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||63%|
|Osmotic Stress-2.0-Hs v2.0||42%|
|Osmotic Stress-2.0-Mm v2.0||41%|
|Oxidative Stress-2.0-Rn v2.0||37%|
|Epithelial Mucus Hypersecretion-2.0-Rn v2.0||36%|
|Growth Factor-2.0-Rn v2.0||29%|
|Epithelial Innate Immune Activation-2.0-Rn v2.0||27%|
|Hypoxic Stress-2.0-Rn v2.0||25%|
|Neutrophil Signaling-2.0-Rn v2.0||22%|
AMPK phosphorylates CFTR in vitro at two essential serines (Ser(737) and Ser(768)) in the R domain,
AMPK-dependent CFTR phosphorylation renders the channel resistant to activation by PKA and PKC without preventing phosphorylation by these kinases. We found that Ser768, a CFTR R domain residue considered to be an inhibitory PKA site, is the dominant site of AMPK phosphorylation in vitro. Ser-to-Ala mutation at this site enhanced baseline CFTR activity and rendered CFTR resistant to inhibition by AMPK
Acute elevation of NaCl causes DNA double-strand breaks in cell culture, and the DNA breaks persist even after the cells are adapted to high NaCl.
Addition of aldosterone to neonatal rat cardiac myocytes caused the activation of NADPH oxidase and intracellular ROS production in a dose-dependent manner (10-(9)-10(-7) mol/L). NADPH oxidase activation was evident as soon as 5 min after aldosterone treatment.
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