation [15].

Initial studies using mouse models demonstrated that Trp53−/− animals develop lymphoma with high frequency and that Trp53−/+ animals display a moderately broader tumor spectrum with slower onset of disease [13], [14].

While in our study both the CTL-induced EAD and the spontaneous NOD mouse models demonstrated sharply increased β-cell proliferation rates at diabetes onset, we did note a few differences between the models.

Evidence from mouse models demonstrates that genetic or pharmacological inhibition of RORγ activity can block the production of pathogenic cytokines, including IL-17, and convey therapeutic benefit.

Our engineered mouse models demonstrate the oncogenic potential of pseudogenes and indicate that ceRNA-mediated microRNA sequestration may contribute to the development of cancer.

Slc6a6 knock out mouse models demonstrate a phenotype of dilated cardiomyopathy with cardiac atrophy [36], lower fasting blood glucose, acceleration of glycolysis in skeletal muscle and susceptibility to development of obesity when placed on a high fat diet [37].

Previously developed ApcMin mouse models demonstrate polyp growth predominately in the small intestine, an anatomical location that cannot be easily reached with endoscopy.

Mouse models demonstrate a systemic negative effect of local sepsis on the inflammatory response.