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Surprisingly, ample data from human tumors and mouse models actually indicate that the 'simple' view on apoptosis being a key mechanism of anti-cancer defense suffers from oversimplification.
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Although these data appear incongruous, the mouse models do actually appropriately model the motor phenotypes associated in the Fragile X-Associated Disorders human population being modeled.
Strikingly, the metabolic actions of DEHP were abolished in this mouse model, which actually tended to be more sensitive to diet-induced obesity than were untreated controls.
The TAC mouse model used is actually a known model for cardiac hypertrophy and it is conclusively proved that inflammation becomes activated [ 11, 12] during cardiac remodeling.
Although demonstrating similar pathology such as macroorchidism and altered dendritic development, the Fmr1 KO mouse model does not actually model the genetics of the Fragile X Full Mutation.
PhenoBase is envisioned to be an ASD research community-based tool that is edited and updated by experts who are actually performing research on these mouse models.
This actually makes any comparison between transgenic mouse models difficult.
Experimental evidence for T-cell epitopes that are actually recognized by the host is only available from mouse models.
Intriguingly, this is actually the opposite to what is observed in more severe mouse models of SMA [ 40].
An important consideration in the study of mouse models of any genetic disease is how well the behavior of the mouse serves to actually model the behaviors present in the clinical population being modeled.
But, actually, we found that the activation of this pathway caused more damage during chronic kidney disease in mouse models.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com