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[PMID]:28933241
[Au] Autor:Hao W; Li Y; Shan Q; Han T; Li W; He S; Zhu K; Li Y; Tan X; Gu J
[Ad] Endereço:a School of Biological Science and Technology , University of Jinan , Jinan , China.
[Ti] Título:Characterization of human S-adenosyl-homocysteine hydrolase in vitro and identification of its potential inhibitors.
[So] Source:J Enzyme Inhib Med Chem;32(1):1209-1215, 2017 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human S-adenosyl-homocysteine hydrolase (SAHH, E.C.3.3.1.1) has been considered to be an attractive target for the design of medicines to treat human disease, because of its important role in regulating biological methylation reactions to catalyse the reversible hydrolysis of S-adenosylhomocysteine (SAH) to adenosine (Ado) and l-homocysteine (Hcy). In this study, SAHH protein was successfully cloned and purified with optimized, Pichia pastoris (P. pastoris) expression system. The biological activity results revealed that, among the tested compounds screened by ChemMapper and SciFinder Scholar, 4-(3-hydroxyprop-1-en-1-yl)-2-methoxyphenol (coniferyl alcohol, CAS: 458-35-5, ZINC: 12359045) exhibited the highest inhibition against rSAHH (IC = 34 nM). Molecular docking studies showed that coniferyl alcohol was well docked into the active cavity of SAHH. And several H-bonds formed between them, which stabilized coniferyl alcohol in the active site of rSAHH with a proper conformation.
[Mh] Termos MeSH primário: Adenosil-Homocisteinase/antagonistas & inibidores
Inibidores Enzimáticos/farmacologia
Fenóis/farmacologia
[Mh] Termos MeSH secundário: Adenosil-Homocisteinase/metabolismo
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/química
Seres Humanos
Concentração de Íons de Hidrogênio
Simulação de Acoplamento Molecular
Estrutura Molecular
Fenóis/química
Relação Estrutura-Atividade
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Phenols); E7SM92591P (coniferyl alcohol); EC 3.3.1.1 (Adenosylhomocysteinase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1370584


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[PMID]:28533090
[Au] Autor:Uchiyama N; Dougan DR; Lawson JD; Kimura H; Matsumoto SI; Tanaka Y; Kawamoto T
[Ad] Endereço:Biomolecular Research Laboratories, Takeda Pharmaceutical Company Ltd., Pharmaceutical Research Division, 26-1, Muraoka-Higashi 2-chome, Fujisawa, Kanagawa, 251-8555, Japan. Electronic address: noriko.uchiyama@takeda.com.
[Ti] Título:Identification of AHCY inhibitors using novel high-throughput mass spectrometry.
[So] Source:Biochem Biophys Res Commun;491(1):1-7, 2017 Sep 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:S-adenosylhomocysteine hydrolase (AHCY) catalyzes the reversible hydrolysis of S-adenosylhomocysteine (SAH) to adenosine and l-homocysteine. This enzyme is frequently overexpressed in many tumor types and is considered to be a validated anti-tumor target. In order to enable the development of small molecule AHCY inhibitors as targeted cancer therapeutics we developed an assay based on a RapidFire high-throughput mass spectrometry detection system, which allows the direct measurement of AHCY enzymatic activity. This technique avoids many of the problems associate with the previously reported method of using a thiol-reactive fluorescence probes to measure AHCY activity. Screening of a ∼500,000 compound library using this technique identified multiple SAH competitive hits. Co-crystal structures of the hit compounds complexed with AHCY were obtained showing that the compounds indeed bind in the SAH site of the enzyme. In addition, some hit compounds increased the SAH levels in HCT116 cells and showed growth inhibition. These compounds could be promising starting points for the optimization of cancer treatments.
