Base de dados : MEDLINE
Pesquisa : D08.811.277.352.100.680.750.937.750.662 [Categoria DeCS]
Referências encontradas : 30 [refinar]
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  1 / 30 MEDLINE  
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[PMID]:26637123
[Au] Autor:Yui D; Nishida Y; Nishina T; Mogushi K; Tajiri M; Ishibashi S; Ajioka I; Ishikawa K; Mizusawa H; Murayama S; Yokota T
[Ad] Endereço:Department of Neurology and Neurological Science, Graduate school of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
[Ti] Título:Enhanced Phospholipase A2 Group 3 Expression by Oxidative Stress Decreases the Insulin-Degrading Enzyme.
[So] Source:PLoS One;10(12):e0143518, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress has a ubiquitous role in neurodegenerative diseases and oxidative damage in specific regions of the brain is associated with selective neurodegeneration. We previously reported that Alzheimer disease (AD) model mice showed decreased insulin-degrading enzyme (IDE) levels in the cerebrum and accelerated phenotypic features of AD when crossbred with alpha-tocopherol transfer protein knockout (Ttpa-/-) mice. To further investigate the role of chronic oxidative stress in AD pathophysiology, we performed DNA microarray analysis using young and aged wild-type mice and aged Ttpa-/- mice. Among the genes whose expression changed dramatically was Phospholipase A2 group 3 (Pla2g3); Pla2g3 was identified because of its expression profile of cerebral specific up-regulation by chronic oxidative stress in silico and in aged Ttpa-/- mice. Immunohistochemical studies also demonstrated that human astrocytic Pla2g3 expression was significantly increased in human AD brains compared with control brains. Moreover, transfection of HEK293 cells with human Pla2g3 decreased endogenous IDE expression in a dose-dependent manner. Our findings show a key role of Pla2g3 on the reduction of IDE, and suggest that cerebrum specific increase of Pla2g3 is involved in the initiation and/or progression of AD.
[Mh] Termos MeSH primário: Envelhecimento/genética
Doença de Alzheimer/genética
Cérebro/metabolismo
Fosfolipases A2 do Grupo III/genética
Insulisina/genética
[Mh] Termos MeSH secundário: Doença de Alzheimer/metabolismo
Animais
Proteínas de Transporte/genética
Células Cultivadas
Modelos Animais de Doenças
Perfilação da Expressão Gênica
Técnicas de Inativação de Genes
Fosfolipases A2 do Grupo III/metabolismo
Células HEK293
Seres Humanos
Camundongos
Análise de Sequência com Séries de Oligonucleotídeos
Especificidade de Órgãos
Estresse Oxidativo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (alpha-tocopherol transfer protein); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (PLA2G3 protein, human); EC 3.1.1.4 (PLA2G3 protein, mouse); EC 3.4.24.56 (Insulysin)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:151214
[Lr] Data última revisão:
151214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151205
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0143518


  2 / 30 MEDLINE  
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[PMID]:25964585
[Au] Autor:Kazama S; Kitayama J; Hiyoshi M; Taketomi Y; Murakami M; Nishikawa T; Tanaka T; Tanaka J; Kiyomatsu T; Kawai K; Hata K; Yamaguchi H; Nozawa H; Ishihara S; Sunami E; Watanabe T
[Ad] Endereço:Division of Surgical Oncology, Department of Surgery, Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan kaz-tky@umin.ac.jp.
[Ti] Título:Phospholipase A2 Group III and Group X Have Opposing Associations with Prognosis in Colorectal Cancer.
