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The role of free fatty acids, pancreatic lipase and Ca2+ signalling in injury of isolated acinar cells and pancreatitis model in lipoprotein lipase‐deficient mice
TLDR
This study investigates a possible pathogenic mechanism of cell damage in isolated mouse pancreatic acinar cells and of pancreatitis in LPL‐deficient and in wild type mice. Expand
Cholecystokinin-evoked Ca(2+) waves in isolated mouse pancreatic acinar cells are modulated by activation of cytosolic phospholipase A(2), phospholipase D, and protein kinase C.
TLDR
The experiments suggest that the propagation of Ca(2+) waves is modulated by protein kinase C (PKC) and arachidonic acid (AA) and the products of PLA(2) and PLD activation, AA and diacylglycerol (DAG), cause inhibition of Ca (2+) wave propagation by yet unknown mechanisms. Expand
Hormonal Control of ADP-ribosyl Cyclase Activity in Pancreatic Acinar Cells from Rats*
TLDR
At least two types of ADP-ribosyl cyclases are present in pancreatic acinar cells: membrane-bound CD38 and a cytosolic enzyme different from CD38, most likely mediated by cGMP. Expand
Inhibition of protein tyrosine phosphatase 1B by reactive oxygen species leads to maintenance of Ca2+ influx following store depletion in HEK 293 cells.
TLDR
Ca2+ influx is followed by generation of reactive oxygen species (ROS) and that it is reduced in cells preincubated with catalase and the results show that ROS act as fine tuning modulators of Ca2+ entry. Expand
Enhanced susceptibility to pancreatitis in severe hypertriglyceridaemic lipoprotein lipase-deficient mice and agonist-like function of pancreatic lipase in pancreatic cells
Background and aims: Recurrent pancreatitis is a common complication of severe hypertriglyceridaemia in patients with various gene mutations in lipoprotein lipase (LPL) or apolipoprotein CII.Expand
Tyrosine phosphatase PTP1B interacts with TRPV6 in vivo and plays a role in TRPV6-mediated calcium influx in HEK293 cells.
TLDR
Data indicate that tyrosine phosphorylation is involved in the regulation of the TRPV6 channel protein. Expand
Cholecystokinin-Evoked Ca2+ Waves in Isolated Mouse Pancreatic Acinar Cells Are Modulated by Activation of Cytosolic Phospholipase A2, Phospholipase D, and Protein Kinase C
TLDR
The experiments suggest that the propagation of Ca(2+) waves is modulated by protein kinase C (PKC) and arachidonic acid (AA) and the products of PLA(2) and PLD activation, AA and diacylglycerol (DAG), cause inhibition of Ca (2+) wave propagation by yet unknown mechanisms. Expand
Agonist-Stimulated Pathways of Calcium Signaling in Pancreatic Acinar Cells
TLDR
In pancreatic acinar cells stimulation of different intracellular pathways leads to different patterns of Ca2+ signaling, and stimulation of phospholipase C and PLD leads to generation of diacylglycerol (DAG) in addition to that produced by activation of PIP2-PLC. Expand
Identification of tyrosines in the putative regulatory site of the Ca2+ channel TRPV6.
TLDR
It is concluded that phosphorylation/dephosphorylation of tyrosines in position 161 and 162 is essential for regulation of Ca2+ influx through TRPV6 Ca2- channels in HEK293 cells. Expand
fMLP-induced arachidonic acid release in db-cAMP-differentiated HL-60 cells is independent of phosphatidylinositol-4, 5-bisphosphate-specific phospholipase C activation and cytosolic phospholipase
TLDR
The bulk of AA generated by fMLP stimulation of db-cAMP-differentiated HL-60 cells is independent of the cPLA(2) pathway, but may originate from activation of PC-PLC and PLD. Expand
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