1-Alkyl-2-acetylglycerophosphocholine Esterase: A lipoprotein-associated PHOSPHOLIPASE A2 which modulates the action of PLATELET ACTIVATING FACTOR by hydrolyzing the SN-2 ester bond to yield the biologically inactive lyso-platelet-activating factor. It has specificity for phospholipid substrates with short-chain residues at the SN-2 position, but inactive against long-chain phospholipids. Deficiency in this enzyme is associated with many diseases including ASTHMA, and HYPERCHOLESTEROLEMIA.EsterasesCarboxylic Ester Hydrolases: Enzymes which catalyze the hydrolysis of carboxylic acid esters with the formation of an alcohol and a carboxylic acid anion.Naphthol AS D Esterase: Hydrolytic enzyme activity used as a histocytochemical test for the presence of esterases in tissue. Substrate used is 3-hydroxy-4'-nitro-2-naphthanilide chloroacetate (naphthol AS-D).Sterol Esterase: An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.Acetylesterase: An enzyme that catalyzes the conversion of acetate esters and water to alcohols and acetate. EC 3.1.1.6.Carboxylesterase: Carboxylesterase is a serine-dependent esterase with wide substrate specificity. The enzyme is involved in the detoxification of XENOBIOTICS and the activation of ester and of amide PRODRUGS.EstersIsoflurophate: A di-isopropyl-fluorophosphate which is an irreversible cholinesterase inhibitor used to investigate the NERVOUS SYSTEM.Alkylation: The covalent bonding of an alkyl group to an organic compound. It can occur by a simple addition reaction or by substitution of another functional group.
(1/562) Lipoprotein-associated phospholipase A2, platelet-activating factor acetylhydrolase, generates two bioactive products during the oxidation of low-density lipoprotein: use of a novel inhibitor.

A novel and potent azetidinone inhibitor of the lipoprotein-associated phospholipase A2 (Lp-PLA2), i.e. platelet-activating factor acetylhydrolase, is described for the first time. This inhibitor, SB-222657 (Ki=40+/-3 nM, kobs/[I]=6. 6x10(5) M-1.s-1), is inactive against paraoxonase, is a poor inhibitor of lecithin:cholesterol acyltransferase and has been used to investigate the role of Lp-PLA2 in the oxidative modification of lipoproteins. Although pretreatment with SB-222657 did not affect the kinetics of low-density lipoprotein (LDL) oxidation by Cu2+ or an azo free-radical generator as determined by assay of lipid hydroperoxides (LOOHs), conjugated dienes and thiobarbituric acid-reacting substances, in both cases it inhibited the elevation in lysophosphatidylcholine content. Moreover, the significantly increased monocyte chemoattractant activity found in a non-esterified fatty acid fraction from LDL oxidized by Cu2+ was also prevented by pretreatment with SB-222657, with an IC50 value of 5.0+/-0.4 nM. The less potent diastereoisomer of SB-222657, SB-223777 (Ki=6.3+/-0.5 microM, kobs/[I]=1.6x10(4) M-1.s-1), was found to be significantly less active in both assays. Thus, in addition to generating lysophosphatidylcholine, a known biologically active lipid, these results demonstrate that Lp-PLA2 is capable of generating oxidized non-esterified fatty acid moieties that are also bioactive. These findings are consistent with our proposal that Lp-PLA2 has a predominantly pro-inflammatory role in atherogenesis. Finally, similar studies have demonstrated that a different situation exists during the oxidation of high-density lipoprotein, with enzyme(s) other than Lp-PLA2 apparently being responsible for generating lysophosphatidylcholine.  (+info)

(2/562) Association of the inflammatory state in active juvenile rheumatoid arthritis with hypo-high-density lipoproteinemia and reduced lipoprotein-associated platelet-activating factor acetylhydrolase activity.

OBJECTIVE: To investigate the relationship between the quantitative and qualitative abnormalities of apolipoprotein B (Apo B)- and Apo A-I-containing lipoproteins and between lipoprotein-associated platelet-activating factor acetylhydrolase (PAF-AH) activity in patients with juvenile rheumatoid arthritis (JRA) as a function of the inflammatory state. METHODS: Twenty-six JRA patients and 22 age- and sex-matched control subjects with normal lipid levels participated in the study. Fourteen patients had active disease, and 12 had inactive disease. Plasma lipoproteins were fractionated by gradient ultracentrifugation into 9 subfractions, and their chemical composition and mass were determined. The PAF-AH activity associated with lipoprotein subfractions and the activity in plasma were also measured. RESULTS: Patients with active JRA had significantly lower plasma total cholesterol and high-density lipoprotein (HDL) cholesterol levels as compared with controls, due to the decrease in the mass of both the HDL2 and HDL3 subfractions. Patients with active JRA also had higher plasma triglyceride levels, mainly due to the higher triglyceride content of the very low-density lipoprotein plus the intermediate-density lipoprotein subfraction. The plasma PAF-AH activity in patients with active JRA was lower than that in controls, mainly due to the decrease in PAF-AH activity associated with the intermediate and dense low-density lipoprotein subclasses. The lipid abnormalities and the reduction in plasma PAF-AH activity were significantly correlated with plasma C-reactive protein levels and were not observed in patients with inactive JRA. CONCLUSION: This is the first study to show that patients with active JRA exhibit low levels of HDL2 and HDL3 and are deficient in plasma PAF-AH activity. These alterations suggest that active JRA is associated with partial loss of the antiinflammatory activity of plasma Apo B- and Apo A-I-containing lipoproteins.  (+info)

(3/562) Glutamate receptor signaling interplay modulates stress-sensitive mitogen-activated protein kinases and neuronal cell death.