[So] Source:Anticancer Res;35(5):2983-90, 2015 May.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although secretory phospholipase A2 (sPLA2) has been shown to be involved in various biological processes, its specific roles in sub-types of cancer development remain to be elucidated. MATERIALS AND METHODS: We examined the expression of sPLA2 group III (GIII) in 142 patients with colorectal cancer using immunohistochemistry, and its correlation with clinicopathological features and outcomes. In addition, we examined the co-expression of sPLA2GIII and sPLA2GX using serial tissue sections to clarify the roles of both proteins in colorectal carcinogenesis. RESULTS: In 66 cases, diffuse staining of sPLA2GIII was seen; this was defined as the group with high expression. High expression was associated with a significantly higher rate of lymph node metastasis (p=0.02) and poorer survival (p=0.03) compared with low expression. Patients with low sPLA2GIII and high sPLA2GX expression had a significantly higher survival rate than those with high sPLA2GIII and low sPLA2GX expression (p=0.038). CONCLUSION: sPLA2GIII expression may be used as a risk factor for lymph node metastasis and a prognostic marker in colorectal cancer. In addition, sPLA2GIII and sPLA2GX may play opposing roles in colorectal carcinogenesis.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Neoplasias Colorretais/genética
Fosfolipases A2 do Grupo III/genética
Fosfolipases A2 do Grupo X/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Neoplasias Colorretais/patologia
Feminino
Regulação Neoplásica da Expressão Gênica
Fosfolipases A2 do Grupo III/biossíntese
Fosfolipases A2 do Grupo X/biossíntese
Seres Humanos
Metástase Linfática
Masculino
Meia-Idade
Prognóstico
Fatores de Risco
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (Group X Phospholipases A2)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150513
[St] Status:MEDLINE


  3 / 30 MEDLINE  
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[PMID]:25904332
[Au] Autor:Gijs HL; Willemarck N; Vanderhoydonc F; Khan NA; Dehairs J; Derua R; Waelkens E; Taketomi Y; Murakami M; Agostinis P; Annaert W; Swinnen JV
[Ad] Endereço:Laboratory of Lipid Metabolism and Cancer, Department of Oncology, KU Leuven-University of Leuven, B-3000 Leuven, Belgium.
[Ti] Título:Primary cilium suppression by SREBP1c involves distortion of vesicular trafficking by PLA2G3.
[So] Source:Mol Biol Cell;26(12):2321-32, 2015 Jun 15.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Distortion of primary cilium formation is increasingly recognized as a key event in many human pathologies. One of the underlying mechanisms involves aberrant activation of the lipogenic transcription factor sterol regulatory element-binding protein 1c (SREBP1c), as observed in cancer cells. To gain more insight into the molecular pathways by which SREBP1c suppresses primary ciliogenesis, we searched for overlap between known ciliogenesis regulators and targets of SREBP1. One of the candidate genes that was consistently up-regulated in cellular models of SREBP1c-induced cilium repression was phospholipase A2 group III (PLA2G3), a phospholipase that hydrolyzes the sn-2 position of glycerophospholipids. Use of RNA interference and a chemical inhibitor of PLA2G3 rescued SREBP1c-induced cilium repression. Cilium repression by SREBP1c and PLA2G3 involved alterations in endosomal recycling and vesicular transport toward the cilium, as revealed by aberrant transferrin and Rab11 localization, and was largely mediated by an increase in lysophosphatidylcholine and lysophosphatidylethanolamine levels. Together these findings indicate that aberrant activation of SREBP1c suppresses primary ciliogenesis by PLA2G3-mediated distortion of vesicular trafficking and suggest that PLA2G3 is a novel potential target to normalize ciliogenesis in SREBP1c-overexpressing cells, including cancer cells.
[Mh] Termos MeSH primário: Cílios/fisiologia
Fosfolipases A2 do Grupo III/fisiologia
Proteína de Ligação a Elemento Regulador de Esterol 1/fisiologia
Vesículas Transportadoras/fisiologia
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Células Cultivadas
Cílios/metabolismo
Cães
Feminino
Fosfolipases A2 do Grupo III/genética
Seres Humanos
Camundongos
Dados de Sequência Molecular
Transporte Proteico
Alinhamento de Sequência
Sus scrofa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Sterol Regulatory Element Binding Protein 1); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (PLA2G3 protein, human)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150424
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E14-10-1472


  4 / 30 MEDLINE  
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[PMID]:25716287
[Au] Autor:Nakamura H; Wakita S; Yasufuku K; Makiyama T; Waraya M; Hashimoto N; Murayama T
[Ad] Endereço:Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, 260-8675, Japan.
[Ti] Título:Sphingomyelin Regulates the Activity of Secretory Phospholipase A2 in the Plasma Membrane.
[So] Source:J Cell Biochem;116(9):1898-907, 2015 Sep.
