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Conditional mouse models allowing temporal control of oncogene expression have become increasingly important for teasing apart the tumorigenesis pathways in adult tissue compartments [8].
To address this problem, Liu et al., 2015 developed new mouse models allowing Cre- loxP mediated gene modifications in tissues expressing the Müllerian inhibiting substance receptor type 2 (Mis2r, aka anti-Müllerian hormone receptor type 2) and follicle stimulating hormone receptor (Fshr).
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The use of transgenic mouse models allows us to dissect the role of AMPK and other signaling pathways in the intact perfused heart and in vivo.
Transgenic mouse models allow in vivo visualization and genetic lineage tracing of individual intestinal stem cells and their offspring.
Future studies could explore whether other mouse models allow for the preservation of additional human disease-related modules.
Conditional transgenic mouse models allow investigators to model possible therapeutic consequences of oncogene downregulation on the maintenance of malignancy and recurrence.
Recent advances in genetic engineering of mouse models allow tracking of cytogenetic alterations in living cells, from the time of irradiation and throughout tumour ontogenesis.
In conclusion, proteomic analysis of fecal proteins in disease and treatment mouse models allowed us to uncover a number of potential disease- and target-engagement biomarkers.
Mouse models allow a direct comparison of brain pathology and biomarkers, which avoids the diagnostic uncertainty present in human preclinical AD cohorts.
Mouse models allow perturbations in gut microbiota to be studied in a controlled experimental setup, and thus help in assessing causality of the complex host-microbiota interactions and in developing mechanistic hypotheses.
However, recent advances in the technologies available for cell-fate tracking using engineered mouse models allow approaches to not only their characterization, but also the mechanism underlying the emergence of these cells.
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