Glutamate receptors modulate multiple signaling pathways, several of which involve mitogen-activated protein (MAP) kinases, with subsequent physiological or pathological consequences. Here we report that stimulation of the N-methyl-D-aspartate (NMDA) receptor, using platelet-activating factor (PAF) as a messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal-regulated kinase, in primary cultures of hippocampal neurons. Activation of the metabotropic glutamate receptor (mGluR) blocks this NMDA-signaling through PAF and MAP kinases, and the resultant cell death. Recombinant PAF-acetylhydrolase degrades PAF generated by NMDA-receptor activation; the hetrazepine BN50730 (an intracellular PAF receptor antagonist) also inhibits both NMDA-stimulated MAP kinases and neuronal cell death. The finding that the NMDA receptor-PAF-MAP kinase signaling pathway is attenuated by mGluR activation highlights the exquisite interplay between glutamate receptors in the decision making process between neuronal survival and death.  (+info)

(4/562) Molecular basis of the interaction between plasma platelet-activating factor acetylhydrolase and low density lipoprotein.

The platelet-activating factor acetylhydrolases are enzymes that were initially characterized by their ability to hydrolyze platelet-activating factor (PAF). In human plasma, PAF acetylhydrolase (EC 3.1.1.47) circulates in a complex with low density lipoproteins (LDL) and high density lipoproteins (HDL). This association defines the physical state of PAF acetylhydrolase, confers a long half-life, and is a major determinant of its catalytic efficiency in vivo. The lipoprotein-associated enzyme accounts for all of the PAF hydrolysis in plasma but only two-thirds of the protein mass. To characterize the enzyme-lipoprotein interaction, we employed site-directed mutagenesis techniques. Two domains within the primary sequence of human PAF acetylhydrolase, tyrosine 205 and residues 115 and 116, were important for its binding to LDL. Mutation or deletion of those sequences prevented the association of the enzyme with lipoproteins. When residues 115 and 116 from human PAF acetylhydrolase were introduced into mouse PAF acetylhydrolase (which normally does not associate with LDL), the mutant mouse PAF acetylhydrolase associated with lipoproteins. To analyze the role of apolipoprotein (apo) B100 in the formation of the PAF acetylhydrolase-LDL complex, we tested the ability of PAF acetylhydrolase to bind to lipoproteins containing truncated forms of apoB. These studies indicated that the carboxyl terminus of apoB plays a key role in the association of PAF acetylhydrolase with LDL. These data on the molecular basis of the PAF acetylhydrolase-LDL association provide a new level of understanding regarding the pathway for the catabolism of PAF in human blood.  (+info)

(5/562) Deficiency of platelet-activating factor acetylhydrolase is a severity factor for asthma.

Asthma, a family of airway disorders characterized by airway inflammation, has an increasing incidence worldwide. Platelet-activating factor (PAF) may play a role in the pathophysiology of asthma. Its proinflammatory actions are antagonized by PAF acetylhydrolase. A missense mutation (V279F) in the PAF acetylhydrolase gene results in the complete loss of activity, which occurs in 4% of the Japanese population. We asked if PAF acetylhydrolase deficiency correlates with the incidence and severity of asthma in Japan. We found that the prevalence of PAF acetylhydrolase deficiency is higher in Japanese asthmatics than healthy subjects and that the severity of this syndrome is highest in homozygous-deficient subjects. We conclude that the PAF acetylhydrolase gene is a modulating locus for the severity of asthma.  (+info)

(6/562) Platelet-activating factor may act as an endogenous pulse generator for sheep of luteolytic PGF2alpha release.

