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Volume element partitioning of the mouse brain data can provide a common coordinate framework for visualization and morphological modeling of neurons and can serve as containers to grow synthetic neurons.
However, none of the POMs were reactive with PrPSc from prion infected mouse brain (data not shown).
In our experiments, Kir2.1 immuno-reactivity was evident in mouse brain (data not shown); however it did not demonstrate significant binding to KCNE1, KCNE3 or Kv12.2 channels (Figure 5A).
However, paricalcitol, a vitamin D analogue, did not significantly enhance [I]hAβ 1-40) elimination from mouse brain (data not shown).
Expression of ENSMUSG00000066992, detectable by RT-PCR exclusively in mouse brain (data not shown), was not ablated in homozygous carriers of insertion 02-0002, however, suggesting that the carp β-actin splice acceptor does not work efficiently in each case.
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We tested MeRIP-PF performance using published adult mouse brains data (GSM854223 and GSM854224) with more than 30 millions reads for each sample [5].
No excess accumulations of GC and GS were detected in 10 weeks 4L/4L and 13 months C−/− mouse brains (data not shown).
Consistently, in situ hybridization analysis revealed that Sim1 mRNA signals were exclusively observed in hypothalamus but not in other regions, including cortex, in both 12-week-old control and R6/2 mouse brains (data not shown).
Mouse brain MRI data was used to provide an anatomical reference frame for PET/CT imaging.
Immunoprecipitation using the lysates with antibodies for Dysbindin and NF-YB and subsequent Western blot revealed the interaction of endogenous Dysbindin with endogenous NF-YB (Figure 2B, 2nd lane of both panels), and this binding was also confirmed using adult mouse brain lysates (data not shown).
We here present an integrative approach to the analysis of mouse brain transcriptome data.
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