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Phospholipase B and

This enzyme (triacylglycerol acyl-hydrolase) has a molecular mass of approximately 42 kDa (Hide, Chan, and Li 1992) and a short half-life of about 1-3 h in dogs. Pancreatic lipase is secreted in its active form, and this activity is enhanced by colipase and bile salts the enzyme hydrolyzes triglycerides to monoglycerides. Other lipases— phospholipase a, phospholipase b, and cholesterol ester hydrolase—are also secreted by the pancreas. [Pg.104]

Kolko, M., DeCoster, M. A., Rodriguez de Turco, E. B. and Bazan, N. G. Synergy by secretory phospholipase A2 and glutamate on inducing cell death and sustained arachidonic acid metabolic changes in primary cortical neuronal cultures./. Biol. Chem. 271 32722-32728,1996. [Pg.589]

Huwiler, A., Johansen, B., Skarstad, A. and Pfeilschifter, J., 2001, Ceramide binds to the CaLB domain of cytosoMc phospholipase Aj and facihtates its membrane docking and aracMdonic add release. FASEB J. 15 7-9... [Pg.242]

This enzyme [EC 3.1.1.5] (also referred to as lecithinase B, lysolecithinase, and phospholipase B) catalyzes the hydrolysis of a 2-lysophosphatidylcholine to produce glycerophosphocholine and a fatty acid anion. [Pg.434]

A12. Attwood, D., Graham, A. B., and Wood, G. C., The phospholipid-dependence of uridine diphosphate glucuronyltransferase. Reactivation of phospholipase-inactivated enzyme by phospholipids and detergents. Biochem. J. 123, 875-882... [Pg.278]

Drugs, particularly organic bases, may release histamine from mast cells by physically displacing the amine from its storage sites. Morphine, codeine, d-tubocu-rarine, guanethidine, and radiocontrast media can release histamine from mast cells. Basic polypeptides, such as bradykinin, neurotensin, substance P, somatostatin, polymyxin B, and the anaphylatoxins resulting from complement activation, also stimulate histamine release. Venoms often contain basic polypeptides as well as the histamine-releasing enzyme phospholipase A. [Pg.451]

Furthermore, the LPS signal transduction involves the activation of G proteins, of phospholipases C and D, the formation of diacyl-glycerol (DG) and inositol triphosphate (IP3). DG mediates the stimulation of protein kinase C (PKC) and IP3 induces an increase of cytosolic Ca++ The LPS signaling pathway also involves tyrosine kinases, constitutive nitric oxide (NO) synthase (cNOS), cGMP-dependent protein kinase, Ca channels, calmodulin and calmodulin kinase [27,28], as well as the MAP kinases [29] ERK1, ERK2 and p38 [23], The intracellular events in response to LPS are due to lipid A because they are inhibited by polymyxin B which is known to bind lipid A [27] and they are reproduced by lipids A [30,31]. [Pg.521]

Two pathways from the activated receptor are shown. At the left is activation of phospholipase Cy and formation, at a membrane-bound site, of inositol trisphosphate and diacylglycerol (DAG). The main pathway, in the center, activates Ras with the aid of the G protein Sos. Activated Ras, in turn, activates Raf and successive components of the MAPK cascade. At the right a seven-helix receptor activates both phospholipase C(3 and Ras via interaction with a (3y subunit. (B) A generalized scheme for the MAP kinase pathway. See Seger and Krebs.380... [Pg.579]

Farooqui A. A., Ong W. Y., Lu X. R., Halliwell B., and Horrocks L. A. (2001). Neurochemical consequences of kainate-induced toxicity in brain involvement of arachidonic acid release and prevention of toxicity by phospholipase A2 inhibitors. Brain Res. Rev. 38 61-78. [Pg.98]

Menard C., Valastro B., Martel M. A., Chartier T., Marineau A., Baudry M., and Massicotte G. (2005). AMPA receptor phosphorylation is selectively regulated by constitutive phospholipase A2 and 5-lipoxygenase activities. Hippocampus 15 370-380. [Pg.197]

Rodriguez A., Freixes M., Dalfo E., Martin M., Puig B., and Ferrer I. (2005). Metabotropic glutamate receptor phospholipase C pathway A vulnerable target to Creutzfeldt-Jakob disease in the cerebral cortex. Neuroscience 131 825-832. [Pg.200]

Borgstrom, B. 1980. Importance of phospholipids, pancreatic phospholipase A2, and fatty acid for the digestion of dietary fat In vitro experiments with the porcine enzymes. Gastroenterology 78, 954-962. [Pg.194]

Indomethacin, introduced in 1963, is an indole derivative (Figure 36-1). It is a potent nonselective COX inhibitor and may also inhibit phospholipase A and C, reduce neutrophil migration, and decrease T cell and B cell proliferation. Probenecid prolongs indomethacin s half-life by inhibiting both renal and biliary clearance. [Pg.821]

R13. Romaschin, A. D., De Majo, W. C., Winton, T., D Costa, M., Chang, G., Rubin, B., Gamliel, Z., and Walker, P. M., Systemic phospholipase a2 and cachectin levels in adult respiratory distress syndrome and multiple-organ failure. Clin. Biochem. 25,55—60 (1992). [Pg.79]


See other pages where Phospholipase B and is mentioned: [Pg.305]    [Pg.312]    [Pg.345]    [Pg.204]    [Pg.305]    [Pg.312]    [Pg.345]    [Pg.204]    [Pg.274]    [Pg.759]    [Pg.1067]    [Pg.105]    [Pg.312]    [Pg.337]    [Pg.178]    [Pg.46]    [Pg.230]    [Pg.218]    [Pg.68]    [Pg.258]    [Pg.172]    [Pg.208]    [Pg.519]    [Pg.178]    [Pg.333]    [Pg.219]    [Pg.98]    [Pg.205]    [Pg.231]    [Pg.174]    [Pg.133]    [Pg.159]    [Pg.407]    [Pg.596]   


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