A computational approach for investigating the mutational landscape of RAC-alpha serine/threonine-protein kinase (AKT1) and screening inhibitors against the oncogenic E17K mutation... by Thirumal Kumar, D

“…Among these 19 compounds, Akti-1/2 exhibited the best binding affinity with both native AKT1 and the E17K mutant. The molecular interaction study also revealed that the co-crystallized AKT1 inhibitor N-(4-(5-(3-acetamidophenyl)-2-(2-aminopyridin-3-yl)-3H-imidazo [4,5-b]pyridin-3-yl)benzyl)-3-fluorobenzamide (12j) exhibited a better interaction with native AKT1 compared with the E17K mutant AKT1 protein, whereas, Akti-1/2 exhibited the opposite effects, i.e., a better interaction with the E17K mutant AKT1 than the native AKT1. …”
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Greensporone C, a Freshwater Fungal Secondary Metabolite Induces Mitochondrial-Mediated Apoptotic Cell Death in Leukemic Cell Lines by Prabhu K.S.

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Effect of Hyperglycemia on eNOS function in EPCs by Elshiekh, Duaa Ibnomer

“…Results showed that both acute and chronic hyperglycemia showed a trend towards decrease in phosphorylation of eNOS and Akt. …”
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AMPK Activation Attenuates Albumin-induced Alterations in Renal Tubular Cells In Vitro by Allouch, Soumaya

“…Notably, metformin also prevented albumin-induced EMT; this was marked by a 50% decrease in a-SMA and a 60% increase in E-cadherin expression. …”
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ASSOCIATION BETWEEN INSULIN RESISTANCE AND NITRIC OXIDE IN HUMAN RETINAL MICROVASCULAR ENDOTHELIAL CELLS IN VITRO by Bushra, Sumbul

“…The various parameters of PI3K/ Akt signaling pathway were analyzed. This study demonstrated that Hyperglycemia causes an increase in ROS/oxidative stress and apoptosis, while insulin promotes a significant decrease in ROS and apoptosis, eNOS mediated NO production increases with hyperglycemia but remarkably reduced with insulin treatment after 1hour, 2 hours and 4 hours. …”
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Association between Insulin and Nitric Oxide in Human Retinal Microvascular Endothelial Cells in vitro by Rizk, Nasser Moustafa

“…In conclusion, this study demonstrated that Hyperglycemia causes an increase in ROS/oxidative stress and apoptosis, while insulin promotes a significant decrease in ROS and apoptosis, eNOS mediated NO production increases with hyperglycemia but remarkably decreases with insulin treatment after 1 hour, 2 hours and 4 hours, insulin could counteract the hyperglycemic effect on AKT/pI3 kinase which mediates NO production and VEGF-A, decreased adhesion molecules p-selectin involved in barrier disorder of retinal endothelial cells. …”
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Renoprotective Effects of Aldose Reductase Inhibitor Epalrestat against High Glucose-Induced Cellular Injury by El Gamal, Heba

“…Rat renal tubular (NRK-52E) cells were exposed to high glucose (30 mM) or normal glucose (5 mM) media for 24 to 48 hours with or without the AR inhibitor epalrestat (1 muM) and assessed for changes in Akt and ERK1/2 signaling, AR expression (using western blotting), and alterations in mitochondrial membrane potential (using JC-1 staining), cell viability (using MTT assay), and cell cycle. …”
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STANDARDIZATION OF AN IN VITRO MODEL OF DIABETIC NEPHROPATHY IN RENAL TUBULAR CELLS AND INVESTIGATION OF THE ROLE OF ALDOSE REDUCTASE PATHWAY IN HIGH GLUCOSE-INDUCED RENAL CELL INJ... by El Gamal, Heba

“…Normal rat kidney (NRK-52E) cells were exposed to high glucose (30 mM) or normal glucose (5 mM) media for 24 to 72 hours, and then assessed for changes in cell viability using MTT assay. …”
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Molecular and Peritoneal Microvascular Changes Cause Peritoneal Membrane Dysfunction by Uremia-Related Mechanisms by Zakaria, El-Rasheid

“…Protein expression of eNOS, MMP-2 and Akt was assessed. Results Uremia caused a remarkable increase in the reactivity of the visceral peritoneal microvasculature to the dialysis solution as compared with the renal injury and the chronic infusion groups. …”
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