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The overexpression of NCX seen in these mice is, however, unlikely to exacerbate cardiac hypertrophy.
The impairment of DA release in pink1 knockout mice is, however, sufficient to compromise nigrostriatal circuit function.
Insufficient accuracy of the sucrose test in mice is, however, one of the key difficulties in measuring behaviour in chronic stress models of depression [ 14, 32, 38, 39].
Neuron-restricted synthesis of G93A mutant SOD1 in mice is, however, sufficient to cause motoneuron pathology and a late ALS-like disease [ 20, 43].
A defective apoptotic phenotype in any cell type in the TRAIL−/− and DR5−/− mice is, however, observed in response to DNA damaging agents such as chemical carcinogen or ionizing radiation [ 59, 60].
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The response of T cells from treated mice was however significantly reduced compared to T cells from sham-treated CCIA arthritic mice (Figure 3A).
The level of reconstitution in scid mice was however low (<1%) and consisted mainly of human T cells, as very few human B cells were able to survive.
Both Lck and Lck/Fyn mice were, however, free of obvious disease throughout a year-long observation period and we noted no increase in unexpected fatalities in the mutant groups relative to controls.
Neurodegeneration in cyclin D2 deficient mice was, however, similar to that in wild-type littermates at 3 weeks p.i. of AAV-Tau.P301L (Figure 8C), excluding cyclinD2 on its own as decisive factor in the observed neurodegeneration.
Our vaccinated-control mice were however unable to do so, and this is in agreement with previous studies in IL2RγcKO genetic stocks lacking HLA class II molecules that were also severely impaired for eliciting human IgG responses to vaccination [15], [20] [22], [26] [28].
GCN5 knockout mice are, however, embryonically lethal (62); therefore, conditional knockout models are needed.
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