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Data from PKCδ −/− mice demonstrate a role for PKCδ in the execution of DNA damage-induced and physiologic apoptosis.
Opn4 DTA/DTA ipRGC ablation mice demonstrate a significant increase in the overlap projections to the dLGN, leaving the ipsilateral and contralateral projections similar to those in the wild-type mice.
These mice demonstrate a transient spatio-temporal expression pattern for Plp-Cre.
Recent studies in mice demonstrate a reciprocal hormonal link between energy metabolism and bone remodeling [65], [66].
G2A KO mice demonstrate a normal pattern of T and B cell lineage differentiation through young adulthood.
Comparable to merosin deficient congenital muscular dystrophy children, dy2J/dy2J mice demonstrate a peripheral neuropathy in addition to the muscular dystrophy [7], [8], [9].
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TNCYFP-CreER; SmoF/- (SmoCKO) mice demonstrate an obvious reduction in cerebellar size within two days of ablation of Shh signaling.
Both models, the VLCAD and LCAD mice, demonstrate an inability to metabolize very long- (C14 C18) and long- chain (C12 C14) fatty acids.
Male relaxin-deficient mice demonstrate an age-related progression of cardiac fibrosis.
Aged peripheral T cells from either humans or mice demonstrate an increased resistance to apoptosis [ 43, 44].
The bone resorption outweighs new bone formation therefore the infected mice demonstrate an overall reduced alveolar bone volume and density.
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