This suggested that activation of Hes1 transcription by Notch signaling could not fully explain the potent oncogenic effects of Notch receptors.
This suggested that activation of WNT signaling resulted in the downregulation of WNT antagonists.
This suggested that activation of alternative pathways could be responsible for the observed increase in phosphorylation status of downstream proteins.
This suggested that activation of canonical WNT signaling might be able to influence BMP signaling by decreasing the expression of BMP antagonists.
This suggested that activation of receptor EphA2 with the ligand ephrin-A1 induced rapid reduction of claudin-2 expression that plays a major role in maintaining cellular integrity.
This suggested that activation of NF-κB by MCAO might differ between the genotypes, which we confirmed by a p65 activity assay.
This suggested that activation of PI3K/Akt signaling pathway by IR in A549 cells was suppressed by knockdown of miR-21, and the suppression was reversed by PI3K activator IGF-1.
This suggested that activation of NK cells was not the result of a direct interaction of NK cells with HSV-1 but rather was dependent on other cell types that could act as a source of IL-18.
Altogether, these data indicated that the modulation of Kit expression was dependent on Jak2 activity and suggested that activation of EpoR could act as a repressor of Kit expression.
The increase of proteolytic activity over time suggested that activation of these enzymes had occurred, probably through self-proteolysis that cleaved parts of the zymogens.
Recent studies have suggested that activation of signal transducer and activator of transcription 3 (STAT3) contributes to gastric carcinogenesis in a mouse model.