[Is] ISSN:1097-4644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We examined the effect of the cellular sphingolipid level on the release of arachidonic acid (AA) and the activity of secretory phospholipase A2 (sPLA2 ) using two Chinese hamster ovary (CHO)-K1 cell mutants, LY-B and LY-A cells, deficient in sphingolipid synthesis. In LY-B cells, deficiency of sphingolipids enhanced the release of AA induced by bee venom sPLA2-III or human sPLA2-V. These alterations were reversed by replenishment of exogenous sphingomyelin (SM). In LY-A cells, deficiency of SM increased the release of AA induced by sPLA2. In CHO-K1 cells, decrease and increase of SM level in the plasma membrane by pharmacological methods increased and inhibited the release of AA, respectively. SM inhibited the activity of sPLA2 in vitro. Niemann-Pick disease type C (NPC) is a lysosomal storage disorder caused by mutation of either the NPC1 or NPC2 gene, and is characterized by accumulation of cholesterol and sphingolipids including SM in late endosomes/lysosomes. Increased levels of AA and sPLA2 activity are involved in various neurodegenerative diseases. In CHO cells lacking NPC1 (A101 cells), SM level was lower in the plasma membrane, while it was higher in late endosomes/lysosomes. The release of AA induced by sPLA2 was increased in A101 cells than that in parental cells (JP17 cells), which was attenuated by adding exogenous SM. In addition, sPLA2 -III-induced cytotoxicity in A101 cells was much higher than that in JP17 cells. These results suggest that SM in the plasma membrane plays important roles in regulating sPLA2 activity and the enzyme-induced cytotoxicity in A101 cells.
[Mh] Termos MeSH primário: Ácido Araquidônico/biossíntese
Membrana Celular/metabolismo
Doença de Niemann-Pick Tipo C/enzimologia
Fosfolipases A2 Secretórias/metabolismo
Esfingomielinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Células CHO
Cricetinae
Cricetulus
Fosfolipases A2 do Grupo III/metabolismo
Fosfolipases A2 do Grupo III/farmacologia
Fosfolipases A2 do Grupo V/metabolismo
Fosfolipases A2 do Grupo V/farmacologia
Seres Humanos
Glicoproteínas de Membrana/deficiência
Modelos Biológicos
Fosfolipases A2 Secretórias/farmacologia
Esfingomielinas/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Glycoproteins); 0 (Sphingomyelins); 27YG812J1I (Arachidonic Acid); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (Group V Phospholipases A2); EC 3.1.1.4 (PLA2G5 protein, human); EC 3.1.1.4 (Phospholipases A2, Secretory)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150724
[Lr] Data última revisão:
150724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150227
[St] Status:MEDLINE
[do] DOI:10.1002/jcb.25145


  5 / 30 MEDLINE  
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[PMID]:25572553
[Au] Autor:Murakami M; Taketomi Y
[Ad] Endereço:Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan; CREST, Japan Science and Technology Agency, Saitama, Japan. Electronic address: murakami-mk@igakuken.or.jp.
[Ti] Título:Secreted phospholipase A2 and mast cells.
[So] Source:Allergol Int;64(1):4-10, 2015 Jan.
[Is] ISSN:1440-1592
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Phospholipase A2s (PLA2s) are a group of enzymes that hydrolyze the sn-2 position of phospholipids to release (typically unsaturated) fatty acids and lysophospholipids, which serve as precursors for a variety of bioactive lipid mediators. Among the PLA2 superfamily, secreted PLA2 (sPLA2) enzymes comprise the largest subfamily that includes 11 isoforms with a conserved His-Asp catalytic dyad. Individual sPLA2 enzymes exhibit unique tissue and cellular localizations and specific enzymatic properties, suggesting their distinct biological roles. Recent studies using transgenic and knockout mice for individual sPLA2 isofoms have revealed their involvement in various pathophysiological events. Here, we overview the current state of knowledge about sPLA2s, specifically their roles in mast cells (MCs) in the context of allergology. In particular, we highlight group III sPLA2 (PLA2G3) as an "anaphylactic sPLA2" that promotes MC maturation and thereby anaphylaxis through a previously unrecognized lipid-orchestrated circuit.
[Mh] Termos MeSH primário: Mastócitos/imunologia
Mastócitos/metabolismo
Fosfolipases A2 Secretórias/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Eicosanoides/biossíntese
Fosfolipases A2 do Grupo III/metabolismo
Seres Humanos
Mastócitos/citologia
Fosfolipases A2 Citosólicas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Eicosanoids); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (Phospholipases A2, Cytosolic); EC 3.1.1.4 (Phospholipases A2, Secretory)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:150109
[Lr] Data última revisão:
150109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150110
[St] Status:MEDLINE


  6 / 30 MEDLINE  
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[PMID]:25517499
[Au] Autor:Biswas NK; Das S; Maitra A; Sarin R; Majumder PP
[Ad] Endereço:National Institute of Biomedical Genomics, Netaji Subhas Sanatorium (2nd Floor), Kalyani 741251, India.