[Mh] Termos MeSH primário: Adenosil-Homocisteinase/antagonistas & inibidores
Adenosil-Homocisteinase/metabolismo
Antineoplásicos/análise
Inibidores Enzimáticos/análise
Espectrometria de Massas
[Mh] Termos MeSH secundário: Antineoplásicos/química
Antineoplásicos/farmacologia
Sítios de Ligação
Sobrevivência Celular/efeitos dos fármacos
Avaliação Pré-Clínica de Medicamentos
Inibidores Enzimáticos/química
Inibidores Enzimáticos/farmacologia
Células HCT116
Ensaios de Triagem em Larga Escala
Seres Humanos
Ligação Proteica
Mapas de Interação de Proteínas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Enzyme Inhibitors); EC 3.3.1.1 (Adenosylhomocysteinase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE


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[PMID]:28288933
[Au] Autor:Haddadi-Guemghar H; Tlili A; Dairou J; Paul JL; Madani K; Janel N
[Ad] Endereço:Laboratoire de Biomathématiques, Biophysique, Biochimie, et Scientométrie (L3BS), Faculté des Sciences de la Nature et de la Vie, Université de Bejaia, 06000 Bejaia, Algeria.
[Ti] Título:Effect of lyophilized prune extract on hyperhomocysteinemia in mice.
[So] Source:Food Chem Toxicol;103:183-187, 2017 May.
[Is] ISSN:1873-6351
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Altered homocysteine metabolism defined as hyperhomocysteinemia is implicated as pathogenic factor in several cardiovascular diseases and atherosclerosis. The purpose of this study was to investigate the efficacy of prune extract, a good source of phenolic antioxidants, on lowering plasma homocysteine level in male hyperhomocysteinemic mice from average weight of 28 g. The administration of lyophilized prune extract was carried out by intraperitoneal injection one day preceding and one hour before sacrifice of mice. Prune extract decreased significantly plasma homocysteine level, correlated with an increased activity of S-adenosylhomocysteine (SAH) hydrolase and NAD(P)H: quinone oxydoreductase-1 activities. Our results suggest a beneficial effect of prune extract on hyperhomocysteinemia with reduction of homocysteine level by its conversion on to SAH by S-adenosylhomocysteine hydrolase, which is activated by NAD , a by-product of NAD(P)H: quinone oxydo reductase-1.
[Mh] Termos MeSH primário: Hiper-Homocisteinemia/dietoterapia
Extratos Vegetais/farmacologia
Prunus domestica/química
[Mh] Termos MeSH secundário: Adenosil-Homocisteinase/metabolismo
Animais
Ácido Clorogênico/farmacologia
Cistationina beta-Sintase/genética
Feminino
Liofilização
Homocisteína/sangue
Hiper-Homocisteinemia/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Mutantes
NAD(P)H Desidrogenase (Quinona)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Extracts); 0LVT1QZ0BA (Homocysteine); 318ADP12RI (Chlorogenic Acid); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (Nqo1 protein, mouse); EC 3.3.1.1 (Adenosylhomocysteinase); EC 4.2.1.22 (Cystathionine beta-Synthase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE


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[PMID]:27623281
[Au] Autor:Ahn JK; Kim HY; Baek S; Park HG
[Ad] Endereço:Department of Chemical and Biomolecular Engineering (BK21+Program), KAIST, 291 Daehak-ro, Yuseong-gu, Daejeon 305-701, Republic of Korea.
[Ti] Título:A new s-adenosylhomocysteine hydrolase-linked method for adenosine detection based on DNA-templated fluorescent Cu/Ag nanoclusters.
[So] Source:Biosens Bioelectron;93:330-334, 2017 Jul 15.
[Is] ISSN:1873-4235
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We herein describe a novel fluorescent method for the rapid and selective detection of adenosine by utilizing DNA-templated Cu/Ag nanoclusters (NCs) and employing s-adenosylhomocysteine hydrolase (SAHH). SAHH is allowed to promote hydrolysis reaction of s-adenosylhomocysteine (SAH) and consequently produces homocysteine, which would quench the fluorescence signal from DNA-templated Cu/Ag nanoclusters employed as a signaling probe in this study. On the other hand, adenosine significantly inhibits the hydrolysis reaction and prevent the formation of homocysteine. Consequently, highly enhanced fluorescence signal from DNA-Cu/Ag NCs is retained, which could be used to identify the presence of adenosine. By employing this design principle, adenosine was sensitively detected down to 19nM with high specificity over other adenosine analogs such as AMP, ADP, ATP, cAMP, guanosine, cytidine, and urine. Finally, the diagnostic capability of this method was successfully verified by reliably detecting adenosine present in a real human serum sample.
