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Готові списки джерел за темами / LysoPAF

Добірка наукової літератури з теми "LysoPAF"

Автор: Grafiati

Опубліковано: 6 липня 2024

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Статті в журналах з теми "LysoPAF":

1

Chai, Yuh-Cherng, David G. Binion, and Guy M. Chisolm. "Relationship of molecular structure to the mechanism of lysophospholipid-induced smooth muscle cell proliferation." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 4 (October 1, 2000): H1830—H1838. http://dx.doi.org/10.1152/ajpheart.2000.279.4.h1830.

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We previously reported that oxidized low-density lipoprotein and one of its constituents, lysophosphatidylcholine (lysoPC), caused smooth muscle cell proliferation that was inhibitable by vitamin E and by a neutralizing antibody against basic fibroblast growth factor-2 (FGF-2). We now show that the mitogenic activity of lysolipids is highly dependent on structure. Phospholipids with palmitoyl fatty acid and phosphocholine induced DNA synthesis optimally. Shorter and longer fatty acids were significantly less potent, as were phosphoserine and phosphoethanolamine head groups. Structurally related phospholipids [platelet-activating factor (PAF) and lysoPAF] were also mitogens and acted via an analogous FGF-2-dependent, vitamin E-inhibitable mechanism. The mechanism of lysoPC stimulation was distinct from that of another phospholipid mitogen, lysophosphatidic acid (lysoPA), in that lysoPC stimulation was not pertussis toxin inhibitable. Furthermore, lysoPA stimulation was not inhibitable by vitamin E. Despite its distinct cellular pathway for stimulation, lysoPA also ultimately led to FGF-2 release. Our data show that specific structural attributes of lysoPC, PAF, and lysoPAF enable these agents to mediate smooth muscle cell release of FGF-2, which in turn stimulates proliferation.

2

Bakken, A. M., and M. Farstad. "The activities of acyl-CoA:1-acyl-lysophospholipid acyltransferase(s) in human platelets." Biochemical Journal 288, no. 3 (December 15, 1992): 763–70. http://dx.doi.org/10.1042/bj2880763.

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The activities of acyl-CoA:1-acyl-lysophospholipid acyltransferases (EC 2.3.1.23) have been studied in human platelet lysates by using endogenously formed [14C]acyl-CoA from [14C]fatty acid, ATP and CoA in the presence of 1-acyl-lysophosphatidyl-choline (lysoPC), -ethanolamine (lysoPE), -serine (lysoPS) or -inositol (lysoPI). Linoleic acid as fatty acid substrate had the highest affinity to acyl-CoA:1-acyl-lysophospholipid acyltransferase with lysoPC as variable substrate, followed by eicosapentaenoic acid (EPA) and arachidonic acid (AA). The activity at optimal conditions was 7.4, 7.3 and 7.2 nmol/min per 10(9) platelets with lysoPC as substrate, with linoleic acid, AA and EPA respectively. EPA and AA were incorporated into all lyso-forms. Linoleic acid was also incorporated into lysoPE at a high rate, but less into lysoPS and lysoPI. DHA was incorporated into lysoPC and lysoPE, but only slightly into lysoPI and lysoPS. Whereas incorporation of all fatty acids tested was maximal for lysoPC and lysoPI at 200 and 80 microM respectively, maximal incorporation needed over 500 microM for lysoPE and lysoPS. The optimal concentration for [14C]fatty acid substrates was in the range 15-150 microM for all lysophospholipids. Competition experiments with equimolar concentrations of either lysoPC and lysoPI or lysoPE resulted in formation of [14C]PC almost as if lysoPI or lysoPE were not added to the assay medium.

3

Schindler, Peter W., and Ewa Ninio. "Kinetic studies of human and rat neutrophil lysoPAF acetyltransferase using lysoPAF and dansyllysoPAF as substrates." Lipids 26, no. 12 (December 1991): 1004–10. http://dx.doi.org/10.1007/bf02536492.

