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In contrast to other transgenic mouse models expressing UPS reporters throughout the body [32], [33], GFPμ expression in our model is controlled by the mouse prion promoter (MoPrP).
The mouse models expressing the Cre transgene are healthy, active and have no overt behavioural or brain histological phenotypes.
Several groups have made knock-in mouse models expressing JAK2V617F and have observed divergent phenotypes, each recapitulating some aspects of disease.
I work in hearing research, and I am now working on genes that are linked to blood (platelet) disorders as well as with mouse models expressing mutant steroid (androgen) receptor genes.
Although multiple cell culture models demonstrated oncogenic potential of several HCV proteins, most transgenic mouse models expressing these proteins did not develop HCC [2].
Similarly, none of the two previously generated transgenic mouse models expressing the whole HCV polyprotein is developing HCC [7], [9], [10].
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All these AD mouse models express full-length APP, and also C-terminal fragments and Aβ peptides after cleavage.
One should note that all of the above-mentioned transgenic mouse models express the Swedish APP mutant prone to BACE cleavage at Asp-1 of Aβ.
Interestingly, we show that a group of highly utilized breast cancer cell lines, and several genetically engineered mouse models, express the claudin-low phenotype.
To systemically evaluate the expression patterns of Nestin during postnatal development in the mouse testes, we assessed GFP expression in the Nes-GFP transgenic mouse model (expressing GFP driven by the Nestin (Nes) promoter) using confocal microscopy.
We next analyzed whether in a different HD mouse model expressing endogenous levels of full-length mutant huntingtin (HdhQ111/111) the expression of both receptors was also altered.
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