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The researchers found that inactivating the PTEN gene in mice led to the formation of the malignant tumor associated with BRCA1 mutations.
We concluded that the C. neoformans infection in mice led to increases in tissue and serum Gal-3 content, with a variable time-course depending on the tissue.
Adenoviral overexpression of miR-124 in C57BL/6 mice led to accumulation of excessive triglycerides and up-regulation of lipogenic genes in the liver.
High levels of p62 in mice led to NRF2 activation and protected hepatocellular carcinoma (HCC -initiating cells from ROS, wHCC -initiatingn Hcellsduction55.
Whereas SFTSV infection of wild-type mice led to rapid weight loss and death, Tpl2−/− mice or Il10−/− mice survived an infection.
Similarly, the cardiomyocyte-specific expression of the constitutive GC domain of the NPRA receptor in mice led to an increase in cGMP levels40.
Administration of the CD133 + cell tumor xenografts in the mice led to the formation of large sized tumors in the control group.
Implantation of the follicular structures in SCID mice led to the formation of hair follicle-like structures, thus demonstrating their hair inductive ability.
Finally, BP administration to mice led to over-expression of keratinocyte chemoattractant (KC), the murine functional homologue of IL-8, in lung.
Prophylactic as well as therapeutic administration of mT + mE1 in BALB/c mice led to protecting mice against SP2/0 tumor cells expressing HCV NS3 protein.
GS-PPMO systemic administration to Pompe mice led to a dose-dependent decrease in glycogen synthase transcripts in the quadriceps, and the diaphragm but not the liver.
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