This study was conducted to determine the contribution of Group IV cytosolic phospholipase A2α (cPLA2α) in the development of angiotensin (Ang) II-induced hypertension and associated pathophysiology. Eight week old male wild type (cPLA2α+/+) and cPLA2α knockout (cPLA2α-/-) mice were infused with Ang II (750 ng/kg/min) or its vehicle for 2 weeks and systolic blood pressure (SBP) was measured weekly by the tail cuff method. Ang II increased SBP in cPLA2α+/+ mice to a greater degree than in cPLA2α-/- mice (125 ± 2 to 186 ± 7 mmHg vs. 125 ± 2 to 132 ± 2 mmHg respectively, P , 0.05). The increase in SBP in Ang II infused cPLA2α+/+ mice was associated with cardiac hypertrophy, measured by heart to body weight ratio (5.0 ± 0.3 vehicle vs. 7.1 ± 0.4 Ang II, P , 0.05), which was reduced by 26.0 ± 3.9 % (P , 0.05) in cPLA2α-/- mice. Ang II caused cardiac fibrosis, as indicated by accumulation of intracardiac α-smooth muscle actin- and transforming growth factor-β-positive cells, and ...

TY - JOUR. T1 - Expression of type V secretory phospholipase A2 in myocardial remodelling after infarction. AU - Ishikawa, Yukio. AU - Komiyama, K.. AU - Masuda, S.. AU - Murakami, M.. AU - Akasaka, Y.. AU - Ito, K.. AU - Akishima-Fukasawa, Y.. AU - Kimura, M.. AU - Fujimoto, A.. AU - Kudo, I.. AU - Ishii, T.. PY - 2005/9. Y1 - 2005/9. N2 - Aims: Secretory phospholipase A2 is associated with ischaemic injury in the human heart, but the distribution of type V secretory phospholipase A2 (sPLA2-V) remains unknown. The significance of sPLA2-V in myocardial infarction was investigated histopathologically. Methods: Sequential changes in the localization of sPLA2-V and its mRNA in myocardial tissues obtained from 30 autopsied hearts were examined by immunohistochemistry and in situ hybridization and compared with those of fibronectin, vascular endothelial growth factor (VEGF), interleukin (IL)-1β, tumour necrosis factor (TNF)-α, and cyclooxygenase-2 (COX-2). Results: No expression of sPLA2-V was ...

1ES9: The functional implications of the dimerization of the catalytic subunits of the mammalian brain platelet-activating factor acetylhydrolase (Ib).

It was concluded that nonpancreatic group II PLA2 is synthesized and stored by Paneth cells, whereas other cell types of the gastrointestinal tract seem incapable of synthesis of this enzyme. The positive immunoreaction in vascular structures may reflect the entry of circulating PLA2-II into vessel …

Oestvang, J., Anthonsen, M. W. & Johansen, B. 2011. LysoPC and PAF trigger arachidonic acid release by divergent signaling mechanisms in monocytes. J Lipids, 2011, 532145. (Read article). Oestvang, J. & Johansen, B. 2006. PhospholipaseA2: a key regulator of inflammatory signalling and a connector to fibrosis development in atherosclerosis. Biochim Biophys Acta, 1761, 1309-16. (Read article). Johansen, B., Hofker, M. & De Winther, M. 2006. Secretory group IIA phospholipase A2 regulates collagen accumulation and fibrotic cap development in atherosclerosis. Prostaglandins Other Lipid Mediat, 79, 159.. Ghesquiere, S. A., Gijbels, M. J., Anthonsen, M., Van Gorp, P. J., Van Der Made, I., Johansen, B., Hofker, M. H. & De Winther, M. P. 2005. Macrophage-specific overexpression of group IIa sPLA2 increases atherosclerosis and enhances collagen deposition. J Lipid Res, 46, 201-10. (Read article). Oestvang, J., Bonnefont-Rousselot, D., Ninio, E., Hakala, J. K., Johansen, B. & Anthonsen, M. W. 2004. ...

Lipoprotein-associated phospholipase A2 (Lp-PLA2) also known as platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A2 enzyme that in humans is encoded by the PLA2G7 gene. Lp-PLA2 is a 45-kDa protein of 441 amino acids. It is one of several PAF acetylhydrolases. In the blood it travels mainly with low-density lipoprotein (LDL). Less than 20% is associated with high-density lipoprotein HDL. It is an enzyme produced by inflammatory cells and hydrolyzes oxidized phospholipids in LDL. Lp-PLA2 is platelet-activating factor (PAF) acetylhydrolase (EC 3.1.1.47), a secreted enzyme that catalyzes the degradation of PAF to inactive products by hydrolysis of the acetyl group at the sn-2 position, producing the biologically inactive products LYSO-PAF and acetate. Lp-PLA2 is involved in the development of atherosclerosis, an observation that has prompted interest as a possible therapeutic target (see, e.g. the investigational drug Darapladib). In human atherosclerotic lesions, 2 main ...

