Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.3 (phospholipase C)
 18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

NaF caused a dose-dependent rise in miniature end-plate potential (MEPP) frequency at the frog neuromuscular junction. The effects on MEPP frequency of both NaF and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) were rapidly reversed by the protein kinase C (PKC) inhibitor polymyxin B (2 microM). Theophylline augmented the response of MEPP frequency to TPA. It is concluded that the effect of fluoride on MEPP frequency may be through activation of phospholipase C and consequent PKC stimulation, and that the synergistic interaction of NaF and theophylline is consistent with such a mode of action.
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PMID:Stimulation of miniature end-plate potential frequency by fluoride may involve activation of protein kinase C. 180 Jan 24

The lipolytic action of theophylline was examined using both intact fat cells and a fat globule system. Theophylline had similar lipolytic actions in both systems. However theophylline did not activate hormone-sensitive lipase in the fat globule system as measured with added Ediol. Pretreatment of the fat globules with phospholipase C suppressed theophylline-induced lipolysis, but phospholipase D had no effect. A theophylline-sensitive system was reconstituted from endogenous fat and a lipase fraction. Inhibitors of theophylline-induced lipolysis such as quinine and propranolol inhibited theophylline binding to artificial lipid micelles. Purine nucleosides such as adenosine, inosine and guanosine inhibited theophylline-induced lipolysis in the fat globule system. These results suggest that theophylline has a lipolytic action similar to that of adrenaline. Both share a lipolytic mechanism additional to that involving the activation of hormone sensitive lipase through the cyclic-AMP dependent protein kinase. Phospholipids play an important role in this additional mechanism.
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PMID:The mechanism of the lipolytic action of theophylline in fat cells. 724 46

1. Adenosine A(1), A(2A), and A(3) receptors (ARs) and extracellular signal-regulated kinase 1/2 (ERK1/2) play a major role in myocardium protection from ischaemic injury. In this study, we have characterized the adenosine receptor subtypes involved in ERK1/2 activation in newborn rat cardiomyocytes. 2. Adenosine (nonselective agonist), CPA (A(1)), CGS 21680 (A(2A)) or Cl-IB-MECA (A(3)), all increased ERK1/2 phosphorylation in a time- and dose-dependent manner. The combined maximal response of the selective agonists was similar to adenosine alone. Theophylline (nonselective antagonist) inhibited completely adenosine-mediated ERK1/2 activation, whereas a partial inhibition was obtained with DPCPX (A(1)), ZM 241385 (A(2A)), and MRS 1220 (A(3)). 3. PD 98059 (MEK1; ERK kinase inhibitor) abolished all agonist-mediated ERK1/2 phosphorylation. Pertussis toxin (PTX, G(i/o) blocker) inhibited completely CPA- and partially adenosine- and Cl-IB-MECA-induced ERK1/2 activation. Genistein (tyrosine kinase inhibitor) and Ro 318220 (protein kinase C, PKC inhibitor) partially reduced adenosine, CPA and Cl-IB-MECA responses, without any effect on CGS 21680-induced ERK1/2 phosphorylation. H89 (protein kinase A, PKA inhibitor) abolished completely CGS 21680 and partially adenosine and Cl-IB-MECA responses, without any effect on CPA response. 4. Cl-IB-MECA-mediated increases in cAMP accumulation suggest that A(3)AR-induced ERK1/2 phosphorylation involves adenylyl cyclase activation via phospholipase C (PLC) and PKC stimulation. 5. In summary, we have shown that ERK1/2 activation by adenosine in cardiomyocytes results from an additive stimulation of A(1), A(2A), and A(3)ARs, which involves G(i/o) proteins, PKC, and tyrosine kinase for A(1) and A(3)ARs, and Gs and PKA for A(2A)ARs. Moreover, the A(3)AR response also involves a cAMP/PKA pathway via PKC activation.
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PMID:Characterization of ERK1/2 signalling pathways induced by adenosine receptor subtypes in newborn rat cardiomyocytes. 1475 70