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This result clearly demonstrates that activation of binding site of R and Otx is distinct from the resultant functional activation of endo16 expression (Figure 1).
This result demonstrates that activation of the endogenous FGFR4 pathway, in the absence of overexpressed or transfected FGFR4, is sufficient to negatively regulate NFκB signaling.
This study demonstrates that activation of mTORC1 signaling is a critical step in adipocyte differentiation and identifies TSC2 as a primary target of Akt driving this process.
With the use of ICI 182780 in some experiments, our study demonstrates that activation of ER by E2 modifies the expression of several genes in HUVEC.
In conclusion, the current study demonstrates that activation of extranuclear ER results in induction of ERK-Akt-CREB-BDNF signaling in the hippocampal CA1 region, which significantly reduces ischemic neuronal injury and preserves cognitive function following GCI.
This study demonstrates that activation of monocytes by cellular contact with stimulated T cells as mimicked by CEsHUT is a pro-inflammatory mechanism distinct from that induced by LPS.
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To demonstrate that activation of CCR7 has an influence on the proliferative activity of MC MTT assays were performed as described in Methods.
To demonstrate that activation of PI3K is an important early signaling event in ATP-mediated VVEC activation, we measured PI3K activity in an in vitro kinase assay.
Here we demonstrate that activation of platelets with thrombin receptor activating peptide (TRAP) significantly increased IL-27 levels in supernatants.
Finally, we use optogenetic stimulation and multicircuit recording techniques concurrently in Thy1-Chr2 mice to demonstrate that activation of cortical projection neurons entrains neural oscillatory activity and drives synchrony across limbic brain areas that regulate affect.
We demonstrate that activation of GITR signalling inhibits NF-κB-dependent transcriptional activity while facilitating Erk activation in these neurons.
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