1FXW: Preparation and crystal structure of the recombinant alpha(1)/alpha(2) catalytic heterodimer of bovine brain platelet-activating factor acetylhydrolase Ib.

A - Tilt: 6° - Segments: 1(38-43), 2(67-78), 3(86-98), 4(113-122), 5(134-143), 6(156-164), 7(169-177), 8(195-203), 9(206-214), 10(222-232), 11(235-243), 12(258-264 ...

Local and systemic skeletal muscle degeneration is a common consequence of envenomations due to snakebites and mass bee attacks. Phospholipases A2 (PLA2) are important myotoxic components in these venoms, inducing a similar pattern of degenerative events in muscle cells. Myotoxic PLA2s bind to acceptors in the plasma membrane, which might be lipids or proteins and which may differ in their affinity for the PLA2s. Upon binding, myotoxic PLA2s disrupt the integrity of the plasma membrane by catalytically dependent or independent mechanisms, provoking a pronounced Ca2+ influx which, in turn, initiates a complex series of degenerative events associated with hypercontraction, activation of calpains and cytosolic Ca2+-dependent PLA2s, and mitochondrial Ca2+ overload. Cell culture models of cytotoxicity indicate that some myotoxic PLA2s affect differentiated myotubes in a rather selective fashion, whereas others display a broad cytolytic effect. A model is presented to explain the difference between ...

phdthesis{9a2b0c99-7a98-49b0-8794-bd53b44cd228, abstract = {This thesis deals with processes coupled to injury in the peripheral nervous system (PNS), with a general aim to investigate the role of phospholipase A2 (PLA2) enzymes in axonal outgrowth. The axonal outgrowth of dorsal root ganglia (DRG) neurons in vitro was reduced by several different inhibitors of PLA2 activity and enhanced by an activator of this enzyme. The PLA2 inhibitors acted locally in the outgrowth region and the effect only comprised the axonal elongation stage. Time-lapse recording of growing axons showed a rapid retraction of filopodia and a reduction in growth cone motility at exposure to the drugs. The PLA2 activity was upregulated in the DRG and nerve after a sciatic nerve injury in vivo, most profoundly in the crush region of the nerve. The upregulated activity was strongly Ca2+-dependent, acid sensitive and reduced by an inhibitor of type IV cytosolic (c) PLA2 (methyl arachidonyl fluorophosphonate, MAFP) and the role ...

Lipoprotein-associated phospholipase A2 (Lp-PLA2), specifically Group VIIA PLA2, is an associate from the phospholipase A2 superfamily and is available mainly connected with LDL and HDL in individual plasma. apoproteins Xarelto in HDL, and also, residues 360C368 are just suffering from HDL.The full total results claim that apoA-I and phospholipid membranes play crucial roles in Lp-PLA2 localization to HDL. 14: 2032C2039. [PubMed] 20. Okamura K., Miura S., Zhang B., Uehara Y., Matsuo K., Kumagai K., Saku K.2007. Proportion of LDL- to HDL-associated platelet-activating aspect acetylhydrolase could be a marker of irritation in sufferers with paroxysmal atrial fibrillation. Circ. J.71: 214C219. [PubMed] 21. Tsimihodimos V., Karabina S. A., Tambaki A. P., Bairaktari E., Miltiadous G., Goudevenos J. A., Cariolou M. A., Chapman M. J., Tselepis A. D., Elisaf M. 2002. Changed distribution of platelet-activating aspect- acetylhydrolase activity between LDL and HDL being a function of the severe nature of ...

cPLA2 Antibody is a Rabbit Polyclonal antibody against cPLA2. This gene encodes a member of the cytosolic phospholipase A2 group IV family. The enzyme catalyzes the hydrolysis of membrane phospholipids to release arachidonic acid which is subsequently met

Les eicosanoïdes sont des médiateurs importants qui encadrent et régulent les fonctions osseuses. Leur production est sous la tutelle des phospholipases A[indice inférieur 2] qui permettent la relâche dacide arachidonique et de lysophospholipides puis de leur métabolisme subséquent des membranes cellulaires. Les PLA[indice inférieur 2] sécrétées ont également comme particularité de pouvoir exercer leurs effets directement via leurs récepteurs membranaires comme ligand. Malgré limplication connue des prostaglandines sur les fonctions ostéoclastiques et dans plusieurs processus pathologiques résultants en érosion osseuse, les phospholipases A[indice inférieur 2] ostéoclastiques restent inconnues et leurs rôles, spéculatifs. Les études présentées démontrent la présence de la cPLA[indice inférieur 2]-α et de la sPLA[indice inférieur 2] IIA chez les ostéoclastes humains. Par contre, leur expression semble différer selon létat de los. En effet, la cPLA[indice ...

