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The elevated oxidative stress and inflammation present in the skeletal muscle of G93A mice suggest that this diseased mouse model lacks an adequate defense system to respond to cellular insults, such as oxidative stress and inflammation.
The ob/ob mouse model lacks functional leptin, leading to hyperphagia, obesity, and insulin resistance.
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We generated a mouse model lacking both collagen IX and COMP to study the potential complementary role of these proteins in skeletal development.
In order to explore this we have utilised an APOE 'humanised' mouse model lacking the mouse APOE gene with human APOEε3 or ε4 knocked in.
Similarly, long-term EE improves memory and reduces astrogliosis and brain degeneration in a mouse model lacking the presenilin genes [77].
Furthermore, a transgenic mouse model lacking white adipose tissue (male A-ZIP/F-1), exhibits reduced fertility independent of leptin and testosterone levels [59], suggesting a potential role for stored fatty acids in the production of viable sperms.
Currently, a mouse model lacking MGL does not exist.
We have generated a novel mouse model lacking both Pomc and Agrp.
Genetically, they developed a mutant mouse model lacking pVHL in osteoblasts to activate the HIF signalling pathway.
We used a triple transgenic mouse model lacking two isoforms of P-glycoprotein (Mdr1a/1b) and the Bcrp.
A mouse model lacking TRPV4 does not show apparent neuromuscular abnormalities (Liedtke and Friedman, 2003; Suzuki et al., 2003).
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