More recently, the expression of both prokineticins and their receptors have been mapped by in situ hybridization in the adult mouse brain, demonstrating that Prok2 and Prokr2 are more widely expressed in the brain than Prok1 and Prokr1 (Cheng et al., 2006).
Western blot analysis of GT-tg mouse brains demonstrated an increase in Tat antibody labeling that seemed to be dependent on the dose and duration of Dox pretreatment.
Similarly, intraventricular injections of folate receptor- α-positive and -negative exosomes into mouse brains demonstrate folate receptor- α-dependent delivery of exosomes into the brain parenchyma [ 57].
In addition, examination of γH2AX foci in both newborn and 12-month old mouse brains demonstrates that, as with MEFs, significantly more γH2AX foci are seen in the brains of Nfkb1 −/− compared to age-matched Nfkb1 +/+ animals (p<0.01, Fig. 4D).
Interestingly, LRP1 is downregulated with age and in AD, and, although the mechanisms behind this downregulation remain unclear [ 35], research in mouse brains demonstrates that the presence of the ApoE 4ϵ allele blocks LRP1-mediated clearance of Aβ from the brain parenchyma [ 38].
Direct interaction between KLK6 and α-syn in mouse brain was demonstrated by co-immunoprecipitation [ 16].
P7 developing mouse brain sections demonstrated strong expression of the NOV MaxiPromoter reporter construct in the retromammillary nucleus (RM) and light expression in the HPF.
The capability of the technique for in vivo 3D imaging of capillary vessel network over a wide field of view in mouse brain was demonstrated.
Using a highly specific affinity-purified antiserum, a surprisingly wide-spread distribution of isoQC protein expression in mouse brain was demonstrated.
Genome-wide binding studies in mouse brain tissue demonstrated that CFP1 associates with more than 80% of CGIs, and almost all CFP1-bound CGIs exhibit significant enrichment of H3K4me3 [ 14].