ObjectiveThe aim of this study is to verify the crucial role of cytosolic phospholipase A2 alpha (cPLA2 alpha) in the… Expand ...

Evropski steber socialnih pravic določa zaveze EU glede plač: pravico delavcev do pravičnih plač, ki zagotavljajo dostojen življenjski standard, zagotavljanje

In the presented study, we demonstrate that the interaction of group IVA cytosolic phospholipase A2 and ceramide-1-phosphate is crucial for production of eicosanoid synthesis in inflammation. Inflammation is a critical component of many disease states including anaphylaxis, cancer, cardiovascular disease, rheumatoid arthritis, diabetes and asthma. Eicosanoids are well established mediators of inflammation, and the initial rate limiting step in the production of eicosanoids is the liberation of arachidonic acid (AA) from membrane phospholipids by a phospholipase A2 (PLA2). The major phospholipase involved in this liberation of AA during the inflammatory response is group IVA cytosolic phospholipase A2 (cPLA2α). Previous studies from our laboratory demonstrated that the bioactive sphingolipid, ceramide-1-phosphate (C1P), binds cPLA2α at a three amino acid sequence, which is located in the cationic β-groove of the C2 domain of cPLA2α. In this study we examined the effects of the genetic ablation of

Background: Although group IIA secretory phospholipase A2 (sPLA2-IIA) is well appraised for its involvement in atherosclerosis by modifying LDL, its role in managing CVD risk in a primary prevention setting with low LDL-C is unknown. Furthermore, the utility of sPLA2-IIA mass for assessing future CVD risk relative to statin therapy in a population free of CVD is unknown.. Methods: We analyzed data from JUPITER (NCT00239681) in which participants with LDL cholesterol ,130 mg/dL and hsCRP≥2 mg/L were randomized to rosuvastatin 20mg/day vs placebo. sPLA2-IIA was quantified by sandwich-type ELISA (Cayman) in 11269 participants before and 1 year after randomization. Cox regression was used to examine the association of sPLA2-IIA with CVD. The impact of lifelong reduction in sPLA2-IIA on CVD risk was assessed by Mendelian randomization analysis in 6692 participants.. Results: 313 first CVD events occurred during maximum follow-up of 5.0 (median, 1.9) years. Baseline sPLA2-IIA levels (median, ...

Publication date: Available online 12 December 2019Source: BiologicalsAuthor(s): Hebleen Brenes, Gilbert D. Loría, Bruno LomonteAbstractSecreted phospholipase A2 (sPLA2) molecules are small, calcium-dependent enzymes involved in many biological processes. Viperid venoms possess gIIA sPLA2s and sPLA2-like proteins, both having homology to human gIIA sPLA2, an innate immunity enzyme. We evalu...

Platelet-activating factor acetylhydrolase 2, cytoplasmic is an enzyme that in humans is encoded by the PAFAH2 gene. It is one of several PAF acetylhydrolases. This gene encodes platelet-activating factor acetylhydrolase isoform 2, a single-subunit intracellular enzyme that catalyzes the removal of the acetyl group at the SN-2 position of platelet-activating factor (identified as 1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine). However, this lipase exhibits a broader substrate specificity than simply platelet activating factor. Two other isoforms of intracellular platelet-activating factor acetylhydrolase exist, and both are multi-subunit enzymes. Additionally, there is a single-subunit serum isoform of this enzyme. GRCh38: Ensembl release 89: ENSG00000158006 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000037366 - Ensembl, May 2017 Human PubMed Reference:. Mouse PubMed Reference:. Hattori K, Adachi H, Matsuzawa A, Yamamoto K, Tsujimoto M, Aoki J, Hattori M, Arai H, Inoue K ...

