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)

Some parameters of the receptor element from the rat olfactory epithelium are evaluated; it is characterized by high affinity for camphor (KD = 1.5. x 10(-9) M). Triton X-100 has no marked effect on the binding of [3H]camphor. Neither RNAase nor phospholipase C affected [3H]camphor-binding activity. Pronase and trypsin abolished [3H]camphor binding activity by 65 and 40%, respectively. Sulfhydryl reagents decrease the binding of [3H]camphor by a factor of 5--8. The isoelectric point of the receptor solubilized with Triton X-100 is 4.8, as determined by isoelectric focusing. The molecular weight of the receptor as determined by gel electrophoresis is about 120 000. It is proposed that the camphor receptor is a membrane protein containing sulfhydryl groups and playing a key role in olfactory reception.
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PMID:Molecular mechanisms of olfactory reception. IV. Some biochemical characteristics of the camphor receptor from rat olfactory epithelium. 4 3

Guinea-pig epidermal cells in culture possess a glycocalyx coat similar to that in vivo, as revealed by the ruthenium red stating technique. Trypsin, phospholipase C, and lysozyme do not produce any changes of the glycocalyx, while hyaluronidase and neuraminidase lead to partial and subcomplete removal respectively. Cells stripped of their glycocalyx coat by neuraminidase do not detach from the support and do not show any signs of toxicity. There is complete reconstitution of the glycocalyx within 24 hr.
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PMID:Glycocalyx of epidermal cells in vitro: demonstration and enzymatic removal. 4 27

The ultrastructural study of liver tissues from 38 patients with type B viral hepatitis consistently showed the presence of hepatitis B core antigen of 21-25 nm size in the liver cell nuclei and to a lesser extent in the cytoplasm. This finding and the demonstration of the tubular form of hepatitis B surface antigen in the proliferative degranulated endoplasmic reticulum constituted the etiologic criterion for the diagnosis of the disease. The double-shelled Dane-like particles were frequently found in association with the tubular form of the surface antigen. The core particles were found in the protoplasmic processes of hepatocytes and this correlated with the immunofluorescent microscopic findings that the antigen may be shed into circulation with the protoplasm. The core antigen was found to resist digestion by various enzymes such as protease, DNase, RNase, phospholipase C, lipase, lysozyme, diastase, neuraminidase and hyaluronidase, all of which did not destroy the immunoreactivity as demonstrated by immunoelectron and immunofluorescent microscopy. Similarly, sodium dodecyl sulfate, Tween 80 and mercaptoethanol also had no effect. The formalin-fixed paraffin-embedded liver tissue sections could be treated with protease to facilitate the immunofluorescent staining for the core antigen in tissue.
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PMID:Structural and immunoreactive characteristics of hepatitis B core antigen. 5 6

The physicochemical structure of the receptor for antibody (FcR) on B cells and its interrelationship with Ig and H-2 gene complex associated antigens were examined. FcR were found to be sensitive to treatment with phospholipase C and pronase, but resistant to neuraminidase, phospholipase A and chymotrypsin. They would therefore appear to be composed of phospholipoproteins. Several lines of evidence indicated that FcR and Ig receptors were discrete entities: thus, FcR (1) were resistant to chymotrypsin; (2) capped independently of Ig, as demonstrated by means of Fab fragments of anti-Ig, and (3) were closely associated with at least some Ia determinants, which are known to be distinct from Ig determinants. The relationship between FcR and H-2 gene complex associated antigens was confirmed by demonstrating inhibition of binding of aggregates by anti-Ia serum and vice versa. If, however, FcR were capped, anti-Ia serum applied under non-capping conditions was still found to bind diffusely to the great majority of B cells. Although this could be explained in part by the presence of residual FcR, some Ia determinants appeared to be distinct from FcR. The finding of residual FcR after capping with aggregates or immune complexes implied that FcR are a more integral part of the cell membrane than Ig receptors and could therefore act as proreceptors for the latter. Consistent with this was the demonstration of a significant polar distribution of Ig on B cells capped for FcR and then labelled under non-capping conditions with anti-Ig.
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PMID:A receptor for antibody on B lymphocytes. III. Relationship to immunoglobulin and ia determinants. 5 90

The lipid and protein fractions of the endobronchial lavage fluid from the normal rats which contained the lung surfactant were analysed. Lecithin, the main main component of the lung surfactant, was exclusively combined with a dextran precipitable protein. This protein then behaved as beta-globulin on cellulose acetate electrophoresis or low density lipoprotein on agarose gel filtration. After administration of phospholipase C (from Clostridium Welchii), the protein content of the lavage fluid increased markedly. The amount of dextran precipitable protein also increased markedly and its properties remained the same on gel filtration after treatment with phospholipase C. The phospholipids in the lavage fluid were not affected, although the total phospholipids in the lung tissue, especially lecithin, did decrease during the 10 days after treatment. Histopathologically, an eosinophilic dense exudative fluid appeared in both the interstitium and the broncho-alveolar spaces. A large number of the alveolar lining cells disappeared and a few of them were desquamated into the alveolar spaces. Thus, the immediate destruction of the alveolar lining cells after the administration of phospholipase C resulted in interstitial pneumonia in 10 days. The significance of phospholipase in pulmonary inflammation is discussed.
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PMID:Lung damage caused by phospholipase C and the changes in phospholipids in the rat lung. 6 May 1

