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The development of additional inbred lines of wild-derived mice should help address these limitations and augment existing resources.
Given these arguments, comprehensive analyses of BACE1−/− mice should help to parse developmental verses adult BACE1 null phenotypes for the estimation of BACE1 inhibitor side effect risk.
A detailed roadmap of NPC disease neuropathology in mice should help to identify pathways conserved in humans that can mitigate disease and be successfully targeted by biopharmaceutical approaches.
Although we focused our studies on HLA-DRB1*0401, the emergence of new predictive matrices such as TEPITOPE (which encompasses predictions for most DR molecules) [ 44], utilized in combination with HLA transgenic mice, should help to determine the role of MHC class II molecules in the pathogenesis of RA.
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Nevertheless, having this new molecularly engineered mouse should help scientists trace out the intricate pathways of fat regulation, says Woychik.
Also, the mouse genome should help identify the role of human genes, most of which are largely unknown.
Now the mouse genome should help researchers develop a lot more models, especially for diseases with more complex genetic origins, like asthma, obesity, hypertension and diabetes.
The Splunc1 −/− mouse model should help investigators to better understand both the biological role of Splunc1 as well as host defense mechanisms in the middle ear.
Both mouse models should help to characterise the cells at risk and to elucidate the molecular mechanisms underlying radiation leukaemogenesis, and assess how applicable they are to human primary and tAML.
Further analysis of the genomic complement of MSYq, and the copy number of the corresponding X genes, in a range of different mouse subspecies should help date these events more precisely, and establish whether X-Y genomic competition is a contributing factor to the gene amplifications.
Unique experiments on genetically engineered mice with altered neuroinflammatory response should help clarify the origin of these differences in the lesion formation.
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