The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.
|BEL Framework Large Corpus Document v20170611||51%|
|Selventa Protein Families Definitions v20150611||29%|
|Epithelial Innate Immune Activation-2.0-Rn v2.0||27%|
|Immune Regulation of Tissue Repair-2.0-Rn v2.0||24%|
|Osmotic Stress-2.0-Rn v2.0||24%|
|Endothelial Innate Immune Activation-2.0-Rn v2.0||23%|
These demonstrate that Ang II is capable of inducing CRP generation in macrophages via AT(1)-ROS-ERK1/2/p38MAPK-NF-kB signal pathway, which contributes to better understanding of the proinflammatory and proatherosclerotic actions of Ang II.
p38 activity was required to enhance the accessibility of the cryptic NF-kappa B binding sites contained in H3 phosphorylated promoters, which indicated that p38-dependent H3 phosphorylation may mark promoters for increased NF-kappa B recruitment.
Thus, suppression of p38 activity using SB203580 and siRNA transfection resulted in the significant reduction of IKK activity, DC maturation, and CXCL2 upregulation by toxin A. These results suggest that p38 MAPK may lead to the activation of IKK and NF-kappaB signaling, resulting in enhanced DC maturation and CXCL2 expression in response to C. difficile toxin A stimulation.
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