TY - JOUR. T1 - Differential roles of ionic, aliphatic, and aromatic residues in membrane - Protein interactions. T2 - A surface plasmon resonance study on phospholipases A2. AU - Stahelin, R. V.. AU - Cho, W.. PY - 2001/4/17. Y1 - 2001/4/17. N2 - The roles of cationic, aliphatic, and aromatic residues in the membrane association and dissociation of five phospholipases A2 (PLA2), including Asp-49 PLA2 from the venom of Agkistodon piscivorus piscivorus, acidic PLA2 from the venom of Naja naja atra, human group IIa and V PLA2s, and the C2 domain of cytosolic PLA2, were determined by surface plasmon resonance analysis. Cationic interfacial binding residues of A. p. piscivorus PLA2 (Lys-10) and human group IIa PLA2 (Arg-7, Lys-10, and Lys-16), which mediate electrostatic interactions with anionic membranes, primarily accelerate the membrane association. In contrast, an aliphatic side chain of the C2 domain of cytosolic PLA2 (Val-97), which penetrates into the hydrophobic core of the membrane and ...

Looking for online definition of Phospholipases in the Medical Dictionary? Phospholipases explanation free. What is Phospholipases? Meaning of Phospholipases medical term. What does Phospholipases mean?

The human group IIA secreted PLA2 is a 14 kDa calcium-dependent extracellular enzyme that has been characterized as an acute phase protein with important antimicrobial activity and has been implicated in signal transduction. The selective binding of this enzyme to the phospholipid substrate interface plays a crucial role in its physiological function. To study interfacial binding in the absence of catalysis, one strategy is to produce structurally intact but catalytically inactive mutants. The active site mutants H48Q, H48N, and H48A had been prepared for the secreted PLA2s from bovine pancreas and bee venom and retained minimal catalytic activity while the H48Q mutant showed the maximum structural integrity. Preparation of the mutant H48Q of the human group IIA enzyme unexpectedly produced an enzyme that retained significant (2-4%) catalytic activity that was contrary to expectations in view of the accepted catalytic mechanism. In this paper it is established that the high residual activity of ...

Calcium dependent phospholipase A2 activity in the mixed micelles of 1-palmitoyl-2-oleoyl-phosphatidylglycerol and cholate was measured in sera of 39 patients with Crohns disease, 40 patients with ulcerative colitis, and 40 healthy controls. The phospholipase A2 activity was significantly raised in those sera of the patients with active Crohns disease and those with moderate and severe ulcerative colitis. The major phospholipase A2 activity derived from the sera was separated into two peaks by reverse phase high performance liquid chromatography. The phospholipase A2 active fractions were immunochemically characterised using specific antibody directed against human group II phospholipase A2 purified from rheumatoid synovial fluid. The results suggest that raised serum phospholipase A2 activity in patients with Crohns disease and ulcerative colitis was mainly attributed to the two forms of phospholipase A2 immunochemically related to group II enzyme. In patients with Crohns disease, serum ...

Fas-mediated apoptosis of human leukemic U937 cells was accompanied by increased arachidonic acid (AA) and oleic acid release from membrane glycerophospholipids, indicating phospholipase A2 (PLA2) activation. During apoptosis, type IV cytosolic PLA2 (cPLA2), a PLA2 isozyme with an apparent molecular mass of 110 kDa critical for stimulus-coupled AA release, was converted to a 78-kDa fragment with concomitant loss of catalytic activity. Cleavage of cPLA2 correlated with increased caspase-3-like protease activity in apoptotic cells and was abrogated by a caspase-3 inhibitor. A mutant cPLA2 protein in which Asp522 was replaced by Asn, which aligns with the consensus sequence of the caspase-3 cleavage site (DXXD downward arrowX), was resistant to apo-ptosis-associated proteolysis. Moreover, a COOH-terminal deletion mutant of cPLA2 truncated at Asp522 comigrated with the 78-kDa fragment and exhibited no enzymatic activity. Thus, caspase-3-mediated cPLA2 cleavage eventually leads to destruction of a catalytic

p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class=publication>Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href=http://www.nrbook.com/b/bookcpdf.php>Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...

Background: Recently we reported that angiotensin II (Ang II)-induced hypertension is mediated by group IV cytosolic phospholipase A2α (cPLA2α) via production of pro-hypertensive eicosanoids. Since Ang II increases blood pressure via its action in the subfornical organ (SFO), it led us to investigate the expression and possible contribution of cPLA2α to oxidative stress and development of hypertension in this brain area. Methods: Adenovirus (Ad)-green fluorescence protein (GFP) cPLA2α short hairpin (sh) RNA (Ad-cPLA2α shRNA) and its control Ad-scrambled shRNA (Ad-Scr shRNA) or Ad-enhanced cyan fluorescence protein cPLA2α DNA (Ad-cPLA2α DNA) and its control Ad-GFP DNA were transduced into SFO of cPLA2α+/+ and cPLA2α-/- male mice, respectively ...

