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Interestingly, depletion of the 26S proteasomal activity in the mouse brain results in the formation of Lewy-body-like inclusions that contain mitochondria (53).

Knockdown of DISC1 in the adult mouse brain results in a cellular phenotype very similar to that of phosphatase and tensin homologue (PTEN) suppressed mice.

The precise role of the UPS in neurodegeneration and aging is not clear, but the partial impairment of its function in the mouse brain results in spatial memory deficits and changes in fear-related behavior [ 11, 24, 28].

Together, these findings demonstrate that disruption of TRIM28 levels in the mouse brain results in behavioral changes that are similar to impairments found in humans with certain psychiatric disorders.

In particular, ADM prevents damage caused by oxidative stress through the phosphatidylinositol-3 kinase-dependent pathway, and it was recently [ 72] reported that lack of ADM in mouse brain results in behavioral changes.

The other findings are similar to those from previous mouse brain results: the IF-IBDV and IF-PRDV images are comparable to each other and the PRCD images show lower contrast.

Similar(53)

Propagation of the three types of clone in mouse brain resulted in swa-resistant 22L prions (Fig 1Ai).

Interestingly, infusion of zebularine, a DNA methyltransferase inhibitor, into mouse brain resulted in immediate DNA demethylation of several genes leading to enhanced transcription [ 52].

More importantly, direct in vivo expression of WNV-Cp protein in mouse brain resulted in an induction of apoptosis similar to what is observed in natural infection.

The lower limit of detection was identified through amplification of targets known not to be expressed in mouse brain resulting in Ct values >32 corresponding to copy numbers <10 per ng total RNA.

Additionally, conditional ablation of HIF1-α in adult mouse brain resulted in hydrocephalus, decreased neurogenesis (partly due to an increase in apoptosis) and deficits in spatial memory (Tomita et al., 2003).

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