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)

The possibility that arachidonic acid (AA) plays a role in the regulation of steroidogenesis in goldfish was investigated using preovulatory ovarian follicles incubated in vitro. AA was shown to act in a time- and dose-dependent manner to stimulate testosterone production. AA in the range of 10(-5) to 10(-4) M increased testosterone production within 2 hr and had a maximal effect by 9 hr. The magnitude of the testosterone response to AA was similar to that observed when ovarian follicles were incubated with human chorionic gonadotropin (hCG). Ovarian follicles incubated with AA and either hCG or forskolin (adenylate cyclase activator) produced more testosterone than follicles incubated with either of these compounds alone. The actions of AA on testosterone production were completely blocked by cyclooxygenase inhibitors (indomethacin or ibuprofen) and were reduced by 50% by the lipoxygenase inhibitor nordihydroguaiaretic acid. Phospholipase C was far more effective than phospholipase A2 in the stimulation of testosterone production. Taken together, these results suggest that AA formed subsequent to the action of phospholipase C on membrane phospholipids has a role in the regulation of steroidogenesis in preovulatory goldfish ovarian follicles.
Gen Comp Endocrinol 1990 Feb
PMID:Arachidonic acid stimulates steroidogenesis in goldfish preovulatory ovarian follicles. 210 68

The effect of electroconvulsive treatment (ECT) on activities of phospholipase C hydrolyzing phosphatidylinositol (PI-PLC) and phosphatidylinositol 4,5-bisphosphate (PIP2-PLC) and guanosine-5'-(3-O-thio)triphosphate (GTP gamma S) binding activity were examined in membrane and cytosol fractions from four discrete areas (prefrontal cortex, hippocampus, striatum, and amygdala) of the rat brain. A single ECT resulted in an increase in cytosolic activities of PI-PLC in the prefrontal cortex and of PIP2PLC in all 4 brain regions examined. There were no significant changes in either PI-PLC or PIP2-PLC activity in membrane fractions after a single ECT. Repeated ECT caused regionally specific changes in PLC activities as follows: in the prefrontal cortex, both cytosolic PI-PLC and PIP2-PLC and membranous PI-PLC activities were decreased; in the hippocampus, no changes in any PLC activities were seen; in the striatum, only membranous PI-PLC activities were increased; and, in the amygdala, cytosolic and membranous PI-PLC and cytosolic PIP2-PLC activities were increased. The pattern of changes in GTP gamma S binding activity following repeated ECT resembled those found in PLC activity as follows: in the prefrontal cortex, GTP gamma S binding activities were significantly reduced in both membrane and cytosol; in the hippocampus, the activity was decreased in membrane; in the striatum, no changes in GTP gamma S binding activity were seen in any fraction; and, in the amygdala, the activity was increased in cytosol. These findings suggest that ECT has complex effects on the G protein-phospholipase C system, possibly affecting neuronal signal transduction.
J Neural Transm Gen Sect 1990
PMID:Electroconvulsive treatment: effects on phospholipase C activity and GTP binding activity in rat brain. 216 50

The recent data on staphylococcal alpha-toxin, its functions, methods for its purification, forms are presented in the review. The problem of a target for toxin molecule is discussed.
Mol Gen Mikrobiol Virusol 1990 Aug
PMID:[Interaction of staphylococcal alpha-toxin with biomembranes]. 223 89

The voltage-dependent action of several scorpion alpha-toxins on Na channels was studied in toad myelinated nerve under voltage clamp. These toxins slow the declining phase of macroscopic Na current, apparently by inhibiting an irreversible channel inactivation step and thus permitting channels to reopen from a closed state in depolarized membranes. In this article, we describe the rapid reversal of alpha-toxin action by membrane depolarizations more positive than +20 mV, an effect not achieved by extensive washing. Depolarizations that were increasingly positive and of longer duration caused the toxin to dissociate faster and more completely, but only up to a limiting extent. Repetitive pulses had a cumulative effect equal to that of a single pulse lasting as long as their combined duration. When the membrane of a nonperfused fiber was repolarized, the effects of the toxin returned completely, but if the fiber was perfused during the conditioning procedure, recovery was incomplete and occurred more slowly, as it did at lower applied toxin concentrations. Other alpha-type toxins, from the scorpion Centruroides sculpturatus (IVa) and the sea anemone Anemonia sulcata (ATXII), exhibited similar voltage-dependent binding, though each had its own voltage range and dissociation rate. We suggest that the dissociation of the toxin molecule from the Na channel is coupled to the inactivation process. An equivalent valence for inactivation gating, of less than 1 e per channel, is calculated from the voltage-dependent change in toxin affinity.
J Gen Physiol 1986 Sep
PMID:Rapid voltage-dependent dissociation of scorpion alpha-toxins coupled to Na channel inactivation in amphibian myelinated nerves. 242 23