Pulsatile release of uterine prostaglandin F2alpha (PGF2alpha) induces luteolysis in ruminants. However, the mechanism(s) that initiates and maintains luteolysis has not been defined. The present study tested the hypothesis that the endogenous PGF2alpha pulse generator is uterine-derived platelet-activating factor (PAF). Ovariectomized ewes were given exogenous progesterone (P), estradiol (E), or both (P+E, mimicking the normal luteal phase). Only ewes treated with steroids released PAF into the uterine lumen and had increased PAF:acetylhydrolase activity in the uterine lumen. Steroid treatment also influenced the capacity of the uterus to release PGF2alpha in response to exogenous PAF. PAF infusion did not affect plasma PGF2alpha metabolite (PGFM) levels in control (no steroid treatment) ewes but increased plasma PGFM levels in P+E ewes (P < 0.001) and ewes treated with P or E alone (P < 0.05). Infusion of PAF followed by or coincident with oxytocin (OT) acted in a synergistic manner to increase plasma PGFM levels. Repeated infusion of PAF into the uterus at 1-h intervals induced tachyphylaxis of the PGFM response to PAF; however, sensitivity of the uterus to PAF returned spontaneously by the 6th h. Interferon-tau (IFN-tau) inhibits pulsatile release of PGF2alpha during pregnancy to prevent luteolysis. Exogenous recombinant ovine IFN-tau (50 microgram) inhibited the uterine response to PAF alone or the combined effects of PAF and OT. These results indicate that uterine PAF fulfills many of the criteria for an endogenous PGF2alpha pulse-generator: steroid induction of PAF production and uterine responsiveness to PAF-induced release of PGF; synergistic stimulation of PAF-induced PGF release by OT; inhibition of PAF effects by IFN-tau; and PAF's ability to induce pulses of PGF with a periodicity during a period of chronic exposure of the uterus to PAF.  (+info)

(7/562) Molecular analysis of an unstable genomic region at chromosome band 11q23 reveals a disruption of the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase (Pafah1a2) in human lymphoma.

A region of 150 kb has been analysed around a previously isolated, lymphoma associated, translocation breakpoint located at chromosome band 11q23. This balanced and reciprocal translocation, t(11;14)(q32;q23), has been shown to result in the fusion between chromosome 11 specific sequence and the switch gamma4 region of the IGH locus. The LPC gene, encoding a novel proprotein convertase belonging to the furin family, has been identified in this region. In order to characterize further the region surrounding the translocation, we have determined the detailed structure of LPC. Here we show that LPC consists of at least 16 exons covering 25 kb, and that there is a partial duplication, involving mobile genetic elements and containing LPC exons 13-17 in a tail-tail configuration at 65 kb downstream. Since the chromosomal breakpoint lay between these two structures, the intervening region was further analysed and shown to contain at least two unrelated genes. The previously known SM22 gene was localized close to the 3' tail of LPC. Furthermore, we identified the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase (Pafah1a2) at the chromosomal breakpoint. The position of another previously identified breakpoint was also located to within the first intron of this gene. Altogether, our results give evidence of a genomic instability of this area of 11q23 and show that Pafah1a2 and not LPC is the gene disrupted by the translocation, suggesting that deregulated Pafah1a2 may have a role in lymphomagenesis.  (+info)

(8/562) All ApoB-containing lipoproteins induce monocyte chemotaxis and adhesion when minimally modified. Modulation of lipoprotein bioactivity by platelet-activating factor acetylhydrolase.

Mildly oxidized LDL has many proinflammatory properties, including the stimulation of monocyte chemotaxis and adhesion, that are important in the development of atherosclerosis. Although ApoB-containing lipoproteins other than LDL may enter the artery wall and undergo oxidation, very little is known regarding their proinflammatory potential. LDL, IDL, VLDL, postprandial remnant particles, and chylomicrons were mildly oxidized by fibroblasts overexpressing 15-lipoxygenase (15-LO) and tested for their ability to stimulate monocyte chemotaxis and adhesion to endothelial cells. When conditioned on 15-LO cells, LDL, IDL, but not VLDL increased monocyte chemotaxis and adhesion approximately 4-fold. Chylomicrons and postprandial remnant particles were also bioactive. Although chylomicrons had a high 18:1/18:2 ratio, similar to that of VLDL, and should presumably be less susceptible to oxidation, they contained (in contrast to VLDL) essentially no platelet-activating factor acetylhydrolase (PAF-AH) activity. Because PAF-AH activity of lipoproteins may be reduced in vivo by oxidation or glycation, LDL, IDL, and VLDL were treated in vitro to reduce PAF-AH activity and then conditioned on 15-lipoxygenase cells. All 3 PAF-AH-depleted lipoproteins, including VLDL, exhibited increased stimulation of monocyte chemotaxis and adhesion. In a similar manner, lipoproteins from Japanese subjects with a deficiency of plasma PAF-AH activity were also markedly more bioactive, and stimulated monocyte adhesion nearly 2-fold compared with lipoproteins from Japanese control subjects with normal plasma PAF-AH. For each lipoprotein, bioactivity resided in the lipid fraction and monocyte adhesion could be blocked by PAF-receptor antagonists. These data suggest that the susceptibility of plasma lipoproteins to develop proinflammatory activity is in part related to their 18:1/18:2 ratio and PAF-AH activity, and that bioactive phospholipids similar to PAF are generated during oxidation of each lipoprotein. Moreover, LDL, IDL, postprandial remnant particles, and chylomicrons and PAF-AH-depleted VLDL all give rise to proinflammatory lipids when mildly oxidized.  (+info)