Previous studies have suggested that sPLA2 may contribute to the development of atherosclerotic lesions,9 10 14 and we have examined this hypothesis directly using transgenic mice expressing human sPLA2. Consistent with previous studies,9 10 we observed abundant immunohistochemically localized sPLA2 in atherosclerotic lesions. The transgenic mice exhibited significantly increased lesions on a high-fat atherogenic diet as well as on a low-fat chow diet. The increase in lesion development appeared to result, in part, from decreased HDL and elevated LDL/VLDL levels. The levels of paraoxonase, an enzyme associated with HDL that protects against LDL oxidation and atherogenesis, were also substantially reduced in the sPLA2 transgenic mice compared with nontransgenic littermates. These points are discussed below.. The sPLA2 transgenic line used in these studies has previously been characterized with respect to sPLA2 expression in plasma and various tissue(s). The transgenic mice displayed severe ...

Background: The group IIA secretory phospholipase A2 gene, Pla2g2a, confers resistance to intestinal tumorigenesis in the ApcMin/+ mouse model. However, it is unclear how Pla2g2a exerts its tumor-suppressive effects and whether its mode of action dep

Arachidonic acid derivatives, like prostaglandins and leukotrienes, and the platelet-activating factor (PAF) are highly active substances with diverse biological actions. Elevated levels of these lipid mediators in response to a variety of stimuli have been implicated in the pathology of many inflammatory diseases. The rate limiting step in the generation of prostaglandins, leukotrienes and the PAF, respectively, is the cleavage of the sn-2- ester of membrane phospholipids by phospholipase A2. To date four main groups of phospholipases are known, which comprise the secretory, the calcium-independent, the cytosolic and the lipoprotein-associated phospholipases A2. From these the a-subtype of cytosolic phospholipases A2 (cPLA2α) appears to be the most likely candidate to catalyze this hydrolysis, since the enzyme is highly selective for arachidonoyl-containing phospholipids and is tightly regulated by receptor-stimulated mechanisms (calcium influx and phosphorylation). Moreover, experiments with ...

Has transacylase and calcium-independent phospholipase A2 activity (PubMed:20410020, PubMed:23958596). Catalyzes the formation of 1-O-acyl-N-acetylsphingosine and the concomitant release of a lyso-phospholipid (PubMed:11790796, PubMed:25727495). Has high activity with 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) and 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC), catalyzing the transfer of oleic acid to N-acetyl-sphingosine. Required for normal phospholipid degradation in alveolar and peritoneal macrophages and in spleen (By similarity). May have weak lysophospholipase activity (PubMed:10092508 ...

Pafah1b2 - Pafah1b2 (untagged) - Mouse platelet-activating factor acetylhydrolase, isoform 1b, subunit 2 (Pafah1b2), (10ug) available for purchase from OriGene - Your Gene Company.

Cytosolic phospholipase A2α (cPLA2α) is the rate-limiting enzyme for release of arachidonic acid, which is converted primarily to PGs via the cyclooxygenase 1 and 2 pathways and to leukotrienes via the 5-lipoxygenase pathway. We used adoptive transfer and relapsing-remitting forms of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, in two different strains of mice (SJL or C57BL/6) to demonstrate that blockade of cPLA2α with a highly specific small-molecule inhibitor during the tissue-damage effector phase abrogates the clinical manifestation of disease. Using the adoptive transfer model in SJL mice, we demonstrated that the blockade of cPLA2α during the effector phase of disease was more efficacious in ameliorating the disease pathogenesis than the blockade of each of the downstream enzymes, cyclooxygenase-1/2 and 5-lipooxygenase. Similarly, blockade of cPLA2α was highly efficacious in ameliorating disease pathogenesis during the effector phase of EAE ...

cdna:known chromosome:VEGA66:1:149829618:149961290:-1 gene:OTTMUSG00000016429 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Pla2g4a description:phospholipase A2, group IVA (cytosolic, calcium-dependent ...

购买Phospholipase A2山羊多克隆抗体(ab104252)，Phospholipase A2抗体经WB验证，可与人,小鼠样本反应。产品出库一年都在质保范围内。中国现货速达。

View mouse Pla2g2e Chr4:138877942-138882817 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression

