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Histone H3 lysine 9 (H3K9) methylation at core pluripotency genes is an epigenetic barrier of mouse pluripotent reprogramming.
It has been shown that TGF-β signaling is a barrier of mouse and human reprogramming and its inhibition can enhance reprogramming [ 38, 41– 43] and also can replace c-Myc or Sox2 in mouse [ 38, 41, 42].
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Our results indicate the in vitro conversion assay used in our study does mimic the species barrier of mice to the TSE agents that we tested.
Consequently, EMT and its main regulator, TGF-β signaling, are barriers of mouse and human pluripotent reprogramming, and their inhibition can enhance reprogramming [ 38, 41– 41].
Hence, these data are consistent with the anticipation that [3H]PIB crossed the blood-brain barrier of ARTE10 mice and significantly bound to Aβ plaques in these animals in vivo.
The species barrier of laboratory mice to most TSEs is well-characterized [ 26].
We conclude that the defective barrier of EPI−/− mice results in elevated expression of keratinocyte stress-associated genes that could prime them for an exacerbated atopic response to TPA.
The authors postulated that a functional P-gp activity in the blood brain barrier of Bcrp1 knockout mice might be dominantly responsible for retaining a similar brain uptake of imatinib as compared to wild-type animals.
In the present study, we report that systemic inflammation, induced by bacterial endotoxin, caused a robust decrease in LAT1 mRNA expression at the blood brain barrier of rats and mice.
Using the CER assay, we found evidence that this method recapitulates known species barriers of laboratory mice to TSEs and data to suggest that BHS could be susceptible to classical scrapie and CWD, and less susceptible to TME.
We confirm that the CER assay correctly predicts known species barriers of laboratory mice to various TSEs and go on to use this assay to assess PrPC conversion in BHS substrates by domestic sheep classical scrapie, transmissible mink encephalopathy (TME) and CWD.
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