[Ti] Título:Somatic mutations in arachidonic acid metabolism pathway genes enhance oral cancer post-treatment disease-free survival.
[So] Source:Nat Commun;5:5835, 2014 Dec 17.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The arachidonic acid metabolism (AAM) pathway promotes tumour progression. Chemical inhibitors of AAM pathway prolong post-treatment survival of cancer patients. Here we test whether non-synonymous somatic mutations in genes of this pathway, acting as natural inhibitors, increase post-treatment survival. We identify loss-of-function somatic mutations in 15 (18%) of 84 treatment-naïve oral cancer patients by whole-exome sequencing, which we map to genes of AAM pathway. Patients (n = 53) who survived ≥ 12 months after surgery without recurrence have significantly (P = 0.007) higher proportion (26% versus 3%) of mutations than those who did not (n = 31). Patients with mutations have a significantly (P = 0.003) longer median disease-free survival (24 months) than those without (13 months). Compared with the presence of a mutation, absence of any mutation increases the hazard ratio for death (11.3) significantly (P = 0.018). The inferences are strengthened when we pool our data with The Cancer Genome Atlas (TCGA) data. In patients with AAM pathway mutations, some downstream pathways, such as the PI3K-Akt pathway, are downregulated.
[Mh] Termos MeSH primário: Ácidos Araquidônicos/metabolismo
Carcinoma de Células Escamosas/genética
Expressão Gênica
Redes e Vias Metabólicas/genética
Neoplasias Bucais/genética
Mutação
[Mh] Termos MeSH secundário: Ácidos Araquidônicos/genética
Carcinoma de Células Escamosas/mortalidade
Carcinoma de Células Escamosas/patologia
Carcinoma de Células Escamosas/cirurgia
Citocromo P-450 CYP2C19/genética
Citocromo P-450 CYP2C19/metabolismo
Sistema Enzimático do Citocromo P-450/genética
Sistema Enzimático do Citocromo P-450/metabolismo
Família 2 do Citocromo P450
Fosfolipases A2 do Grupo III/genética
Fosfolipases A2 do Grupo III/metabolismo
Fosfolipases A2 do Grupo IV/genética
Fosfolipases A2 do Grupo IV/metabolismo
Fosfolipases A2 do Grupo VI/genética
Fosfolipases A2 do Grupo VI/metabolismo
Seres Humanos
Neoplasias Bucais/mortalidade
Neoplasias Bucais/patologia
Neoplasias Bucais/cirurgia
Peroxidases/genética
Peroxidases/metabolismo
Modelos de Riscos Proporcionais
Análise de Sobrevida
Tromboxano-A Sintase/genética
Tromboxano-A Sintase/metabolismo
Resultado do Tratamento
gama-Glutamiltransferase/genética
gama-Glutamiltransferase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arachidonic Acids); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.11.1.- (GPX7 protein, human); EC 1.11.1.- (Peroxidases); EC 1.14.14.1 (CYP2C19 protein, human); EC 1.14.14.1 (CYP2U1 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP2C19); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 2.3.2.2 (gamma-Glutamyltransferase); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (Group IV Phospholipases A2); EC 3.1.1.4 (Group VI Phospholipases A2); EC 3.1.1.4 (PLA2G3 protein, human); EC 3.1.1.4 (PLA2G4E protein, human); EC 3.1.1.4 (PLA2G4F protein, human); EC 3.1.1.4 (PLA2G6 protein, human); EC 5.3.99.4 (PTGIS protein, human); EC 5.3.99.5 (Thromboxane-A Synthase)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141218
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms6835


  7 / 30 MEDLINE  
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[PMID]:24508801
[Au] Autor:Brglez V; Pucer A; Pungercar J; Lambeau G; Petan T
[Ad] Endereço:Department of Molecular and Biomedical Sciences, Jozef Stefan Institute, Ljubljana, Slovenia.
[Ti] Título:Secreted phospholipases A2are differentially expressed and epigenetically silenced in human breast cancer cells.