[Mh] Termos MeSH primário: Adenosina/isolamento & purificação
Adenosil-Homocisteinase/química
Técnicas Biossensoriais
[Mh] Termos MeSH secundário: Adenosina/química
Cobre/química
DNA/química
Fluorescência
Seres Humanos
Nanopartículas Metálicas/química
S-Adenosil-Homocisteína
Prata/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
3M4G523W1G (Silver); 789U1901C5 (Copper); 9007-49-2 (DNA); 979-92-0 (S-Adenosylhomocysteine); EC 3.3.1.1 (Adenosylhomocysteinase); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160914
[St] Status:MEDLINE


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[PMID]:27876123
[Au] Autor:Novak EM; Halley NS; Gimenez TM; Rangel-Santos A; Azambuja AM; Brumatti M; Pereira PL; Vince CS; Giorgi RR; Bendit I; Cristofani LM; Odone-Filho V
[Ad] Endereço:Instituto de Tratamento de Câncer Infantil (ITACI), Pediatric Department at São Paulo University Medical School, Hematology-Oncology Division, São Paulo, SP, Brazil; Division of Molecular Genetics, Fundação Pró-Sangue Hemocentro de São Paulo, São Paulo, SP, Brazil; Laboratory of Medical Investigatio
[Ti] Título:BLM germline and somatic PKMYT1 and AHCY mutations: Genetic variations beyond MYCN and prognosis in neuroblastoma.
[So] Source:Med Hypotheses;97:22-25, 2016 Dec.
[Is] ISSN:1532-2777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroblastoma (NB) is the most common extra cranial solid tumor of childhood and often lethal in childhood. Clinical and biologic characteristics that are independently prognostic of outcome in NB are currently used for risk stratification to optimally the therapy. It includes age at diagnosis, International Neuroblastoma Staging System tumor histopathology and MYCN amplification. However, even in patients with theoretically good prognosis, such as localized tumor and non-amplified MYCN, either disease progress or recurrence may occur. Potential genetic determinants of this unfavorable behavior are not yet fully clarified. The presence of elevated expression of AHCY, PKMYT1, and BLM has accompanied poor prognosis MYCN-amplified neuroblastoma patients. Considering the potential implication of these genes on the clinical management of NB, we hypothesize that the identification of genetic variations may have significant impact during development of the recurrent or progressive disease. Using targeted DNA sequencing, we analyzed the mutation profiles of the genes PKMYT1, AHCY, and BLM in tumor samples of five patients with MYCN amplified and 15 MYCN non-amplified NB. In our study, BLM germline variants were detected in two patients with MYCN-non-amplified neuroblastoma. Our data allow us to hypothesize that, regardless of MYCN status, these mutations partially abolish BLM protein activity by impairing its ATPase and helicase activities. BLM mutations are also clinically relevant because BLM plays an important role in DNA damage repair and the maintenance of genomic integrity. We also found a novel variant in our cohort, PKMYT1 mutation localized in the C-terminal domain with effect unknown on NB. We hypothesize that this variant may affect the catalytic activity of PKMYT1 in NB, specifically when CDK1 is complexed to cyclins. The prognostic value of this mutation must be further investigated. Another mutation identified was a nonsynonymous variant in AHCY. This variant may be related to the slow progression of the disease, even in more aggressive cases. It affects the maintenance of the catalytic capacity of AHCY, leading to the consequent functional effects observed in the NB patients studied. In conclusion, our hypothesis may provide that mutations in BLM, AHCY and PKMYT1 genes found in children with MYCN-amplified or MYCN-non amplified neuroblastomas, may be associated with the prognosis of the disease.
