Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.4.3 (phospholipase C)
18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to clarify the mechanism of the inhibitory effect of forskolin on contraction, cytosolic Ca(2+) level ([Ca(2+)](i)), and Ca(2+) sensitivity in guinea pig ileum. Forskolin (0.1 nM~10 microM) inhibited high K(+) (25 mM and 40 mM)- or histamine (3 microM)-evoked contractions in a concentration-dependent manner. Histamine-evoked contractions were more sensitive to forskolin than high K(+)-evoked contractions. Spontaneous changes in [Ca(2+)](i) and contractions were inhibited by forskolin (1 microM) without changing the resting [Ca(2+)](i). Forskoln (10 microM) inhibited muscle tension more strongly than [Ca(2+)](i) stimulated by high K(+), and thus shifted the [Ca(2+)](i)-tension relationship to the lower-right. In histamine-stimulated contractions, forskolin (1 microM) inhibited both [Ca(2+)](i) and muscle tension without changing the [Ca(2+)](i)-tension relationship. In alpha-toxin-permeabilized tissues, forskolin (10 microM) inhibited the 0.3 microM Ca(2+)-evoked contractions in the presence of 0.1 mM GTP, but showed no effect on the Ca(2+)-tension relationship. We conclude that forskolin inhibits smooth muscle contractions by the following two mechanisms: a decrease in Ca(2+) sensitivity of contractile elements in high K(+)-stimulated muscle and a decrease in [Ca(2+)](i) in histamine-stimulated muscle.
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PMID:Forskolin Changes the Relationship between Cytosolic Ca and Contraction in Guinea Pig Ileum. 1988 36

Cellular signaling can inhibit the membrane Na(+)-K(+) pump via protein kinase C (PKC)-dependent activation of NADPH oxidase and a downstream oxidative modification, glutathionylation, of the beta(1) subunit of the pump alpha/beta heterodimer. It is firmly established that cAMP-dependent signaling also regulates the pump, and we have now examined the hypothesis that such regulation can be mediated by glutathionylation. Exposure of rabbit cardiac myocytes to the adenylyl cyclase activator forskolin increased the co-immunoprecipitation of NADPH oxidase subunits p47(phox) and p22(phox), required for its activation, and increased superoxide-sensitive fluorescence. Forskolin also increased glutathionylation of the Na(+)-K(+) pump beta(1) subunit and decreased its co-immunoprecipitation with the alpha(1) subunit, findings similar to those already established for PKC-dependent signaling. The decrease in co-immunoprecipitation indicates a decrease in the alpha(1)/beta(1) subunit interaction known to be critical for pump function. In agreement with this, forskolin decreased ouabain-sensitive electrogenic Na(+)-K(+) pump current (arising from the 3:2 Na(+):K(+) exchange ratio) of voltage-clamped, internally perfused myocytes. The decrease was abolished by the inclusion of superoxide dismutase, the inhibitory peptide for the epsilon-isoform of PKC or inhibitory peptide for NADPH oxidase in patch pipette solutions that perfuse the intracellular compartment. Pump inhibition was also abolished by inhibitors of protein kinase A and phospholipase C. We conclude that cAMP- and PKC-dependent inhibition of the cardiac Na(+)-K(+) pump occurs via a shared downstream oxidative signaling pathway involving NADPH oxidase activation and glutathionylation of the pump beta(1) subunit.
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PMID:Activation of cAMP-dependent signaling induces oxidative modification of the cardiac Na+-K+ pump and inhibits its activity. 2019 11

The mechanism of proton pump inhibitors (PPIs) suppressing intestinal Mg²⁺ uptake is unknown. The present study aimed to investigate the role of purinergic P2Y receptors in the regulation of Mg²⁺ absorption in normal and omeprazole-treated intestinal epithelium-like Caco-2 monolayers. Omeprazole suppressed Mg²⁺ transport across Caco-2 monolayers. An agonist of the P2Y₂ receptor, but not the P2Y₄ or P2Y₆ receptor, suppressed Mg²⁺ transport across control and omeprazole-treated monolayers. Omeprazole enhanced P2Y₂ receptor expression in Caco-2 cells. Forskolin and P2Y₂ receptor agonist markedly enhanced apical HCO₃^- secretion by control and omeprazole-treated monolayers. The P2Y₂ receptor agonist suppressed Mg²⁺ transport and stimulated apical HCO₃^- secretion through the G_q-protein coupled-phospholipase C (PLC) dependent pathway. Antagonists of cystic fibrosis transmembrane conductance regulator (CFTR) and Na⁺-HCO₃^- cotransporter-1 (NBCe1) could nullify the inhibitory effect of P2Y₂ receptor agonist on Mg²⁺ transport across control and omeprazole-treated Caco-2 monolayers. Our results propose an inhibitory role of P2Y₂ on intestinal Mg²⁺ absorption.
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PMID:The inhibitory role of purinergic P2Y receptor on Mg²⁺ transport across intestinal epithelium-like Caco-2 monolayer. 3003 68


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