As mitochondrial electron transfer chain (ETC) complexes I and III also have similar Q binding sites, we hypothesized that ATZ might bind to these mitochondrial sites, resulting in the suppression of mitochondrial oxidative phosphorylation.
Since this region contains three predicted GATA binding sites, we hypothesized that these sites were required in cis to mediate osmosensitive gpdh-1 expression.
Inasmuch as the MCP-1 promoter and enhancer regions contain NF-κB binding sites, we hypothesized that ciclesonide was acting on the NF-κB pathway.
Since the promoter sequence of cyclin D1 contains a putative NF-κB-binding site, we hypothesized that NF-κB is responsible for the transcription of cyclin D1.
Because 14-3-3 14-3-3 14-3-3 to the C-terminal region of Rnd3 close to the farnesylation site, we hyproteinsed that 14-3-3 binding could affectoRnd3 subcellular localizathen and consequently negatively regulate Rnd3 function.
As CTRC c.180C>T is in a genetic region that contains multiple nuclear-binding protein sites, we hypothesize that the risk of CP is enhanced by failed response to pancreatic stress, allowing trypsin-activating conditions to drive inflammation and rapid progression to CP. Guarantor of the article: David C. Whitcomb, MD, PhD.
Given that F221 and F222 bind in a hydrophobic pocket on a neighboring subunit in the crystal lattice, coupled with their proximity to the Ca3 5 sites, we hypothesized that this interaction might prevent calcium-binding at Ca2.
Together with our analyses of the axin allosteric binding site (24, 51), we hypothesize that GSK-3β, as most (if not all) dynamic proteins (58), has few allosteric binding sites, where weak transient bindings can promote activity.
Based on the conservation of tensin binding sites in DLC2, we hypothesized that DLC2 might interact with tensin2.