*  1-alkyl-2-acetylglycerophosphocholine esterase
In enzymology, a 1-alkyl-2-acetylglycerophosphocholine esterase (EC 3.1.1.47) is an enzyme that catalyzes the chemical reaction ... The systematic name of this enzyme class is 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetohydrolase. Other names in common ... Blank ML, Lee T, Fitzgerald V, Snyder F (1981). "A specific acetylhydrolase for 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (a ... 1-alkyl-sn-glycero-3-phosphocholine + acetate Thus, the two substrates of this enzyme are 1-alkyl-2-acetyl-sn-glycero-3- ...
*  List of MeSH codes (D08)
... naphthol as d esterase MeSH D08.811.277.352.100.680 --- phospholipases MeSH D08.811.277.352.100.680.510 --- lysophospholipase ... cholesterol esterase MeSH D08.811.277.352.100.170 --- cholinesterases MeSH D08.811.277.352.100.170.176 --- acetylcholinesterase ... glucan 1,4-beta-glucosidase MeSH D08.811.277.450.420.200.600 --- glucan endo-1,3-beta-d-glucosidase MeSH D08.811.277.450. ... endo-1,4-beta xylanases MeSH D08.811.277.450.950.500 --- xylan endo-1,3-beta-xylosidase MeSH D08.811.277.656.149 --- atp- ...
*  List of EC numbers (EC 3)
... acetylxylan esterase EC 3.1.1.73: feruloyl esterase EC 3.1.1.74: cutinase EC 3.1.1.75: poly(3-hydroxybutyrate) depolymerase EC ... polyneuridine-aldehyde esterase EC 3.1.1.79: hormone-sensitive lipase EC 3.1.1.80: acetylajmaline esterase EC 3.1.1.81: quorum- ... methyl ester esterase EC 3.1.1.86: rhamnogalacturonan acetylesterase EC 3.1.1.87: fumonisin B1 esterase EC 3.1.1.88: pyrethroid ... alpha-amino-acid esterase EC 3.1.1.44: 4-methyloxaloacetate esterase EC 3.1.1.45: carboxymethylenebutenolidase EC 3.1.1.46: ...
Circulating Levels of Secretory- and Lipoprotein-Associated Phospholipase A2 Activities: Relation to Atherosclerotic Plaques...  Circulating Levels of Secretory- and Lipoprotein-Associated Phospholipase A2 Activities: Relation to Atherosclerotic Plaques...
In a sample of 1,029 post-MI patients, sPLA2 (adjusted HR 1.32 for 1 unit increase, p = 0.036), but not Lp-PLA2 (HR, 1.03; p = ... sPLA2 [hazard ratio (HR) 1.45 for 1 SD increase, p = 0.001], but not Lp-PLA2 (HR, 0.95; p = 0.55), activity was a significant ... sPLA2 [odds ratio 1.23 for 1 standard deviation (SD) increase, p = 0.007], but not Lp-PLA2 (p = 0.26), activity was related to ... 0.90), activity predicted death or recurrent MI during 1-year follow-up. ...
more infohttp://www.acc.org/latest-in-cardiology/journal-scans/2012/06/26/17/31/circulating-levels-of-secretory-and-lipoprotein-associated-phospholipase-a2
1-alkyl-2-acetylglycerophosphocholine esterase - Wikipedia  1-alkyl-2-acetylglycerophosphocholine esterase - Wikipedia
In enzymology, a 1-alkyl-2-acetylglycerophosphocholine esterase (EC 3.1.1.47) is an enzyme that catalyzes the chemical reaction ... The systematic name of this enzyme class is 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetohydrolase. Other names in common ... Blank ML, Lee T, Fitzgerald V, Snyder F (1981). "A specific acetylhydrolase for 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (a ... 1-alkyl-sn-glycero-3-phosphocholine + acetate Thus, the two substrates of this enzyme are 1-alkyl-2-acetyl-sn-glycero-3- ...
more infohttps://en.wikipedia.org/wiki/1-alkyl-2-acetylglycerophosphocholine_esterase
PAFAH2 - Platelet-activating factor acetylhydrolase 2, cytoplasmic - Homo sapiens (Human) - PAFAH2 gene & protein  PAFAH2 - Platelet-activating factor acetylhydrolase 2, cytoplasmic - Homo sapiens (Human) - PAFAH2 gene & protein
Has a marked selectivity for phospholipids with short acyl chains at the sn-2 position. May share a common physiologic function ... Belongs to the serine esterase family.Curated. Phylogenomic databases. evolutionary genealogy of genes: Non-supervised ... O-alkyl-2-acetyl-sn-glycero-3-phosphocholine*Search proteins in UniProtKB for this molecule. ... O-alkyl-2-acetyl-sn-glycero-3-phosphocholine*Search proteins in UniProtKB for this molecule. ...
more infohttps://www.uniprot.org/uniprot/Q99487
Tissue expression of PAFAH1B3 - Summary - The Human Protein Atlas  Tissue expression of PAFAH1B3 - Summary - The Human Protein Atlas
