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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.
Similarly, long-term EE improves memory and reduces astrogliosis and brain degeneration in a mouse model lacking the presenilin genes [77].
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.
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.
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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.
Mouse models lacking the α3- or γ2-chain of laminin-332 have been developed and a spontaneous ß3-knockout mouse exists, but all die shortly after birth.
Indeed, they have proved to be essential elements in normal physiology, as shown by mouse models lacking these proteins, that evidence several developmental abnormalities and pathological features.
We therefore used two different conditional mouse models lacking Prkg1 in the nervous system.
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