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4

Thumser, A. E., J. E. Voysey, and D. C. Wilton. "The binding of lysophospholipids to rat liver fatty acid-binding protein and albumin." Biochemical Journal 301, no. 3 (August 1, 1994): 801–6. http://dx.doi.org/10.1042/bj3010801.

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The binding of lysophospholipids to rat liver fatty acid-binding protein (FABP) and to BSA and human serum albumin was investigated by using competitive displacement fluorescence assays by monitoring the displacement of the fluorescent fatty acid probe 11-(dansylamino)undecanoic acid (DAUDA). In addition, direct binding assays using changes in tryptophan fluorescence were possible with albumin. Liver FABP was able to bind a range of lysophospholipids, oleoyl-lysophosphatidic acid (lysoPA), oleoyl-lysophosphatidylcholine (lysoPC), oleoyl-lysophosphatidylethanolamine (lysoPE) and oleoyl-lysophosphatidylglycerol, with similar affinity and a Kd of about 1 microM. Liver FABP was also able to bind lysophospholipids generated by the action of phospholipase A2 or phospholipase A1 (triacylglycerol lipase) on phospholipid vesicles. A possible physiological role for liver FABP in lysophospholipid metabolism within the cell is discussed. Albumin was shown to bind lysoPA with higher affinity than either lysoPC or lysoPE, and the initial minimal DAUDA displacement by lysoPA indicated that lysoPA was binding to the primary high-affinity fatty acid-binding sites on albumin and that, like oleic acid, about 3 mol of ligand/mol was bound to these sites. Kd values in the microM range were indicated for lysoPC and lysoPE, whereas, by comparison with oleic acid, the Kd for lysoPA was significantly lower and high-affinity binding in the nM range was indicated. Overall, the data suggest that, because of structural similarity, lysoPA binds to albumin in a similar manner to long-chain fatty acids.

5

NAGUMO, Seiji, Akira FUKUJU, Mitsue TAKAYAMA, Masahiro NAGAI, Ryohei YANOSHITA, and Yuji SAMEJIMA. "Inhibition of LysoPAF Acetyltransferase Activity by Components of Licorice Root." Biological & Pharmaceutical Bulletin 22, no. 10 (1999): 1144–46. http://dx.doi.org/10.1248/bpb.22.1144.

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6

Aoyama, Chieko, Hiroyuki Sugimoto, Hiromi Ando, Satoko Yamashita, Yasuhiro Horibata, Sayaka Sugimoto та Motoyasu Satou. "The heterotrimeric G protein subunits Gαq and Gβ1 have lysophospholipase D activity". Biochemical Journal 440, № 2 (14 листопада 2011): 241–50. http://dx.doi.org/10.1042/bj20110545.

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In a previous study we purified a novel lysoPLD (lysophospholipase D) which converts LPC (lysophosphatidylcholine) into a bioactive phospholipid, LPA (lysophosphatidic acid), from the rat brain. In the present study, we identified the purified 42 and 35 kDa proteins as the heterotrimeric G protein subunits Gαq and Gβ1 respectively. When FLAG-tagged Gαq or Gβ1 was expressed in cells and purified, significant lysoPLD activity was observed in the microsomal fractions. Levels of the hydrolysed product choline increased over time, and the Mg2+ dependency and substrate specificity of Gαq were similar to those of lysoPLD purified from the rat brain. Mutation of Gαq at amino acids Lys52, Thr186 or Asp205, residues that are predicted to interact with nucleotide phosphates or catalytic Mg2+, dramatically reduced lysoPLD activity. GTP does not compete with LPC for the lysoPLD activity, indicating that these substrate-binding sites are not identical. Whereas the enzyme activity of highly purified FLAG-tagged Gαq overexpressed in COS-7 cells was ~4 nmol/min per mg, the activity from Neuro2A cells was 137.4 nmol/min per mg. The calculated Km and Vmax values for lysoPAF (1-O-hexadecyl-sn-glycero-3-phosphocholine) obtained from Neuro2A cells were 21 μM and 0.16 μmol/min per mg respectively, similar to the enzyme purified from the rat brain. These results reveal a new function for Gαq and Gβ1 as an enzyme with lysoPLD activity. Tag-purified Gα11 also exhibited a high lysoPLD activity, but Gαi and Gαs did not. The lysoPLD activity of the Gα subunit is strictly dependent on its subfamily and might be important for cellular responses. However, treatment of Hepa-1 cells with Gαq and Gα11 siRNAs (small interfering RNAs) did not change lysoPLD activity in the microsomal fraction. Clarification of the physiological relevance of lysoPLD activity of these proteins will need further studies.

