Trichostatin A treatment (330 nmol l−1, 18 h) did not induce any significant change in MBD1 recruitment on the promoter site, suggesting that the ABCB1 expression decrease observed in H69VP cells was not linked to a MBD1-mediated methylation-independent silencing.
In addition, as ependymal cells are not linked by tight junctions, CP transport may impact periventricular brain regions and potentially deeper structures by affecting CSF composition.
Moreover, the severity of collagen-induced arthritis was reported to be exaggerated in the absence of IFN-γ signaling [ 49, 50], suggesting that Th1 cells are not linked to bone damage in arthritis.
Even though GlySar has a molecular weight of 146 and ependymal cells are not linked by tight junctions, there was a rapid decline in tissue [C]GlySar levels with distance from the ependyma in both Pept2-/ and WT mice with concentrations dropping by 50% over 0.53 and 0.34 mm, respectively.
Anisomycin did not stimulate viral reactivation, demonstrating that sensitivity to anisomycin-induced cell death was not linked to viral protein expression, and consistent with the finding that p38 and JNK signaling was increased in latently infected cells.
Thus, the expression of stem cell markers was not linked to a specific phenotype.
Cell doubling time was not linked to 5′ or 3′ TS genotypes.
Importantly, the aberrant cell-wall morphology was not linked to Asc1p effect on de-novo synthesis of proteins in response to the hypotonic shock, because arresting the translation process by Cycloheximide had no effect on the morphology of asc1Δ and its parental strain during the hypotonic stress (Fig. 4 compare C to B and F to E).
However, PCB-degrading cells were not observed in the root areas containing fast-growing cells, indicating that PCB degradation was not linked to high cellular activity.