[Mh] Termos MeSH primário: Adenosil-Homocisteinase/genética
Neoplasias Encefálicas/genética
Mutação em Linhagem Germinativa
Proteínas de Membrana/genética
Proteína Proto-Oncogênica N-Myc/genética
Neuroblastoma/genética
Proteínas Serina-Treonina Quinases/genética
Proteínas Tirosina Quinases/genética
RecQ Helicases/genética
[Mh] Termos MeSH secundário: Criança
Estudos de Coortes
Dano ao DNA
Reparo do DNA
Progressão da Doença
Resistência a Medicamentos Antineoplásicos
Regulação Neoplásica da Expressão Gênica
Variação Genética
Genoma Humano
Seres Humanos
Modelos Teóricos
Recidiva Local de Neoplasia
Prognóstico
Domínios Proteicos
Fatores de Risco
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MYCN protein, human); 0 (Membrane Proteins); 0 (N-Myc Proto-Oncogene Protein); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.11.1 (PKMYT1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.3.1.1 (Adenosylhomocysteinase); EC 3.6.1.- (Bloom syndrome protein); EC 3.6.4.12 (RecQ Helicases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE


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[PMID]:27474977
[Au] Autor:Zhang Q; Bertics SJ; Luchini ND; White HM
[Ad] Endereço:Department of Dairy Science, University of Wisconsin, Madison 53706.
[Ti] Título:The effect of increasing concentrations of dl-methionine and 2-hydroxy-4-(methylthio) butanoic acid on hepatic genes controlling methionine regeneration and gluconeogenesis.
[So] Source:J Dairy Sci;99(10):8451-8460, 2016 Oct.
[Is] ISSN:1525-3198
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolizable methionine (Met) concentrations can be increased by feeding rumen-protected dl-Met or the isopropyl ester of 2-hydroxy-4-(methylthio) butanoic acid (HMBi). Hepatic responses to increasing concentrations of metabolizable Met as a result of supplementation of different Met sources have not been comparatively examined. The objective of this experiment was to examine the regulation of key genes for Met metabolism, gluconeogenesis, and fatty acid oxidation in response to increasing concentrations of dl-Met or 2-hydroxy-4-(methylthio) butanoic acid (HMB) in bovine primary hepatocytes. Hepatocytes isolated from 4 Holstein calves less than 7d old were maintained as monolayer cultures for 24h before addition of treatments. Cells were then exposed to treatments of dl-Met or HMB (0, 10, 20, 40, or 60 µM) in Met-free medium for 24h and collected for RNA isolation and quantification of gene expression by quantitative PCR. Expression of betaine-homocysteine methyltransferase (BHMT), 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR), and 5,10 methylenetetrahydrofolate reductase (MTHFR) genes, which catalyze regeneration of Met from betaine and homocysteine, decreased linearly with increasing dl-Met concentration. We observed similar effects with increasing HMB concentration, except expression of MTHFR, which was not altered. Expression of Met adenosyltransferase 1A (MAT1A), which catalyzes the first step of Met metabolism to generate S-adenosylmethionine (SAM), a primary methyl donor, was decreased with increasing dl-Met or HMB concentration. Expression of S-adenosylhomocysteine hydrolase (SAHH) was decreased linearly with increasing HMB concentration, but not altered by dl-Met. Increasing concentrations of dl-Met and HMB decreased cytosolic phosphoenolpyruvate carboxykinase (PCK1) expression, but did not alter the expression of mitochondrial phosphoenolpyruvate carboxykinase (PCK2) or pyruvate carboxylase (PC). Expression of glucose-6-phosphatase(G6PC) decreased linearly with increasing HMB concentration, but not altered by dl-Met. Neither dl-Met nor HMB altered the expression of carnitine palmitoyltransferase 1A(CPT1a). These findings demonstrate reduced necessity for Met regeneration with increased Met concentrations in the medium, regardless of the Met source. The lack of upregulation of gluconeogenesis indicates that increased dl-Met or HMB is not prioritized for glucose synthesis in primary bovine hepatocytes.
