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Molecular analysis suggest that tumors from double myrAKT p53(R172H) mice result from acceleration of initiated p53(R172H) tumors and not from bypass of AKT-induced oncogenic senescence.
It is possible that the learning impairments observed in our GluR2-cKO mice result from reduced synaptic transmission and/or excitability and not altered plasticity.
In previous studies, we showed that the increases in muscle mass seen in Mstn null mice result from a combination of increased fiber numbers and muscle fiber hypertrophy [2].
To test the hypothesis that differences in susceptibility to allergen-driven AHR in A/J and C3H mice result from differential regulation of pulmonary DC recruitment or activity, we developed a model in which allergen sensitization occurs via the airways.
I have presented data showing that mice homozygous for this D76A mutation exhibit significant increases in muscle mass and, as in the case of mice completely lacking myostatin, that the increases in MstnD76A/D76A mice result from a combination of increased fiber numbers and increased fiber sizes.
Our experiments at the moment do not discriminate whether the phenotypes observed in mutant mice result from decreased STIP1co-chaperone function, diminished STIP1 extracellular signaling or both.
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Less well understood, however, are the nontrophic, geomorphic effects of mice resulting from their burrowing activities.
Loading induced the expected strain-dependent increase in bone formation in WT mice, resulting from increases in both mineralizing surface (MS/BS) and mineral apposition rate (MAR).
On the other hand, it was reported that the number of microglia was reduced in osteopetrotic (op/op) toothless mice resulting from the lack of functional macrophage colony-stimulating factor (M-CSF).
Persistent diet-induced obesity in male C57BL/6 mice resulting from temporary obesigenic diets.
PiT1neo/neo mice resulting from PiT1neo/+ intercrosses were born at a lower than expected Mendelian frequency (Table S2).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com