NTERA-2. PC-3. REH. RH-30. RPMI-8226. RPTEC TERT1. RT4. SCLC-21H. SH-SY5Y. SiHa. SK-BR-3. SK-MEL-30. T-47d. THP-1. TIME. U-138 ... NTERA-2. PC-3. REH. RH-30. RPMI-8226. RPTEC TERT1. RT4. SCLC-21H. SH-SY5Y. SiHa. SK-BR-3. SK-MEL-30. T-47d. THP-1. TIME. U-138 ... CACO-2. CAPAN-2. Daudi. EFO-21. FHDF/TERT166. HaCaT. HAP1. HBEC3-KT. HBF TERT88. HDLM-2. HEK 293. HEL. HeLa. Hep G2. HHSteC. HL ... CACO-2. CAPAN-2. Daudi. EFO-21. FHDF/TERT166. HaCaT. HAP1. HBEC3-KT. HBF TERT88. HDLM-2. HEK 293. HEL. HeLa. Hep G2. HHSteC. HL ...
more infohttp://www.proteinatlas.org/ENSG00000079462-PAFAH1B3/tissue/vulva%252Fanal+skin
The role of cytoplasmic dynein in the human brain developmental diseas by Richard B. Vallee, Nicole E. Faulkner et al.  "The role of cytoplasmic dynein in the human brain developmental diseas" by Richard B. Vallee, Nicole E. Faulkner et al.
LIS-1 is homologous to the fungal genes NudF and PAC1, which are involved in cytoplasmic dynein mediated nuclear transport, but ... Overexpression of LIS-1 interferes with cell division, with noteworthy effects on chromosome attachment to the mitotic spindle ... Together, these results suggest a role for LIS-1 in cytoplasmic dynein functions involving microtubule plus-ends. Furthermore, ... Recent evidence has implicated the human LIS-1 gene in Miller-Dieker lissencephaly and isolated lissencephaly sequence. ...
more infohttps://escholarship.umassmed.edu/gsbs_sp/1273/
multiple sclerosis  - BioMedLib™ search engine  multiple sclerosis - BioMedLib™ search engine
2 years. 3 years. 5 years. 10 years. Or published in the following date range: From (yyyy/mm/dd - month and day are optional) ... A1.1.3.1.1. Vertebrate. A1.1.3.1.1.1. Amphibian. A1.1.3.1.1.2. Bird. A1.1.3.1.1.3. Fish. A1.1.3.1.1.4. Mammal. A1.1.3.1.1.4.1. ... 2. Sandberg-Wollheim M, Ciusani E, Salmaggi A, Pociot F: An evaluation of tumor necrosis factor microsatellite alleles in ... 1 multiple sclerosis 383908 results Searchbox Export PDF RSS Email Delete Email this search result to the following email ...
more infohttp://bmlreview.com/?kwr=multiple+sclerosis&smntc=gene+or+genome&kwr=&ck=&cxts=10&fntszff=100&hghlght=maroon&srtrdr=relevance&annttn=none&pdthm=2010&hqryhstry=5062b3f288e4d101&pgwdth=100&mld=&wft=wims&b4s=851542823
multiple sclerosis  - BioMedLib™ search engine  multiple sclerosis - BioMedLib™ search engine
2 years. 3 years. 5 years. 10 years. Or published in the following date range: From (yyyy/mm/dd - month and day are optional) ... A1.1.3.1.1. Vertebrate. A1.1.3.1.1.1. Amphibian. A1.1.3.1.1.2. Bird. A1.1.3.1.1.3. Fish. A1.1.3.1.1.4. Mammal. A1.1.3.1.1.4.1. ... 2. Sandberg-Wollheim M, Ciusani E, Salmaggi A, Pociot F: An evaluation of tumor necrosis factor microsatellite alleles in ... 1 multiple sclerosis 383908 results Searchbox Export PDF RSS Email Delete Email this search result to the following email ...
more infohttp://bmlreview.com/?kwr=multiple+sclerosis&smntc=gene+or+genome&kwr=&ck=&cxts=10&fntszff=100&hghlght=maroon&srtrdr=relevance&annttn=none&pdthm=2010&hqryhstry=5062b3f288e4d101&pgwdth=100&mld=&wft=wims&b4s=397885983
Human Metabolome Database: Showing metabocard for LysoPC(10:0) (HMDB0003752)  Human Metabolome Database: Showing metabocard for LysoPC(10:0) (HMDB0003752)
Exhibits also esterase activity toward p-nitrophenyl. May act on the brush border membrane to facilitate the absorption of ... InChI=1S/C18H38NO7P/c1-5-6-7-8-9-10-11-12-18(21)24-15-17(20)16-26-27(22,23)25-14-13-19(2,3)4/h17,20H,5-16H2,1-4H3/p+1/t17-/m1/ ... 1. Cytosolic phospholipase A2. General function:. Involved in metabolic process. Specific function:. Selectively hydrolyzes ... 2. Eosinophil lysophospholipase. General function:. Involved in sugar binding. Specific function:. May have both ...
more infohttp://www.hmdb.ca/metabolites/HMDB03752
Relation of markers of inflammation (C-reactive protein, white blood cell count, and lipoprotein-associated phospholipase A2)...  Relation of markers of inflammation (C-reactive protein, white blood cell count, and lipoprotein-associated phospholipase A2)...
TY - JOUR. T1 - Relation of markers of inflammation (C-reactive protein, white blood cell count, and lipoprotein-associated phospholipase A2) to the ankle - Brachial index. AU - Santos, Simone. AU - Rooke, Thom W. AU - Bailey, Kent R. AU - McConnell, Joseph P.. AU - Kullo, Iftikhar Jan. PY - 2004. Y1 - 2004. N2 - Markers of inflammation are predictive of cardiovascular events but their association with atherosclerotic burden remains poorly defined. We hypothesized that markers of inflammation, including C-reactive protein (CRP), white blood cell (WBC) count, and lipoprotein-associated phospholipase A2 (Lp-PLA2), would be associated with the ankle-brachial index (ABI), a marker of atherosclerotic burden. Subjects were 247 patients referred for lower extremity arterial evaluation to the non-invasive vascular laboratory excluding those with active infection or lower extremity revascularization within the previous year. ABI was measured at two sites in both legs and the lowest of four measurements ...