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近年來，利用高分子微針貼片作為一種可自我施行且無痛之經皮藥物輸送裝置已廣為研究。然而，大多數的高分子微針皆在短時間內溶解，無法長效地釋放藥物，且由於高分子微針之機械強度較弱，微針往往無法完全刺進皮膚，降低藥物傳輸之效率。本研究將幾丁聚醣微針和機械強度較高的聚乳酸 [poly(L-lactide-co-DL-lactide), PLA] 支持軸陣列組合，製備出一具有生物可分解性且可將高分子微針完全刺入並鑲嵌於皮膚中的經皮微針貼片裝置。此鑲嵌式微針可於常溫常壓下，將幾丁聚醣溶液經離心灌模，並於半乾情形下與PLA支持軸組合而成。由體外豬皮穿刺結果證實，此鑲嵌式幾丁聚醣微針的穿刺比例可達100%，穿刺深度為550 ± 50 μm，可成功穿越皮膚角質層、到達有大量可引發免疫反應的抗原呈現細胞所存在的表皮層與真皮層。幾丁聚醣微針在穿刺後可與PLA支持軸分離

Alleen US$4.99, koop de beste 1.75mm PLA/ABS Reinigingsblok van filamentreiniger Antistatische stofreiniger voor 3D-printer online winkel tegen groothandelsprijs.

In this study, we demonstrate the presence of a transacetylase activity in human plasma low-density lipoprotein (LDL) that transfers short-chain fatty acids from platelet-activating factor (PAF) and its close ether- and ester-linked analogues to ether/ester-linked lysophospholipids (lyso-PL). We show evidence that both PAF acetylhydrolase (PAF-AH) and transacetylase activities are inhibited to the same extent by serine esterase inhibitors, are resistant to heat treatment, and exhibit identical distributions in lipoprotein classes and in LDL subfractions. Additionally, the competitive inhibition of PAF-AH by lyso-PL, and the evidence that the recombinant PAF-AH also showed a similar transacetylase activity, suggest that PAF-AH is responsible for both activities. Using PAF as a donor molecule and lyso-PAF (1-O-alkyl-sn-glycero-3-phosphocholine) as an acceptor, the transacetylase activity showed typical allosteric kinetics, due to the positive co-operativity of the substrates, with apparent Vmax = ...

I have postulated that arachidonic acid release from rat liver cells is associated with cancer chemoprevention. Since it has been reported that inhibition of proteasome activities may prevent cancer, the effects of proteasome inhibitors on arachidonic acid release from cells and on prostaglandin I2 production in rat liver cells were studied. The proteasome inhibitors, epoxomicin, lactacystin and carbobenzoxy-leucyl-leucyl-leucinal, stimulate the release of arachidonic acid from rat glial, human colon carcinoma, human breast carcinoma and the rat liver cells. They also stimulate basal and induced prostacycin production in the rat liver cells. The stimulated arachidonic acid release and basal prostaglandin I2 production in rat liver cells is inhibited by actinomycin D. Stimulation of arachidonic acid release and arachidonic acid metabolism may be associated with some of the biologic effects observed after proteasome inhibition, e.g. prevention of tumor growth, induction of apoptosis, stimulation of bone

Πανεπιστήμιο Ιωαννίνων. Ιδρυματικό Αποθετήριο Ολυμπιάς.1999 . Creators: Milionis, H. J.. Contributors: Πανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείας, Milionis, H. J..Background. Platelet-activating factor (PAF) is a potent inflammatory mediator associated with several physiopathological conditions, including renal diseases. PAF is degraded to the inactive metabolite lyso-PAF by PAF-acetylhydrolase (PAF-AH), which is considered as a potent anti-inflammatory and anti-atherogenic enzyme associated with lipoproteins. In this study, we evaluated the plasma- and lipoprotein(a) [Lp(a)]associated PAF-AH activity in relationship to plasma lipid parameters and Lp(a) isoform size in patients with mild/moderate chronic renal failure (CRF), as well as in hemodialysis (HD) and chronic ambulatory peritoneal dialysis (CAPD) patients. Methods. We studied 74 patients undergoing maintenance HD, 44

Various molecular mechanisms have been suggested to be involved in dexamethasone induced thymocyte apoptosis. In this study we show that pharmacological inhibition of cytoplasmic PLA2 in mouse thymocytes for 18 h with arachidonyl trifluoromethyl ketone (AACOCF3) (10μM) and palmitoyl trifluoromethyl ketone (PACOCF3) (10 μM) induced a drastic increase of thymocyte apoptosis comparable to that observed following Dex (10-7 M) treatment, while inhibition of secretory PLA2 with p-bromophenacyl bromide (pBPB) (20 μM) did not. AACOCF3-induced thymocyte apoptosis, similarly to Dex-induced thymocyte apoptosis, was eliminated by cell pre-treatment with the PI-PLCβ inhibitor, U73122, but not by the PC-PLC inhibitor D609. These observations were corroborated by the ability of AACOCF3, like Dex, to induce a rapid and transient increase in DAG generation. In addition, AACOCF3-induced apoptosis involved the activation of the acidic sphingomyelinase (aSMase) but not of the neutral sphingomyelinase (nSMase), ...

