Molecular Docking Performance of Selective Organic Compounds with Target Protein

In this article, the docking analysis has been carried out to know some selective compounds' interaction to bind with a targeted protein. There are three approaches have been analyzed here with three different kinds of protein as the target species. They are 2-aminobenzimidazole (2ABZ) with Acetylcholinesterase receptor (AChE), Phenoxazine (POZ) with Penicillin-binding proteins (PBPs) receptor, and Phenothiazines with Calcium/calmodulin-dependent protein kinase IV (CAMK IV) receptor. All three studies showed that the binding is perfect at the binding site and explained with hydrogen bonding interaction via donor-acceptor interactions.

Exercise and CaMK activation both increase the binding of MEF2A to the Glut4 promoter in skeletal muscle in vivo

In vitro binding assays have indicated that the exercise-induced increase in muscle GLUT4 is preceded by increased binding of myocyte enhancer factor 2A (MEF2A) to its cis-element on the Glut4 promoter. Because in vivo binding conditions are often not adequately recreated in vitro, we measured the amount of MEF2A that was bound to the Glut4 promoter in rat triceps after an acute swimming exercise in vivo, using chromatin immunoprecipitation (ChIP) assays. Bound MEF2A was undetectable in nonexercised controls or at 24 h postexercise but was significantly elevated ∼6 h postexercise. Interestingly, the increase in bound MEF2A was preceded by an increase in autonomous activity of calcium/calmodulin-dependent protein kinase (CaMK) II in the same muscle. To determine if CaMK signaling mediates MEF2A/DNA associations in vivo, we performed ChIP assays on C2C12 myotubes expressing constitutively active (CA) or dominant negative (DN) CaMK IV proteins. We found that ∼75% more MEF2A was bound to the Glut4 promoter in CA compared with DN CaMK IV-expressing cells. GLUT4 protein increased ∼70% 24 h after exercise but was unchanged by overexpression of CA CaMK IV in myotubes. These results confirm that exercise increases the binding of MEF2A to the Glut4 promoter in vivo and provides evidence that CaMK signaling is involved in this interaction.