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This hypothesis is supported by the earlier observation that the MZ compartment is normal in several other lymphopenic mutant mice such as IL-7−/− mice [39] or Lambda5−/− mice [40].

With repeated Hole Board testing grooming increased in both groups, but control mice increased their grooming periods more than mutant mice such that the difference between the groups became even more pronounced (Fig 8B, Open Field, p<0.001; Hole Board, p<0.001).

Previous transgenics harboring the human CEA gene only, while showing the same pattern of tissue specific expression as in humans [27], [28], did not show a predilection for developing more tumors even when crossed with tumor susceptible mutant mice, such as APCMin/+ mice [29].

Most of the mutant mice, such as mice in the control groups, die of some form of neoplasia, rather than of metabolic diseases such as diabetes or atherosclerosis.

This increase in bone formation rate induced a restoration of some of the architectural parameters in mutant mice, such as cortical thickness and trabecular thickness, but could not restore a normal bone diameter.

CSF-1 was undetectable in the serum and there was no correction of phenotypic features of the CSF-1-null mutant mice such as osteopetrosis, body weight, toothlessness, or the extended estrous cycle.

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This is in sharp contrast to other circadian mutant mice models, such as Clock/Clock and Per2 m/manimals, which accelerate their aging program and develop phenotypes that are reminiscent of those in Bmal1-deficient mice only after being exposed to a low dose of ionizing radiation [8,9].

The reason for this discrepancy arises likely from the broader specificity of the RET-P1 antibody used by Won et al. In contrast to the 1D4 antibody, RET-P1 is known also to label the cell bodies, fibers and synaptic pedicles of rod photoreceptors and such labeling may cause easily the misinterpretation of data of mutant mouse strains, such as Rpgrip1 nmf247.

Our analysis showed that in contrast to the wild-type situation where the RGC axons are highly fasciculated across the chiasm and in the optic tract, the Dicer mutant mice were missing such dense axon bundles (Figure 6).

GluR1 mutant mice are one such example, where standard tasks like the Morris Water Maze fail to identify deficits yet certain forms of hippocampal LTP are compromised [52], [53].

It is therefore intriguing to ask whether such mutant mice, like the C. elegans daf-2 mutants, have elevated HSP expression levels, and whether such HSP expression patterns contribute to their aging-related phenotypes, as well as to their stress resistance properties [ 26].

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