Link to Pubmed [PMID] - 16040234. Res. Microbiol. 2005 Aug;156(7):822-9. Phospholipases play an important role as virulence factors in human pathogens. Candida albicans, the major fungal pathogen of humans, encodes phospholipases of type A, B, C and D. Type B Plb2 and type D Pld1 phospholipases have been shown to contribute to virulence in this organism. We analyzed, in C. albicans, PLC2 and PLC3, two highly conserved genes coding for phosphatidylinositol-dependent phospholipases C with homology to the known virulence factor PlcA in the human pathogen Listeria monocytogenes. We show that expression of PLC2 and PLC3 is upregulated under different filament-inducing conditions and in the constitutive filamentous mutant tup1Delta. In order to analyze PLC2 and PLC3 function in C. albicans, we constructed strains that carry PLC2 or PLC3 under a constitutive promoter and strains that lack all four PLC2/3 alleles. These strains were not affected in their ability to produce filaments under non-inducing ...

In the present study, to our knowledge, we first demonstrated that bvPLA2 is the major BV compound capable of inducing Treg expansion without altering the total composition of the other cell types in vivo and in vitro. Our previous report showed that BV has therapeutic effects on the MPTP-induced mouse model of PD via modulating the neuroinflammatory response and increasing the proportion of functional Tregs (23). In this study, we showed that bvPLA2 has neuroprotective effects by suppressing microglial activation and reducing the infiltrating CD4+ T cells in the MPTP-induced mouse model of PD. In addition to the neuroprotective effects, bvPLA2 directly binds to the mannose receptor (CD206) on DCs, and this binding induces the release of PGE2, which promotes Treg induction in CD4 T cells.. Microglia are resident innate immune cells of the CNS found in and around degenerating neurons (10-12) that are rapidly activated in response to neuronal damage and significantly contribute to secondary ...

We report a sequential one-pot preparation of aromatic trifluoromethyl ketones starting from readily accessible aryl bromides and fluorosulfates, the latter easily prepared from the corresponding phenols. The methodology utilizes low pressure carbon monoxide generated ex situ from COgen to generate Weinreb amides as reactive intermediates that undergo monotrifluoromethylation affording the corresponding aromatic trifluoromethyl ketones (TFMKs) in good yields. The stoichiometric use of CO enables the possibility for accessing 13C-isotopically labeled TFMK by switching to the use of 13COgen. ...

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OBJECTIVES: The objectives of this study were to examine the time course of the inflammatory response in acute coronary syndromes (ACS) and to assess the markers of inflammation and their relation to disease severity. METHODS: We prospectively studied 134 patients with ACS who survived for at least 30 months. The patients were divided into four groups: acute myocardial infarction (MI) with (n=54) or without (n=46) ST-segment elevation and unstable angina with (n=14) or without (n=20) increased risk. Plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6), secretory phospholipase A2 group IIA (sPLA2-IIA), and intercellular adhesion molecule-1 (ICAM-1) were measured on days 1 and 4 and after 3 and 30 months. RESULTS: The highest levels of CRP and sPLA2-IIA were seen on day 4 but for IL-6 on day 1. These three markers, but not ICAM-1, were significantly related to disease severity, CKMB, and ejection fraction. Patients in Killip class II-IV had higher levels than those in Killip class I. ...

Definition of Arachidonic acid cascade with photos and pictures, translations, sample usage, and additional links for more information.

Results Exposure of VSMC to sPLA2 IIA or X did not increase mitogenesis, whereas exposure to grV markedly increased it in a dose/time fashion. Likewise, VSMC exposed to HDL or LDL hydrolysed by sPLA2 V (and less by X) became mitogenic. Interaction of sPLA2 with lipoproteins showed that hydrolysis of HDL and LDL by sPLA2s and the impact on mitogenesis were invariably enhanced in order V,X,IIA. Release of PGE2 was enhanced by sPLA2 X and LTB4 by gr X and V. Investigation of the products of lipoproteins hydrolysis showed that there is formation of core aldehydes, isoprostanes, hydroxides and hydroperoxides of PtdCho. sPLA2 grV hydrolysed hydroxides and hydroxyperoxides of linoleolyl GroPCho in preference to arachidonoyl GroPCho while groups IIA and X did the opposite.. ...