Subviral cores have been prepared from the oncornavirus-like particle found in human milks with the use of phospholipase C and ether or Sterox SL. The major protein of these cores has a molecular weight of 27,000 daltons, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. This protein is found in the core fractions of reverse transcriptase-positive milks and is absent in negative milks. It is distributed in sucrose gradients only in those fractions containing cores and reverse transcriptase activity. The major core protein of the human milk oncornavirus-like particle is electrophoretically identical to the major core protein of the mouse mammary tumor virus.
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PMID:Identification and isolation of the major core protein from the oncornavirus-like particle in human milk. 6 99

Rabbits were treated with cyclophosphamide and 5-fluorouracil, myelosuppressive cytostatic agents, applied with a single dose of 1/3 LD50 or daily doses of 1/30 LD50 given for 14 days. Functional tests for evaluation of granulopoiesis were regularly performed at standard intervals and were following: leukocytosis, bone marrow picture with mitotic index, 3H-thymidine incorporation in vitro followed by autoradiography of labeled promyelocytes and myelocytes, serum lysozyme activity, mobilization of granulocyte reserve pool by staphylococcal alpha-toxin, cytochemistry of granulocytes, phagocytosis ability and Nitro-BT reduction. It has been found that 6-10 days after application of cytostatics, a marked depression of proliferation of young granulocyte forms and lowered reserve pool, are regularly observed. This was followed by spontaneous regeneration of granulopoiesis. No changes were noted in functional tests of mature granulocytes in peripheral blood. It is suggested that for investigation of the impairment of granulopoiesis after application of cytostatic agents, most suitable is evaluation of mobilization of the bone marrow reserve pool, lysozyme activity in blood serum and labelling of promyelocytes and myelocytes with 3H-thymidine in vitro.
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PMID:Inhibition of normal granulopoiesis by cytostatic agents. 6 8

The opposing actions of phosphatidylserine (PS) and cromolyn on histamine release were studied in rat peritoneal mast cells in vitro. Histamine-releasing drugs could be separated into 2 groups on the basis of whether they were potentiated by PS and inhibited by muM cromolyn (dextran, antigen (BSA), concanavalin A) or neither potentiated by PS nor inhibited by muM cromolyn (48/80, polymyxin, phospholipase C and ATP). Compound 48/80 and polymyxin chemically combined with PS, but this could be circumvented by preincubating the mast cells in PS for one hour, and then washing them free of PS in solution prior to addition of the drugs. These data define at least 2 pathways for induction of histamine release: (1) a PS-potentiated pathway inhibited by muM cromolyn, and (2) a PS-independent pathway unaffected by muM cromolyn. Dose-response curves of the muM cromolyn inhibition of PS-potentiated release revealed a parallel shift, suggesting that cromolyn may compete with PS.
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PMID:Relationship between phosphatidylserine and cromolyn in histamine release. 6 50

Benzalkonium chloride (BAC) is a mixture of quaternary benzyldimethylalkylammonium chlorides which was found to inhibit histamine release induced by polyamines (48/80, ATP, bradykinin, curare, guanethidine, polylysine, polymyxin B, poly-THIQ, protamine, stilbamidine or substance P), but not that caused by antigens, concanavalin A, dextran, lonophores (A23187 or X-537A), enzymes (chymotrypsin or phospholipase C), monoamines (dextromethorphan, meperidine or chlorpromazine) or detergents (decylamine, Triton X-100 or a fire ant venom alkylpiperidine). Inhibition by 1.5 and 3 microgram of BAC per ml caused parallel shifts of the 48/80 dose-response curves to the right with no loss of efficacy, indicating that the antagonism was surmountable. Phospholipase C was partially inhibited by BAC, but Triton X-100 also inhibited phospholipase C (but not 48/80), indicating that the inhibition of phospholipase C by BAC was probably a nonspecific, detergent effect. BAC caused histamine release by itself at concentrations over 5 microgram/ml. Heat inactivation (50 degrees C for 15 min) of the mast cells did not prevent this release, suggesting a lytic mechanism for this action. Structure-activity relations studies on various members of the BAC family for their ability to inhibit 48/80-induced histamine release indicated that benzyldimethyltridecylammonium chloride was the most potent.
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PMID:Benzalkonium chloride: selective inhibitor of histamine release induced by compound 48/80 and other polyamines. 9 63

The effect of nalidixic acid, rifampicin and chloramphenicol on the synthesis of phospholipase C (EC 3.1.4.3) has been studied in washed Bacillus cereus cells resuspended in nutrient broth. In the absence of inhibitors, the synthesis showed a biphasic pattern. No synthesis of release of enzyme was found in the presence of chloramphenicol. When rifampicin was added, phospholipase C synthesis continued for 10-15 min. Nalidixic acid, at concentrations which inhibited DNA synthesis completely, permitted the synthesis of phospholipase C at the same rate and for a similar length of time as rifampicin.
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PMID:The effect of nalidixic acid, rifampicin and chloramphenicol on the synthesis of phospholipase C in Bacillus cereus. 9 61


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