7

Guimbaud, Rosine, Angelo Izzo, Jean Pierre Martinolle, Nicole Vidon, Daniel Couturier, Jacques Benveniste, and Stanislas Chaussade. "Intraluminal excretion of PAF, lysoPAF, and acetylhydrolase in patients with ulcerative colitis." Digestive Diseases and Sciences 40, no. 12 (December 1995): 2635–40. http://dx.doi.org/10.1007/bf02220453.

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8

Christman, B. W., J. W. Christman, R. Dworski, I. A. Blair, and C. Prakash. "Prostaglandin E2 limits arachidonic acid availability and inhibits leukotriene B4 synthesis in rat alveolar macrophages by a nonphospholipase A2 mechanism." Journal of Immunology 151, no. 4 (August 15, 1993): 2096–104. http://dx.doi.org/10.4049/jimmunol.151.4.2096.

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Abstract Prostaglandin E2 (PGE2), a potent mediator of inflammation released in large amounts by endotoxin-stimulated alveolar macrophages (AM), has been shown to inhibit leukotriene B4 (LTB4) release by activated neutrophils. We investigated the hypothesis that LTB4 synthesis by AM can be regulated by PGE2 and performed experiments to determine the biochemical site of regulation. AM obtained from Sprague-Dawley rats were preincubated with PGE2 before stimulation with the calcium ionophore A23187. LTB4, platelet-activating factor (PAF), lysoPAF, (AA), and 5-hydroxyeicosatetraenoic acid were isolated from AM cells and supernatants, then quantified by gas chromatography/electron capture negative ion mass spectrometry. Stimulated AM released 30.50 +/- 4.52 ng LTB4/10(6) cells and were inhibited by PGE2 in a dose dependent manner. PGE2 (1 microM) inhibited LTB4 synthesis by 37% and decreased release of both 5-hydroxyeicosatetraenoic acid and arachidonic acid by stimulated AM, but did not alter synthesis of PAF or lysoPAF. These mass measurements suggest that PGE2 does not affect the activity of phospholipase A2, PAF acetyltransferase, leukotriene A4 hydrolase. We conclude that PGE2 attenuates LTB4 production in alveolar macrophages by altering the activity of lipases other than phospholipase A2. PGE2-mediated inhibition of LTB4 synthesis by AM may regulate the initiation of lung inflammation.

9

Petsini, Filio, Agathi Ntzouvani, Maria Detopoulou, Vasiliki D. Papakonstantinou, Nick Kalogeropoulos, Elizabeth Fragopoulou, Tzortzis Nomikos, Meropi D. Kontogianni, and Smaragdi Antonopoulou. "Consumption of Farmed Fish, Fed with an Olive-Pomace Enriched Diet, and Its Effect on the Inflammatory, Redox, and Platelet-Activating Factor Enzyme Profile of Apparently Healthy Adults: A Double-Blind Randomized Crossover Trial." Foods 11, no. 14 (July 15, 2022): 2105. http://dx.doi.org/10.3390/foods11142105.

