Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.13.12.5 (aequorin)
 1,451 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumour-promoting phorbol esters and 1,2-dioctanoyl-sn-glycerol both induce calcium transients in platelets. However, these can only be detected in platelets loaded with aequorin, but not in those loaded with the fluorescent probes quin-2 and fura-2 presumably because of intracellular calcium buffering. Several effects induced by phorbol esters and diacylglycerols, including the rise in (Ca2+)i, the stimulation of Na+/H+ transporter and the inhibition of the effects of thrombin alone on (Ca2+)i are potently antagonised by staurosporine, a compound known to inhibit protein kinase C. Higher concentrations of staurosporine themselves inhibit the thrombin-induced calcium transient. Staurosporine inhibits the effects of phorbol esters and dioctanoyl glycerol with equal potency although the latter does not cause enzyme translocation of cytosolic protein kinase C to membranes. These results therefore suggest that some, if not all, the effects of protein kinase C activation can occur without translocation of the enzyme.
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PMID:Calcium transients in human platelets monitored by aequorin, fura-2 and quin-2: effects of protein kinase C activation and inhibition. 359 58

1. Non-contractile Ca2+ mobilization (unaccompanied by muscle contraction) was initiated by nerve stimulation in the presence of neostigmine (more than 0.03 microM) at the endplate region of mouse diaphragm muscles. In the process of nicotinic receptor desensitization, the depressant effect of non-contractile Ca2+ on contractile Ca2+ mobilization was investigated by measurement of Ca(2+)-aequorin luminescence. 2. When the phrenic nerve was stimulated with paired pulses having intervals of 150, 300, 600, 1000 and 2000 ms, contractile Ca2+ transients were elicited during the generation of non-contractile Ca2+ mobilization. The amplitude of the contractile Ca2+ transients elicited by the second pulse (S2) was depressed at the shorter pulse intervals, but recovered to the initial contractile response (S1) at longer pulse intervals. 3. The extent of depression of S2 was enhanced by increasing the concentration of neostigmine (0.03 to 0.3 microM). When a low concentration (0.05 microM) of pancuronium, a competitive nicotinic antagonist, completely blocked non-contractile Ca2+ mobilization, the depression of S2 was diminished. 4. The depression of S2 was enhanced when the peak amplitude of non-contractile Ca2+ mobilization was raised by increasing the external Ca2+ concentration from 1.3 to 5 mM. 5. Staurosporine (10 nM), a protein kinase-C inhibitor, diminished the depression of S2 despite large amounts of non-contractile Ca2+ mobilization. The diminishing effect of staurosporine was counteracted by TPA (0.1 microM), a protein kinase-C activator. 6. These findings suggest that non-contractile Ca2+ mobilization may enhance the desensitization of the postsynaptic nicotinic receptor via activation of protein kinase-C at the neuromuscular junction.
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PMID:Postsynaptic nicotinic receptor desensitized by non-contractile Ca2+ mobilization via protein kinase-C activation at the mouse neuromuscular junction. 788 45