more infohttps://mayoclinic.pure.elsevier.com/en/publications/relation-of-markers-of-inflammation-c-reactive-protein-white-bloo
Association between lipoprotein associated phospholipase A2 mass and subclinical coronary and carotid atherosclerosis in...  Association between lipoprotein associated phospholipase A2 mass and subclinical coronary and carotid atherosclerosis in...
Methods: LpPLA2 mass was assessed using a dual monoclonal antibody immunoassay. CAC presence was defined as CAC score,0. CAP ... In a fully adjusted model, LpPLA2 was not associated with CAC (OR per 1-SD increase, 0.85; 95% CI 0.71-1.02) or CAP (0.90, 0.75 ... In a fully adjusted model, LpPLA2 was not associated with CAC (OR per 1-SD increase, 0.85; 95% CI 0.71-1.02) or CAP (0.90, 0.75 ... In a fully adjusted model, LpPLA2 was not associated with CAC (OR per 1-SD increase, 0.85; 95% CI 0.71-1.02) or CAP (0.90, 0.75 ...
more infohttps://jhu.pure.elsevier.com/en/publications/association-between-lipoprotein-associated-phospholipase-a2-mass-
The Effect of Inhibition of Lp-PLA2 With Darapladib on Ischemic Events in Chronic CHD - American College of Cardiology  The Effect of Inhibition of Lp-PLA2 With Darapladib on Ischemic Events in Chronic CHD - American College of Cardiology
Keywords: 1-Alkyl-2-acetylglycerophosphocholine Esterase, Alleles, Blood Pressure, Cholesterol, Cooperative Behavior, Coronary ... Darapladib is a potent and reversible oral inhibitor of Lp-PLA2.6 Darapladib has been shown to reduce levels of Lp-PLA2 in ... Figure 1: Kaplan-Meier curves for the primary end point of death from cardiovascular causes, myocardial infarction, or stroke ( ... Figure 2: Cumulative Kaplan-Meier estimates of the secondary end point of major coronary events (a composite of death from ...
more infohttp://www.acc.org/latest-in-cardiology/articles/2014/07/18/18/29/the-effect-of-inhibition-of-lp-pla2-with-darapladib-on-ischemic-events-in-chronic-chd
LINC complex-Lis1 interplay controls MT1-MMP matrix digest-on-demand response for confined tumor cell migration.  LINC complex-Lis1 interplay controls MT1-MMP matrix digest-on-demand response for confined tumor cell migration.
... complex protein nesprin-2 and dynein adaptor Lis1. Our results uncover a digest-on-demand strategy for nuclear translocation ...
more infohttp://vivo.mblwhoilibrary.org/display/publication239092
Kennedy, G.<...  Kennedy, G.<...
Predictors of Early Stage Decline in Kidney Function in Type 1 Diabetes (Joint with Universities of Cambridge and Edinburgh). ... Genetic factors predicting Lp-PLA 2 activity and their association with cardiovascular-related mortality and morbidity. ... 1 Feb 2019, In : ERJ Open Research. 5, 1, p. 1-9 9 p., 00252-2018.. Research output: Contribution to journal › Article ...
more infohttps://discovery.dundee.ac.uk/en/persons/gwen-kennedy
YUHSpace: Lipoprotein-Associated Phospholipase A2 Is Related to Plaque Stability and Is a Potential Biomarker for Acute...  YUHSpace: Lipoprotein-Associated Phospholipase A2 Is Related to Plaque Stability and Is a Potential Biomarker for Acute...
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers. Yonsei Authors Kwon, Hyuck Moon(권혁문) ... 1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers. ... 1-Alkyl-2-acetylglycerophosphocholine Esterase/blood* ; Acute Coronary Syndrome/blood* ; Acute Coronary Syndrome/ ...
more infohttps://ir.ymlib.yonsei.ac.kr/handle/22282913/100141
YUHSpace: Lipoprotein-Associated Phospholipase A2 Is Related to Plaque Stability and Is a Potential Biomarker for Acute...  YUHSpace: Lipoprotein-Associated Phospholipase A2 Is Related to Plaque Stability and Is a Potential Biomarker for Acute...
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers. Show simple item record Find it @ YMLIB ... 1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers. ...
more infohttps://ir.ymlib.yonsei.ac.kr/handle/22282913/100141?mode=full