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A fish-rich diet has a beneficial effect on cardiovascular health. The platelet activating factor (PAF) is involved in the development of atherosclerosis, and in vitro results support the regulating action of bioactive nutrients on PAF metabolism. The purpose of this study is to examine whether the consumption of farmed fish fed with an olive-pomace enriched diet (EF) affects PAF metabolism and the markers of inflammation and oxidative stress compared to the consumption of conventionally fed farmed fish (CF). Thirty apparently healthy adults completed a randomized double-blind crossover trial, during which they consumed both CF and EF twice a week for 8 weeks with a six-week washout period in between. The activities of PAF acetylhydrolase (PAF-AH), lysoPAF acetyltransferase (lysoPAF-AT), DTT-insensitive CDP-choline: 1-alkyl-2-acetyl-sn-glycerol-choline-phosphotransferase (PAF-CPT) in leukocytes, and lipoprotein-associated phospholipase A2 (LpPLA2) in serum were determined. The quantities of interleukin-6 (IL-6), high sensitivity C-reactive protein (hsCRP), oxidized LDL (ox-LDL), thiobarbituric acid-reactive substances (TBARS), and glutathione peroxidase (GPx), as well as the serum oxidation, were also determined. Both types of fish exerted similar effects as there were no statistically significant differences between the two interventions except for an elevated PAF-CPT and reduced arachidonic acid (AA) in the red blood cell (RBC) membrane lipids after the EF intake.

10

Noris, Marina, Daniela Macconi, Vittorio Nanni, Mario Salmona, Marta Todeschini, and Giuseppe Remuzzi. "Defective glomerular [3H]lysoPAF metabolism in the autologous phase of rabbit nephrotoxic nephritis." Kidney International 44, no. 4 (October 1993): 747–54. http://dx.doi.org/10.1038/ki.1993.309.

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Більше джерел

Дисертації з теми "LysoPAF":

1

Stephenson, J. "Studies on molecular cloning of the genes for the enzymes #alpha#-L-iduronidase and arylsulphatase A." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.232964.

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2

Varadarajan, Shankar. "P38 MAPKs coordinately regulate distinct phases of autophagy and lysomal biogenesis." 2008. http://hdl.handle.net/2152/17812.

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p38 mitogen-activated protein kinases (MAPKs) control the endocytic trafficking of various growth-related cell surface receptors and transporters. Herein, I demonstrate that p38 MAPKs also regulate autophagy, or the process of self-cannibalism. In my studies, inhibition of p38 MAPKs triggered rapid formation of autophagosomes in prostate cancer cells, even under nutrient-rich conditions, and remarkably, the autophagosomal membranes emanated from endoplasmic reticulum exit sites via the concerted actions of the small GTPases, ARF1 and SAR1. Once formed, the autophagosomes fused with late endosomes and/or lysosomes, in a Rab7-dependent manner, to form “hybrid organelles” that were co-labeled with ER, autophagic, late endosomal, and lysosomal markers. Unlike other inducers of autophagy, however, inhibition of p38 MAPKs suppressed the fission of hybrid organelles, resulting in a profound but reversible accumulation of large cytoplasmic vacuoles. Thus, in addition to their previously reported roles in endocytosis, p38 MAPKs appear to coordinately regulate autophagy and the downstream biogenesis and fission of hybrid organelles.
text

3

Prodoehl, Mark. "Functional analysis of the deubiquitylating enzyme fat facets in mouse in protein trafficking." Thesis, 2008. http://hdl.handle.net/2440/49145.

