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With the application of MCAO models, Lou et al [ 28] confirmed that the increased TNFα protein and its mRNA expression and NFκB DNA-binding-activity could reduce the survival number of spinal cells in the hippocampal CA1 area, suggesting that NFκB activation can lead to neuronal apoptosis in inflammation following cerebral ischemic reperfusion injury.
This reduced binding activity could also be associated with either high levels of MAN-1 expression or by higher levels of free MAN-1, which could happen after losing its physical interaction with lamin A/C [15].
Nonetheless, HNF4α DNA binding activity could be assayed for in EMSA supershift assays and was significantly reduced to 58% after treatment with 8.3 µM (10 µg/ml) cyclosporine (Fig. 3C, 3D).
However, in both cases residual binding activity could be detected.
However, no ice-binding activity could be detected in lithostathine [19].
Alteration of one or more of these transcription factor binding sites could reduce the levels of IκBα expression, increase NK-κB activity and contribute to HBV-induced hepatocarcinogenesis.
When different amounts of methylated DNA were incorporated, the binding activity was reduced proportionately in vitro (Figure 7A).
FOXO DNA binding activity is reduced by acetylation and enhanced by deactylation [ 36, 37, 42, 43].
This binding activity was reduced in the protein extract (10 μg) from eEF1A1-knocked down cells.
This position also falls within a dileucine binding motif that can bind AP-2 and substitutions here could reduce both AP-2 binding and CD4 downregulation [54].
Moreover, CAPA could reduce MPO activity compared to vehicle (P < 0.05; Figure 4B).
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