PLA2G7 elisa kit | Human phospholipase A2, group VII (platelet-activating factor acetylhydrolase, plasma) ELISA Kit-NP...  PLA2G7 elisa kit | Human phospholipase A2, group VII (platelet-activating factor acetylhydrolase, plasma) ELISA Kit-NP...
96-Strip-Wells / $795 +1 FREE 8GB USB. 5x96-Strip-Wells / $2,890 +3 FREE 8GB USB. 10x96-Strip-Wells / $5,465 +6 FREE 8GB USB. ... 24-Strip-Wells (LIMIT 1) / $250 +1 FREE 8GB USB. 48-Strip-Wells / $550 +1 FREE 8GB USB. ... Catalytic activity: 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine + H2O = 1-alkyl-sn-glycero-3-phosphocholine + acetate. ... Has a specificity for substrates with a short residue at the sn-2 position. It is inactive against long-chain phospholipids.. ...
more infohttps://www.mybiosource.com/prods/ELISA-Kit/Human/phospholipase-A2-group-VII-platelet-activating-factor-acetylhydrolase-plasma/PLA2G7/datasheet.php?products_id=703495
Rilapladib - GlaxoSmithKline - AdisInsight  Rilapladib - GlaxoSmithKline - AdisInsight
Mechanism of Action 1-alkyl-2-acetylglycerophosphocholine esterase inhibitors * Orphan Drug Status Orphan designation is ...
more infohttps://adisinsight.springer.com/drugs/800018454?error=cookies_not_supported&code=7e21b0ea-6cde-4d3b-bc91-40365881176b
Human Metabolome Database: Showing metabocard for LysoPC(22:1(13Z)) (HMDB0010399)  Human Metabolome Database: Showing metabocard for LysoPC(22:1(13Z)) (HMDB0010399)
Exhibits also esterase activity toward p-nitrophenyl. May act on the brush border membrane to facilitate the absorption of ... LysoPC(22:1(13Z)), in particular, consists of one chain of erucic acid at the C-1 position. The erucic acid moiety is derived ... LysoPC(22:1(13Z)). Description. LysoPC(22:1(13Z)) is a lysophospholipid (LyP). It is a monoglycerophospholipid in which a ... 1. Acyl-protein thioesterase 1. General function:. Involved in hydrolase activity. Specific function:. Hydrolyzes fatty acids ...
more infohttp://www.hmdb.ca/metabolites/HMDB10399
Lipoprotein-Associated phospholipase A2 ELISA & Assay Kits  Lipoprotein-Associated phospholipase A2 ELISA & Assay Kits
Low Density Lipoprotein Receptor-Related Protein Associated Protein 1 ELISA Kits * LPS-Responsive Vesicle Trafficking, Beach ... 1-alkyl-2-acetylglycerophosphocholine esterase , 2-acetyl-1-alkylglycerophosphocholine esterase , LDL-PLA(2) , LDL-associated ... phospholipase A2 , PAF 2-acylhydrolase , PAF acetylhydrolase , gVIIA-PLA2 , group-VIIA phospholipase A2 , lipoprotein- ...
more infohttps://www.antibodies-online.com/peptide-hormone-metabolism-pathway-41/lp-pla2-elisa-kit-28733/
List of MeSH codes (D08) - Wikipedia  List of MeSH codes (D08) - Wikipedia
... naphthol as d esterase MeSH D08.811.277.352.100.680 --- phospholipases MeSH D08.811.277.352.100.680.510 --- lysophospholipase ... cholesterol esterase MeSH D08.811.277.352.100.170 --- cholinesterases MeSH D08.811.277.352.100.170.176 --- acetylcholinesterase ... glucan 1,4-beta-glucosidase MeSH D08.811.277.450.420.200.600 --- glucan endo-1,3-beta-d-glucosidase MeSH D08.811.277.450. ... endo-1,4-beta xylanases MeSH D08.811.277.450.950.500 --- xylan endo-1,3-beta-xylosidase MeSH D08.811.277.656.149 --- atp- ...
more infohttps://en.wikipedia.org/wiki/List_of_MeSH_codes_(D08)
  • 8 In the Integrated Biomarkers and Imaging Study-2 (IBIS-2 study) in CHD patients, darapladib, compared with placebo over 12 months, halted progression of the secondary endpoint of coronary artery plaque necrotic core, as determined by intravascular ultrasound virtual histology. (acc.org)
  • The concordance of findings from Mendelian randomization and clinical trials suggests that for these 2 drugs, and for other novel biomarkers in future, validation of potential therapeutic targets by genetic studies (such as Mendelian randomization) before embarking on costly phase III randomized controlled trials could increase efficiency and offset the high risk of drug development, thereby facilitating discovery of new therapeutics and mitigating against the exuberant costs of drug development. (ox.ac.uk)
  • As is the case with diacylglycerols, glycerophosphocholines can have many different combinations of fatty acids of varying lengths and saturation attached at the SN-1 and SN-2 positions. (hmdb.ca)
  • These are glycerophosphocholines in which the glycerol is esterified with a fatty acid at O-1 position, and linked at position 3 to a phosphocholine. (hmdb.ca)