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Fat facets in Mouse (FAM) or mUSP9x is a deubiquitylating enzyme of the USP class. Knockdown of FAM protein levels in mouse pre-implantation embryos by antisense oligonucleotides is known to prevent embryos from progressing to the blastocyst stage indicating an important role for FAM in early mammalian development. In mammals, the Fam gene is located on the X-chromosome. In mice, the Y homologue, Dffry or usp9y, is expressed exclusively in the testes and maps to the Sxrb deletion (Brown et al., 1998). Sxrb is associated with an early post-natal blockage of spermatogonial proliferation and differentiation leading to absence of germ cells (Bishop et al., 1988; Mardon et al., 1989). The human Y homologue of Fam is closely associated with oligozoospermia (Sargent et al., 1999; Sun et al., 1999) and the human X homologue has been linked to the failure of oocytes to pass through the first meitoc prophase in Turner syndrome (Cockwell et al., 1991; Speed, 1986) Despite these associations, the substrates and precise role of Fam and its homologues in these processes have not yet been defined. Due to the complex nature of Fam expression and the lack of data tying FAM to specific cellular functions, much attention has been paid in identifying interacting partners and cellular targets of FAM activity to aid in the definition of its role in the cell and development. Three common molecular biology techniques were applied here in an attempt to further characterise known interactions of FAM, including interactions with the cell adhesion molecule β-catenin and the protein trafficking pathway proteins epsin-1 and itch. The aim of these investigations was to generate FAM mutants that could abolish individual interactions, enabling investigation of individual interactions in cellular function and development. These experiments failed to identify the amino acids of FAM that were critical for its interactions with β-catenin, epsin-1, or itch. Experiments aimed at characterising a novel ubiquitin-like domain located in the N-terminal half of the FAM protein, did however identify novel interactions of FAM with the three Golgi associated adaptor proteins GGA1, GGA2, and GGA3. Further investigations prompted by this interaction, examined the role of FAM in the trafficking of proteins from the Golgi apparatus. Cellular FAM protein levels were altered either by exogenous expression of FAM protein or knockdown of endogenous FAM using FAM specific shRNA triggers. The cellular protein levels and extent of post-translational modification of eleven lysosomal proteins were monitored in each case. It was found that increased FAM protein levels resulted in decreased cellular protein levels of five of the eleven lysosomal proteins studied. In contrast, a reduction in FAM protein levels was found to result in an increase in the cellular protein levels of eight of the eleven lysosomal proteins. This study provides the first evidence of a deubiquitylating enzyme that is able to interact with the GGA proteins. It is also the first to describe a deubiquitylating enzyme that can affect the biosynthesis of lysosomal proteins and provides valuable new insight into the cellular function of FAM/USP9X.
Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Sciences, 2008

4

Prodoehl, Mark. "Functional analysis of the deubiquitylating enzyme fat facets in mouse in protein trafficking." 2008. http://hdl.handle.net/2440/49145.

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Fat facets in Mouse (FAM) or mUSP9x is a deubiquitylating enzyme of the USP class. Knockdown of FAM protein levels in mouse pre-implantation embryos by antisense oligonucleotides is known to prevent embryos from progressing to the blastocyst stage indicating an important role for FAM in early mammalian development. In mammals, the Fam gene is located on the X-chromosome. In mice, the Y homologue, Dffry or usp9y, is expressed exclusively in the testes and maps to the Sxrb deletion (Brown et al., 1998). Sxrb is associated with an early post-natal blockage of spermatogonial proliferation and differentiation leading to absence of germ cells (Bishop et al., 1988; Mardon et al., 1989). The human Y homologue of Fam is closely associated with oligozoospermia (Sargent et al., 1999; Sun et al., 1999) and the human X homologue has been linked to the failure of oocytes to pass through the first meitoc prophase in Turner syndrome (Cockwell et al., 1991; Speed, 1986) Despite these associations, the substrates and precise role of Fam and its homologues in these processes have not yet been defined. Due to the complex nature of Fam expression and the lack of data tying FAM to specific cellular functions, much attention has been paid in identifying interacting partners and cellular targets of FAM activity to aid in the definition of its role in the cell and development. Three common molecular biology techniques were applied here in an attempt to further characterise known interactions of FAM, including interactions with the cell adhesion molecule β-catenin and the protein trafficking pathway proteins epsin-1 and itch. The aim of these investigations was to generate FAM mutants that could abolish individual interactions, enabling investigation of individual interactions in cellular function and development. These experiments failed to identify the amino acids of FAM that were critical for its interactions with β-catenin, epsin-1, or itch. Experiments aimed at characterising a novel ubiquitin-like domain located in the N-terminal half of the FAM protein, did however identify novel interactions of FAM with the three Golgi associated adaptor proteins GGA1, GGA2, and GGA3. Further investigations prompted by this interaction, examined the role of FAM in the trafficking of proteins from the Golgi apparatus. Cellular FAM protein levels were altered either by exogenous expression of FAM protein or knockdown of endogenous FAM using FAM specific shRNA triggers. The cellular protein levels and extent of post-translational modification of eleven lysosomal proteins were monitored in each case. It was found that increased FAM protein levels resulted in decreased cellular protein levels of five of the eleven lysosomal proteins studied. In contrast, a reduction in FAM protein levels was found to result in an increase in the cellular protein levels of eight of the eleven lysosomal proteins. This study provides the first evidence of a deubiquitylating enzyme that is able to interact with the GGA proteins. It is also the first to describe a deubiquitylating enzyme that can affect the biosynthesis of lysosomal proteins and provides valuable new insight into the cellular function of FAM/USP9X.
Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Sciences, 2008

