15 research outputs found
Prediction of phycoremediation of As(III) and As(V) from synthetic wastewater by Chlorella pyrenoidosa using artificial neural network
859 Regression of an immunologically ‘cold’ oral cancer model induced by modulation of the tumor microenvironment with DOXIL, anti-CTLA-4, and radiation
Isolation of (+)-pinitol and other constituents from the root bark of Tamarindus indica Linn.
Decreased 5-HT2C receptor binding in the cerebral cortex and brain stem during pancreatic regeneration in rats
Molecular mechanisms of muscarinic acetylcholine receptor-stimulated increase in cytosolic free Ca2+ concentration and ERK1/2 activation in the MIN6 pancreatic b-cell line
Muscarinic acetylcholine receptor (mAChR) activation of pancreatic β-cells elevates intracellular Ca2+ and potentiates glucose-stimulated insulin secretion. In addition, it activates a number of signaling molecules, including ERK1/2, whose activation has been shown to play an important role in regulating pancreatic β-cell function and mass. The aim of this work was to determine how mAChR activation elevates intracellular Ca2+ concentration ([Ca2+] i ) and activates ERK1/2 in the pancreatic β-cell line MIN6. We demonstrate that agonist-stimulated ERK1/2 activation is dependent on the activation of phospholipase C and an elevation in [Ca2+] i , but is independent of the activation of diacylglycerol-dependent protein kinase C isoenzymes. Using a pharmacological approach, we provide evidence that agonist-induced increases in [Ca2+] i and ERK activity require (1) IP3 receptor-mediated mobilization of Ca2+ from the endoplasmic reticulum, (2) influx of extracellular Ca2+ through store-operated channels, (3) closure of KATP channels, and (4) Ca2+ entry via L-type voltage-operated Ca2+ channels. Moreover, this Ca2+-dependent activation of ERK is mediated via both Ras-dependent and Ras-independent mechanisms. In summary, this study provides important insights into the multifactorial signaling mechanisms linking mAChR activation to increases in [Ca2+] i and ERK activity