  • Lysophosphatidylcholines can have different combinations of fatty acids of varying lengths and saturation attached at the C-1 (sn-1) position. (hmdb.ca)
  • The enzyme catalyzes the transfer of the fatty acids of position sn-2 of phosphatidylcholine to the free cholesterol in plasma, with formation of cholesterol esters and lysophosphatidylcholine. (hmdb.ca)
  • Darapladib is a potent and reversible oral inhibitor of Lp-PLA 2 . (acc.org)
  • 6 Darapladib has been shown to reduce levels of Lp-PLA 2 in atherosclerotic plaque, the necrotic core. (acc.org)
  • 7 Darapladib has also been shown to reduce Lp-PLA 2 activity in human carotid plaque. (acc.org)
  • During 3.7 years median follow-up the primary endpoint occurred in 9.7% patients in the darapladib group and 10.4% patients in the placebo group: hazard ratio (HR) 0.94, 95% confidence interval (CI) (0.85, 1.03), p=0.20 (Figure 1). (acc.org)
  • Major coronary events occurred in 9.3% patients in the darapladib versus 10.3% in the placebo group: HR 0.90, 95% CI (0.82, 1.00), nominal p=0.045 (Figure 2). (acc.org)
  • Here we show that selective inhibition of Lp-PLA(2) with darapladib reduced development of advanced coronary atherosclerosis in diabetic and hypercholesterolemic swine. (nih.gov)
  • Darapladib markedly inhibited plasma and lesion Lp-PLA(2) activity and reduced lesion lysophosphatidylcholine content. (nih.gov)
  • Plasma glucose, cholesterol and Lp-PLA 2 activity increase upon DM-HC induction, but only Lp-PLA 2 activity is influenced by darapladib. (nih.gov)
  • Four weeks later, pigs were assigned to either a control or a treated group, and 10 mg kg −1 darapladib was orally administered daily to the treated group. (nih.gov)
  • Recent evidence from our laboratory has revealed that cytoplasmic dynein coimmunoprecipitates with LIS-1 in bovine brain cytosol, supporting a role in the dynein pathway in vertebrates. (umassmed.edu)
  • Together, these results suggest a role for LIS-1 in cytoplasmic dynein functions involving microtubule plus-ends. (umassmed.edu)
  • We further show that this response, including invadopodia formation in association with confining matrix fibrils, requires an intact connection between the nucleus and the centrosome via the linker of nucleoskeleton and cytoskeleton (LINC) complex protein nesprin-2 and dynein adaptor Lis1. (mblwhoilibrary.org)
  • Overexpression of LIS-1 interferes with cell division, with noteworthy effects on chromosome attachment to the mitotic spindle and on the interaction of astral microtubules with the cell cortex. (umassmed.edu)
  • These data show that selective inhibition of Lp-PLA(2) inhibits progression to advanced coronary atherosclerotic lesions and confirms a crucial role of vascular inflammation independent from hypercholesterolemia in the development of lesions implicated in the pathogenesis of myocardial infarction and stroke. (nih.gov)
  • Plasma glucose ( a ), cholesterol ( b ) and Lp-PLA 2 activity ( c ) levels were monitored throughout the 28-week study period. (nih.gov)
  • Data shown are means ± s.e.m. for glucose and cholesterol and means ± s.d. for Lp-PLA 2 activity. (nih.gov)
  • Our objective was to assess whether LpPLA 2 mass was associated with coronary artery calcium (CAC) and carotid artery plaque (CAP) in retired NFL players. (elsevier.com)
  • Methods: LpPLA 2 mass was assessed using a dual monoclonal antibody immunoassay. (elsevier.com)
  • Compared to the lowest quartile of Lp-PLA(2) activity, those in the highest had an increased risk of recurrent stroke (adjusted HR 2.54, 95% CI 1.01-6.39). (nih.gov)
  • Conclusion: LpPLA 2 mass was not associated with coronary or carotid subclinical atherosclerosis in retired NFL players. (elsevier.com)
  • 1-Decanoyllysolecithin is a glycerophosphocholine. (hmdb.ca)
  • b ROC for model containing covariates in a and Lp-PLA 2 and the interaction between LDL ≥130 mg/dl and Lp-PLA 2 . (nih.gov)
  • LysoPC(22:1(13Z)), in particular, consists of one chain of erucic acid at the C-1 position. (hmdb.ca)
  • Another sample of 1,029 post-ST-segment elevation myocardial infarction (STEMI) patients was followed for clinical events for 1 year. (acc.org)
  • Results were similar when highest and lowest LpPLA 2 tertiles were compared, and also in various subgroups. (elsevier.com)