An alpha-toxin-binding membrane protein, isolated from the head and thoracic ganglia of the locus (Locusta migratoria), was reconstituted into planar lipid bilayers. Cholinergic agonists such as acetylcholine, carbamylcholine, and suberyldicholine induced fluctuations of single channels, which suggests that the protein represents a functional cholinergic receptor channel. The antagonist d-tubocurarine blocked the activation of the channels, whereas hexamethonium had only a weak effect; similar properties have been described for nicotinic insect receptors in situ. The channel was selectively permeable to monovalent cations but was impermeable to anions. The conductance of the channel (75 pS in 100 mM NaCl) was independent of the type of agonist used to activate the receptor. Kinetic analysis of the channel gating revealed that, at high agonist concentrations (50 microM carbamylcholine), more than one closed state exists and that multiple gating events, bursting as well as fast flickering, appeared. At very high agonist concentrations (500 microM carbamylcholine), desensitization was observed. Channel kinetics were dependent on the transmembrane potential. Comparing the conductance, the kinetics, and the pharmacology of nicotinic acetylcholine receptor from insect ganglia and fish electroplax reconstituted into bilayers revealed obvious similarities but also significant differences.
J Gen Physiol 1987 Dec
PMID:Characterization of the channel properties of a neuronal acetylcholine receptor reconstituted into planar lipid bilayers. 245 Jan 69

Polyethylene glycols (PEG) with molecular weight less than or equal to 3000 were shown to effectively protect human erythrocytes from osmotic lysis induced by alpha-staphylotoxin (ST). PEG with MW less than 3000 do not change the conductivity of ion channels induced by ST in bilayer lipid membranes (BLM). Changing the bilayer from a pure phosphatidylcholine (PC) to a negatively charged phosphatidylserine (PS) film results in an asymmetry of the current-voltage characteristics. This is evidenced by the asymmetrical position of the ST-channel pore in bilayer membranes. The results obtained allow to conclude that the ST-channel is an interprotein pore filled with water (with an inner diameter of 2.5-3 nm and a length of approximately 10 nm). It is composed of six molecules of alpha-toxin from Staphylococcus aureus. The ST-channel incorporates into a membrane with only one mouth in contact with the polar lipid heads and the other one protruding 4.5-5 nm from the bilayer plane in water solution.
Gen Physiol Biophys 1988 Oct
PMID:The structure of Staphylococcus aureus alpha-toxin-induced ionic channel. 246 32

The plc gene encoding the alpha-toxin (phospholipase C), an important virulence factor of Clostridium perfringens, has been cloned, sequenced and expressed in Escherichia coli. Transcriptional analysis of mRNAs produced in vivo by C. perfringens and E. coli, and in vitro using purified RNA polymerase from C. perfringens revealed that plc is transcribed constitutively from a single promoter situated about 100 nucleotides from the coding sequence. A T7 expression system was used to overproduce alpha-toxin in E. coli; enzymological studies with the amplified plc gene product unambiguously demonstrated that both lecithinase (phospholipase C) and sphingomyelinase activities were associated with this 43,000 dalton cytotoxin. The 370-residue alpha-toxin is haemolytic and shares sequence and functional homology with the two components of Bacillus cereus haemolysin, cereolysin AB, in which phospholipase C and sphingomyelinase activities are associated with different polypeptides.
Mol Gen Genet 1989 Nov
PMID:Gene cloning shows the alpha-toxin of Clostridium perfringens to contain both sphingomyelinase and lecithinase activities. 256 Jan 37

The Drosophila and Lucilia photoreceptor mutants, trp and nss, respond like wild-type flies to a short pulse of intense light or prolonged dim light; however, upon continuous intense illumination, the trp and nss mutants are unable to maintain persistent excitation. This defect manifests itself by a decline of the receptor potential toward baseline during prolonged intense illumination with little change in the shape or amplitude of the quantal responses to single photons (quantum bumps). Previous work on the trp and nss mutants suggests that a negative feedback loop may control the rate of bump production. Chemical agents affecting different steps of the phototransduction cascade were used in conjunction with light to identify a possible branching point of the feedback loop and molecular stages which are affected by the mutation. Fluoride ions, which in the dark both excite and adapt the photoreceptors of wild-type flies, neither excite nor adapt the photoreceptors of the trp and nss mutants. The hydrolysis-resistant analogue, GTP gamma S, which excites the photoreceptors of wild-type flies, resulting in noisy depolarization, markedly reduces the light response of both mutant flies. Intracellular recordings revealed, however, that the inhibitory effect of GTP gamma S on the nss mutant was accompanied neither by any significant depolarization nor by an increase in the noise, and thus was very different from the effect of a dim background light. The combination of inositol trisphosphate and diphosphoglycerate (InsP3 + DPG), which efficiently excites the photoreceptors of wild-type Lucilia, also excites the photoreceptors of nss Lucilia mutant. The InsP3 + DPG together act synergistically with light to accelerate the decline of the response to light in the mutant flies. These results suggest that the fly phototransduction pathway involves a feedback regulatory loop, which branches subsequent to InsP3 production and regulates guanine nucleotide-binding protein (G protein)-phospholipase C activity. A defect in this regulatory loop, which may cause an unusually low level of intracellular Ca2+, severely reduces the triggering of bumps in the mutants during intense prolonged illumination.
J Gen Physiol 1989 Sep
PMID:Chemical excitation and inactivation in photoreceptors of the fly mutants trp and nss. 260 31

