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As one would expect from their depletion of WAT (Fig. 7A C), Ate1-deficient mice were strongly hypersensitive to cold (Fig. 9F).
Beta cells from wild-type mice were strongly protected by the LXR-agonist TO1317, as well as by clofibrate/9-cis RA.
In a recent study of immune complex arthritis, IL-1-deficient mice were strongly protected [ 11].
In addition, RIPK3-deficient mice were strongly protected in a model of myocardial infarction.
After 10 days, motor performance scores of deficient mice were strongly impaired and were not modified by PKR inhibition.
Moreover, we found that the developmental defects in FUT1 knockout mice were strongly associated with NCAM-expressing neurons.
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Additionally, survival of tumour-bearing mice was strongly dependent on molecular weight and polymer conjugate architecture.
This maternal deficit in Asic3−/− female mice was strongly linked to their hearing deficit because their approach behaviors were not significantly correlated with pup USV as were Asic3+/+ and Asic3+/− mice behaviors.
However, studies of mice are strongly supportive of cellular interference.
Interestingly, the presence of lung metastases in these mice was strongly associated with the detection of circulating tumor cells [ 54].
Proton conductance in mitochondria from Ucp3-knockout mice was strongly inhibited by carboxyatractylate, bongkrekate and partially by GDP.
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