TY - JOUR. T1 - Genes encoding multiple forms of phospholipase A2 are expressed in rat brain. AU - Molloy, G Y. AU - Rattray, M. AU - Williams, Robert J. PY - 1998. Y1 - 1998. N2 - The polymerase chain reaction was utilized to determine which of six cloned phospholipase A2 (PLA2) messenger RNAs (mRNAs), encoding four distinct low molecular weight forms of secretory PLA2 (PLA2-IB, PLA2-IIA, PLA2-IIC and PLA2-V), a calcium-dependent high molecular weight PLA2 (PLA2-IV, cPLA2) and a calcium-independent high molecular weight PLA2 (PLA2-VI, iPLA2), were expressed in different regions of rat brain and in a number of peripheral tissues. Pancreatic PLA2-IB mRNA was not expressed in the brain. PLA2-IIA, PLA2-IV and PLA2-VI mRNAs appeared to be ubiquitously expressed in brain, with relatively similar levels detected in all regions. PLA2-IIC mRNA was expressed in all brain regions but not in any of the peripheral tissues studied. PLA2-V mRNA was found at low levels in most areas of the brain, but at very ...

The present review aims to systematically and critically analyze the current knowledge on phospholipases and their role in physiological and pathological mineralization undertaken by mineralization competent cells. Cellular lipid metabolism plays an important role in biological mineralization. The physiological mechanisms of mineralization are likely to take place in tissues other than in bones and teeth under specific pathological conditions. For instance, vascular calcification in arteries of patients with renal failure, diabetes mellitus or atherosclerosis recapitulates the mechanisms of bone formation. Osteoporosis-a bone resorbing disease-and rheumatoid arthritis originating from the inflammation in the synovium are also affected by cellular lipid metabolism. The focus is on the lipid metabolism due to the effects of dietary lipids on bone health. These and other phenomena indicate that phospholipases may participate in bone remodelling as evidenced by their expression in smooth muscle cells, in

Lipid comprising polyunsaturated fatty acids | Oral pharmaceutical composition of isotretinoin | Preparation for treatment of a non-oral treatment site comprising an active chlorine compound and amino acids | Compounded solutions of diclofenac and lidocaine and methods | Compositions and methods including leelamine and arachidonyl trifluoromethyl ketone relating to treatment of cancer |

Lipases and Phospholipases in Drug Development: From Biochemistry to Molecular Pharmacology. Editor(s). Dr. Günter Müller; Dr. Stefan.

promotes stimulus-induced arachidonic acid release and prostaglandin (PG) production similar to those elicited by HSPG-dependent sPLA(2)s, suggesting that this enzyme plays a role in the inflammatory process ...

In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.4+/-0.1 microM) was the most potent. We identified in live trypanosomes PLA2 activity that was sensitive to OBAA and could be stimulated by Ca2+, suggesting the presence of positive feedback control. The cell-associated PLA2 activity was able to release [14C]AA from labelled phospholipid substrates. Exogenous AA (5-50 microM) also initiated Ca2+ entry in a manner that was inhibited by the Ca2+ antagonist La3+ (100 microM). Ca2+ entry did not depend on AA metabolism or protein kinase activation. The cell response was specific for AA, and fatty acids with greater saturation than tetraeicosanoic acid (AA) or with chain lengths less than C20 ...

Glycerophospholipids in Brain: Phospholipases A2 in Neurological Disorders Akhlaq A. Farooqui and Lloyd A. Horrocks Glycerophospholipids in Brain: Phospholipases A2 in Neurological Disorders provides

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Principal Investigator：OKANO Yukio, Project Period (FY)：1991 - 1992, Research Category：Grant-in-Aid for General Scientific Research (C), Research Field：General medical chemistry

médecine/sciences (M/S), revue internationale dans le domaine de la recherche biologique, médicale et en santé

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just read a article about arachidonic acid,,,had sum great info on it,,,,was wondering if anyone here uses it while on / off cycle and does it really work or is

AuxInfo=1/1/N:1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22/E:(21,22)/rA:22nCCCCCCCCCCCCCCCCCCCCOO/rB:s1;s2;s3;s4;s5;d6;s7;s8;d9;s10;s11;d12;s13;s14;d15;s16;s17;s18;s19;s20;d20;/rC:-7.3658,-.6188,0;-6.6513,-.2062,0;-5.9368,-.6188,0;-5.2224,-.2062,0;-4.5079,-.6188,0;-3.7934,-.2062,0;-2.9684,-.2062,0;-2.2539,-.6188,0;-1.5395,-.2062,0;-.7145,-.2062,0;0,-.6188,0;.7145,-.2062,0;1.5395,-.2062,0;2.2539,-.6188,0;2.9684,-.2062,0;3.7934,-.2062,0;4.5079,-.6188,0;5.2224,-.2062,0;5.9368,-.6188,0;6.6513,-.2062,0;7.3658,-.6188,0;6.6513,.6188,0 ...

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