[So] Source:Biochem Biophys Res Commun;445(1):230-5, 2014 Feb 28.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Secreted phospholipases A2 (sPLA2s) have recently been associated with several cancers, but their role in breast cancer is unknown. Here we demonstrate that mRNA expression of group IIA, III and X sPLA2s differs both in vivo in tumour biopsies and in breast cancer cells in vitro. Their expression is differentially regulated by DNA methylation and histone acetylation and, significantly, all three genes are silenced in aggressive triple negative cells due to both mechanisms. The transcription start site promoter region and the upstream CpG islands, exclusive to the group X sPLA2 gene, have variable roles in the regulation of sPLA2 expression. Our results suggest that the differential expression of hGIIA, hGIII and hGX sPLA2s in breast cancer cells is a consequence of various degrees of epigenetic silencing due to DNA hypermethylation and histone deacetylation.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Epigênese Genética
Perfilação da Expressão Gênica
Fosfolipases A2 do Grupo II/genética
Fosfolipases A2 do Grupo III/genética
Fosfolipases A2 do Grupo X/genética
[Mh] Termos MeSH secundário: Azacitidina/análogos & derivados
Azacitidina/farmacologia
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Linhagem Celular
Linhagem Celular Tumoral
Ilhas de CpG/genética
Metilação de DNA/efeitos dos fármacos
Feminino
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Fosfolipases A2 do Grupo II/metabolismo
Fosfolipases A2 do Grupo III/metabolismo
Fosfolipases A2 do Grupo X/metabolismo
Seres Humanos
Ácidos Hidroxâmicos/farmacologia
Células MCF-7
Regiões Promotoras Genéticas/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydroxamic Acids); 3X2S926L3Z (trichostatin A); 776B62CQ27 (decitabine); EC 3.1.1.4 (Group II Phospholipases A2); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (Group X Phospholipases A2); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1405
[Cu] Atualização por classe:140303
[Lr] Data última revisão:
140303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140211
[St] Status:MEDLINE


  8 / 30 MEDLINE  
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[PMID]:23793742
[Au] Autor:Hariprasad G; Srinivasan A; Singh R
[Ad] Endereço:Department of Biophysics, All India Institute of Medical Sciences, Ansari nagar, New Delhi, 110029, India. g.hariprasad@rediffmail.com
[Ti] Título:Structural and phylogenetic basis for the classification of group III phospholipase A2.
[So] Source:J Mol Model;19(9):3779-91, 2013 Sep.
[Is] ISSN:0948-5023
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Secretory phospholipase A2 (PLA2) catalyses the hydrolysis of the sn-2 position of glycerophospholipids to liberate arachidonic acid, a precursor of eicosanoids, that are known mediators of inflammation. The group III PLA2 enzymes are present in a wide array of organisms across many species with completely different functions. A detailed understanding of the structure and evolutionary proximity amongst the enzymes was carried out for a meaningful classification of this group. Fifty protein sequences from different species of the group were considered for a detailed sequence, structural and phylogenetic studies. In addition to the conservation of calcium binding motif and the catalytic histidine, the sequences exhibit specific 'amino acid signatures'. Structural analysis reveals that these enzymes have a conserved globular structure with species specific variations seen at the active site, calcium binding loop, hydrophobic channel, the C-terminal domain and the quaternary conformational state. Character and distance based phylogenetic analysis of these sequences are in accordance with the structural features. The outcomes of the structural and phylogenetic analysis lays a convincing platform for the classification the group III PLA2s into (1A) venomous insects; (IB) non-venomous insects; (II) mammals; (IIIA) gila monsters; (IIIB) reptiles, amphibians, fishes, sea anemones and liver fluke, and (IV) scorpions. This classification also helps to understand structure-function relationship, enzyme-substrate specificity and designing of potent inhibitors against the drug target isoforms.
[Mh] Termos MeSH primário: Fosfolipases A2 do Grupo III/química
Fosfolipases A2 do Grupo III/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Cálcio/metabolismo
Domínio Catalítico
Dissulfetos
Fosfolipases A2 do Grupo III/classificação
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Modelos Moleculares
Dados de Sequência Molecular
Filogenia
Ligação Proteica
Conformação Proteica
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Disulfides); EC 3.1.1.4 (Group III Phospholipases A2); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1404
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130625
[St] Status:MEDLINE
[do] DOI:10.1007/s00894-013-1913-x


  9 / 30 MEDLINE  
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[PMID]:23685814
[Au] Autor:Starkl P; Marichal T; Galli SJ
[Ti] Título:PLA2G3 promotes mast cell maturation and function.