Interactions between the different signaling roles of myo-inositol 1,4,5-trisphosphate and 1,2-diacylglycerol, the products of agonist-stimulated phosphatidylinositol 4,5-bisphosphate breakdown, are assessed in isolated rat hepatocytes. Measurements of the kinetics of accumulation of individual [3H]inositol phosphates after the addition of different Ca2+-mobilizing agonists in general support the role of inositol 1,4,5-trisphosphate as the second messenger responsible for release of sequestered intracellular Ca2+. Various agonists, when added at maximal concentrations, however, produce qualitatively and quantitatively different responses, which reflect varying abilities of the agonists to activate phospholipase C. Qualitative differences are revealed by a pronounced biphasic pattern to the Ins(1,4,5)P3 accumulation after vasopressin and phenylephrine stimulation, which is indicative of negative feedback. It is suggested that this effect is mediated by a partial diacylglycerol activation of protein kinase C, which in vitro causes an activation of inositol phosphate 5-phosphatase and hence promotes removal of Ins(1,4,5)P3 to Ins(1,4)P2. An alternative mechanism proposed by Biden and Wollheim (1986) of a secondary Ca2+ activation of Ins(1,4,5)P3 3-kinase is considered less likely as a general mechanism, since highly purified kinase prepared from rat brain shows only an inhibition by Ca2+. Glucagon, 8-Br-cAMP, and EGF induce small increases of Ins(1,4,5)P3 in hepatocytes, together with slower and smaller increases of cytosolic free Ca2+ than those produced by vasopressin or phenylephrine, with Ca2+ being mobilized from the same intracellular pools with each of the agonists. The Ca2+-mobilizing effect of glucagon, therefore, may be entirely due to a cAMP-dependent process, although a direct receptor-mediated activation of phospholipase C, as suggested by Wakelam et al. (1986), remains a possibility. The EGF receptor appears to be coupled to phospholipase C, presumably via a G-protein. It is speculated that the mechanism by which cAMP increases Ins(1,4,5)P3 levels in hepatocytes could either be by phosphorylation and inhibition of inositol phosphate 5-phosphatase or by phosphorylation and facilitation of the coupling between the G-protein and phospholipase C. When protein kinase C is maximally activated by pretreatment of hepatocytes with PMA, the stimulatory effects of phenylephrine, glucagon, 8-Br-cAMP, and EGF on the accumulation of inositol phosphates and increase of cytosolic free Ca2+ are largely inhibited.(ABSTRACT TRUNCATED AT 400 WORDS)
Soc Gen Physiol Ser 1987
PMID:Mechanisms involved in receptor-mediated changes of intracellular Ca2+ in liver. 285 Jun 13

The interaction of feline leukaemia viruses (FeLV) with erythrocytes was investigated. Haemadsorption (HAd) was observed on the surface of feline embryonic fibroblast cells infected with FeLV. HAd was detected in various degrees when cat, hamster or horse erythrocytes were incubated with cells infected with viruses of subgroup C (FeLV-C) and on cells infected with some FeLV subgroup A viruses (FeLV-A), but not on cells infected with FeLV subgroup B viruses (FeLV-B). HAd of sheep erythrocytes was detected on cells infected with some FeLV-C viruses. The HAd of hamster erythrocytes on cells infected with FeLV-C/Sarma virus was inhibited by antisera against gp70 or p15(E) but not by sera to the other FeLV structural polypeptides. HAd inhibition was also exhibited by cat sera which had FeLV-neutralizing activity but not by sera of specific pathogen-free cats. Haemagglutination by FeLV-C viruses was demonstrated after the virus was treated with neuraminidase and phospholipase C, or Tween-80 and ether. Contrary to expectations from the pattern observed by HAd, all FeLV-A viruses had similar haemagglutinin (HA) activity to FeLV-C viruses. FeLV-B viruses did not possess an HA.
J Gen Virol 1985 Feb
PMID:Haemadsorption and haemagglutination by feline leukaemia viruses. 298 74


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