5

Conway, Betsy Ann. "The effects of laforin, malin, Stbd1, and Ptg deficiencies on heart glycogen levels in Pompe disease mouse models." Thesis, 2015. http://hdl.handle.net/1805/7979.

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Indiana University-Purdue University Indianapolis (IUPUI)
Pompe disease (PD) is a rare metabolic myopathy characterized by loss of acid alpha-glucosidase (GAA), the enzyme responsible for breaking down glycogen to glucose within the lysosomes. PD cells accumulate massive quantities of glycogen within their lysosomes, and as such, PD is classified as a “lysosomal storage disease” (LSD). GAA-deficient cells also exhibit accumulation of autophagic debris. Symptoms of severe infantile PD include extreme muscle weakness, hypotonia, and hypertrophic cardiomyopathy, resulting in death before one year of age. Certain LSDs are currently being successfully treated with enzyme replacement therapy (ERT), which involves intravenous infusion of a recombinant enzyme to counteract the endogenous deficiency. ERT has been less successful in PD, however, due to ineffective delivery of the recombinant enzyme. Alternatively, specific genes deletion may reduce lysosomal glycogen load, and could thus be targeted in PD therapy development. Absence of malin (EPM2B) or laforin (EPM2A) has been proposed to impair autophagy, which could reduce lysosomal glycogen levels. Additionally, deficiency of Stbd1 has been postulated to disable lysosomal glycogen import. Furthermore, Ptg deficiency was previously reported to abrogate Lafora body formation and correct neurological abnormalities in Lafora disease mouse models and could have similar effects on PD pathologies. The goal of this study was to characterize the effects of homozygous disruption of Epm2a, Epm2b, Stbd1, and Ptg loci on total glycogen levels in PD mouse model heart tissue, as in severe infantile PD, it is accumulation of glycogen in the heart that results in fatal hypertrophic cardiomyopathy. Gaa-/- mice were intercrossed with Epm2a-/-, Epm2b-/-, Stbd1-/-, and Ptg-/- mice to generate wildtype (WT), single knockout, and double knockout mice. The results indicated that Gaa-/- hearts accumulated up to 100-fold more glycogen than the WT. These mice also displayed cardiac hypertrophy. However, deficiency of Epm2a, Epm2b, Stbd1, or PTG in the Gaa-/- background did not reveal changes of statistical significance in either heart glycogen or cardiac hypertrophy. Nevertheless, since total glycogen was measured, these deficiencies should not be discarded in future discussions of PD therapy, as increasing sample sizes and/or distinguishing cytosolic from lysosomal glycogen content may yet reveal differences of greater significance.

Книги з теми "LysoPAF":

1

Dice, J. Fred. Lysomal Pathways of Protein Degradation. Landes Bioscience, 2000.

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Частини книг з теми "LysoPAF":

1

Cataldo, Anne M., Deborah J. Hamilton, Jody L. Barnett, Peter A. Paskevich, and Ralph A. Nixon. "Abnormalities of the Endosomal-Lysomal System in Alzheimer’s disease." In Intracellular Protein Catabolism, 271–80. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0335-0_34.