[So] Source:Nat Immunol;14(6):527-9, 2013 Jun.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Fosfolipases A2 do Grupo III/imunologia
Mastócitos/imunologia
Comunicação Parácrina/imunologia
Prostaglandina D2/imunologia
Receptores de Prostaglandina/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:COMMENT; NEWS
[Nm] Nome de substância:
0 (Receptors, Prostaglandin); 0 (prostanoid D receptor 1, mouse); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (PLA2G3 protein, mouse); RXY07S6CZ2 (Prostaglandin D2)
[Em] Mês de entrada:1307
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130521
[St] Status:MEDLINE
[do] DOI:10.1038/ni.2612


  10 / 30 MEDLINE  
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[PMID]:23624557
[Au] Autor:Taketomi Y; Ueno N; Kojima T; Sato H; Murase R; Yamamoto K; Tanaka S; Sakanaka M; Nakamura M; Nishito Y; Kawana M; Kambe N; Ikeda K; Taguchi R; Nakamizo S; Kabashima K; Gelb MH; Arita M; Yokomizo T; Nakamura M; Watanabe K; Hirai H; Nakamura M; Okayama Y; Ra C; Aritake K; Urade Y; Morimoto K; Sugimoto Y; Shimizu T; Narumiya S; Hara S; Murakami M
[Ad] Endereço:Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
[Ti] Título:Mast cell maturation is driven via a group III phospholipase A2-prostaglandin D2-DP1 receptor paracrine axis.
[So] Source:Nat Immunol;14(6):554-63, 2013 Jun.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microenvironment-based alterations in phenotypes of mast cells influence the susceptibility to anaphylaxis, yet the mechanisms underlying proper maturation of mast cells toward an anaphylaxis-sensitive phenotype are incompletely understood. Here we report that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A2, regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD2 synthase (L-PGDS) to provide PGD2, which facilitates mast-cell maturation via PGD2 receptor DP1. Mice lacking PLA2G3, L-PGDS or DP1, mast cell-deficient mice reconstituted with PLA2G3-null or DP1-null mast cells, or mast cells cultured with L-PGDS-ablated fibroblasts exhibited impaired maturation and anaphylaxis of mast cells. Thus, we describe a lipid-driven PLA2G3-L-PGDS-DP1 loop that drives mast cell maturation.
[Mh] Termos MeSH primário: Fosfolipases A2 do Grupo III/imunologia
Mastócitos/imunologia
Comunicação Parácrina/imunologia
Prostaglandina D2/imunologia
Receptores de Prostaglandina/imunologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Células da Medula Óssea/imunologia
Células da Medula Óssea/metabolismo
Diferenciação Celular/genética
Diferenciação Celular/imunologia
Células Cultivadas
Fibroblastos/citologia
Fibroblastos/imunologia
Fibroblastos/metabolismo
Perfilação da Expressão Gênica
Fosfolipases A2 do Grupo III/genética
Fosfolipases A2 do Grupo III/metabolismo
Seres Humanos
Oxirredutases Intramoleculares/genética
Oxirredutases Intramoleculares/imunologia
Oxirredutases Intramoleculares/metabolismo
Lipocalinas/genética
Lipocalinas/imunologia
Lipocalinas/metabolismo
Mastócitos/metabolismo
Mastócitos/ultraestrutura
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microscopia Eletrônica de Transmissão
Análise de Sequência com Séries de Oligonucleotídeos
Comunicação Parácrina/genética
Prostaglandina D2/metabolismo
Receptores de Prostaglandina/genética
Receptores de Prostaglandina/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lipocalins); 0 (Receptors, Prostaglandin); 0 (prostanoid D receptor 1, mouse); EC 3.1.1.4 (Group III Phospholipases A2); EC 3.1.1.4 (PLA2G3 protein, mouse); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.99.2 (prostaglandin R2 D-isomerase); RXY07S6CZ2 (Prostaglandin D2)
[Em] Mês de entrada:1307
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130430
[St] Status:MEDLINE
[do] DOI:10.1038/ni.2586



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