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2

Schindler, Peter, and Ewa Ninio. "Kinetic Studies of Human and Rat Neutrophil LysoPAF Acetyltransferase Using LysoPAF and DansyllysoPAF as Substrates." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids, 1004–10. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch8.

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3

Doebber, Thomas, Margaret Wu, Anthony Mauriello, and Alfred Alberts. "Platelet-Activating Factor (PAF) Stimulates the LysoPAF Acetyltransferase in Leukocyte-Rich Plasma." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids, 997–1003. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch7.

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4

Goracci, Gianfrancesco, and Ermelinda Francescangeli. "Properties of PAF-Synthesizing Phosphocholinetransferase and Evidence for LysoPAF Acetyltransferase Activity in Rat Brain." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids, 986–91. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch5.

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5

"Lysopin." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1133. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_9681.

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6

"Lysova Island." In The Eastern Arctic Seas Encyclopedia, 203. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24237-8_315.

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7

Desnick, R. J., E. H. Schuchman, K. H. Astrin, and S. H. Cheng. "Enzyme Replacement and Pharmacologic Chaperone Therapies for Lysomal Storage Disease." In Reference Module in Biomedical Sciences. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-801238-3.05501-x.

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Тези доповідей конференцій з теми "LysoPAF":

1

Niu, Qi, Shao-Liang Peng, Xiang-Li-Lan Zhang, Shuai-Cheng Li, Ying Xu, Xiang-Cheng Xie, and Yi-Gang Tong. "LysoPhD: predicting functional prophages in bacterial genomes from high-throughput sequencing." In 2019 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2019. http://dx.doi.org/10.1109/bibm47256.2019.8983280.

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2

Sugimori, Daisuke, Kiyoto Kajiyama, Shunsuke Kawashima, and Yuho Matsumoto. "Phosphatidylglycerol-specific Phospholipase C from Amycolatopsis Sp. NT115: Biochemical Characterization and Heterologous Expression." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/fmmj5845.

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In recent years, phosphatidylglycerol (PG) has been attracting attention in the field of cell physiology such as photosynthesis and germ cells, or clinical diagnosis. Most of phospholipids containing PG are analyzed using HPLC and LC-MS; however, it has been desired to develop an enzymatic assay method for determination of PG concentration in a simple, easy, and high-through put.In our presentation, biochemical characterization of a PG-specific phospholipase C (PG-PLC) from Amycolatopsis sp. NT115 will be reported. PG-PLC (molecular mass, 55 kDa) showed maximal activity at pH 6.0 and 55°C. PG-PLC showed almost no activity on other diacylphospholipids, dipalmitoylPG, lysoPG and glycerol 3-phosphate, demonstrating PG-PLC can recognize not only the substrate headgroup but also the acyl chains. PG-PLC was inhibited by Zn2+; however, it was hardly inhibited by EDTA and non-ionic surfactants such as Triton X-100, Tween 80, Briji 35 and Nonidet P-40. PG-PLC activity was enhanced by 1 mM Mn2+, Al3+, 0.1% sodium deoxycholate by 1.3-2.5 folds. Recombinant PG-PLC (rPG-PLC) was extracellularly produced using Streptomyces lividans/pUC702 expression system. However, unexpectedly it was produced with the N-terminal region deleted by ca. 230 amino acids. As a result, the stability of the deletion mutant (Δ230aa) was markedly decreased. In 96 h culture, rPG-PLC with His6-tag was produced with 0.188 U/mL and 3.36×10-2 U/mg-protein in the culture supernatant. Moreover, 1.52 mg-protein of the purified Δ220aa (2.5 U/mL, 16.4 U/mg-protein) was yielded from 0.9 L of the culture supernatant by His-tag affinity chromatography. Using the purified Δ220aa, kinetic parameters were determined to be Km=0.368 mM, 99.2 µM/min (6.51 mmol/min/mg-protein), kcat=5.29×10-2 s-1, kcat/Km=0.256 mM-1s-1 for POPG.