[Mh] Termos MeSH primário: Fígado/efeitos dos fármacos
Metionina/análogos & derivados
Metionina/farmacologia
[Mh] Termos MeSH secundário: 5-Metiltetra-Hidrofolato-Homocisteína S-Metiltransferase/genética
Adenosil-Homocisteinase/genética
Animais
Animais Recém-Nascidos
Betaína/metabolismo
Betaína-Homocisteína S-Metiltransferase/genética
Carnitina O-Palmitoiltransferase/genética
Bovinos
Regulação para Baixo
Gluconeogênese/genética
Glucose-6-Fosfatase/genética
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Homocisteína/metabolismo
Fígado/metabolismo
Metionina Adenosiltransferase/genética
Metilenotetra-Hidrofolato Redutase (NADPH2)/genética
Fosfoenolpiruvato Carboxiquinase (GTP)/genética
S-Adenosilmetionina/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0LVT1QZ0BA (Homocysteine); 3SCV180C9W (Betaine); 583-91-5 (alpha-hydroxy-gamma-methylmercaptobutyric acid); 7LP2MPO46S (S-Adenosylmethionine); AE28F7PNPL (Methionine); EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2)); EC 2.1.1.13 (5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase); EC 2.1.1.5 (Betaine-Homocysteine S-Methyltransferase); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase); EC 2.5.1.6 (Methionine Adenosyltransferase); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 3.3.1.1 (Adenosylhomocysteinase); EC 4.1.1.32 (Phosphoenolpyruvate Carboxykinase (GTP))
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160801
[St] Status:MEDLINE


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[PMID]:27279487
[Au] Autor:He P; Zhao L; No YR; Karvar S; Yun CC
[Ad] Endereço:Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia; phe3@emory.edu.
[Ti] Título:The NHERF1 PDZ1 domain and IRBIT interact and mediate the activation of Na+/H+ exchanger 3 by ANG II.
[So] Source:Am J Physiol Renal Physiol;311(2):F343-51, 2016 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Na(+)/H(+) exchanger (NHE)3, a major Na(+) transporter in the luminal membrane of the proximal tubule, is subject to ANG II regulation in renal Na(+)/fluid absorption and blood pressure control. We have previously shown that inositol 1,4,5-trisphosphate receptor-binding protein released with inositol 1,4,5-trisphosphate (IRBIT) mediates ANG II-induced exocytosis of NHE3 in cultured proximal tubule epithelial cells. In searching for scaffold protein(s) that coordinates with IRBIT in NHE3 trafficking, we found that NHE regulatory factor (NHERF)1, NHE3, and IRBIT proteins were coexpressed in the same macrocomplexes and that loss of ANG II type 1 receptors decreased their expression in the renal brush-border membrane. We found that NHERF1 was required for ANG II-mediated forward trafficking and activation of NHE3 in cultured cells. ANG II induced a concomitant increase of NHERF1 interactions with NHE3 and IRBIT, which were abolished when the NHERF1 PDZ1 domain was removed. Overexpression of a yellow fluorescent protein-NHERF1 construct that lacks PDZ1, but not PDZ2, failed to exaggerate the ANG II-dependent increase of NHE3 expression in the apical membrane. Moreover, exogenous expression of PDZ1 exerted a dominant negative effect on NHE3 activation by ANG II. We further demonstrated that IRBIT was indispensable for the ANG II-provoked increase in NHERF1-NHE3 interactions and that phosphorylation of IRBIT at Ser(68) was necessary for the assembly of the NHEF1-IRBIT-NHE3 complex. Taken together, our findings suggest that NHERF1 mediates ANG II-induced activation of renal NHE3, which requires coordination between IRBIT and the NHERF1 PDZ1 domain in binding and transporting NHE3.
[Mh] Termos MeSH primário: Adenosil-Homocisteinase/metabolismo
Angiotensina II/farmacologia
Fosfoproteínas/metabolismo
Trocadores de Sódio-Hidrogênio/agonistas
Trocadores de Sódio-Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Biotinilação
Linhagem Celular
Concentração de Íons de Hidrogênio
Camundongos
Camundongos Knockout
Microvilosidades/metabolismo
Plasmídeos/genética
Receptor Tipo 1 de Angiotensina/efeitos dos fármacos
Receptor Tipo 1 de Angiotensina/genética
Receptor Tipo 1 de Angiotensina/metabolismo
Sódio/metabolismo
Trocador 3 de Sódio-Hidrogênio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphoproteins); 0 (Receptor, Angiotensin, Type 1); 0 (Slc9a3 protein, mouse); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (sodium-hydrogen exchanger regulatory factor); 11128-99-7 (Angiotensin II); 9NEZ333N27 (Sodium); EC 3.3.1.1 (Adenosylhomocysteinase); EC 3.3.1.1 (IRBIT protein, mouse)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160610
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00247.2016


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[PMID]:26898994
[Au] Autor:Khare P; Jaiswal AK; Tripathi CD; Sundar S; Dube A
[Ad] Endereço:Division of Parasitology, CSIR - Central Drug Research Institute, Lucknow.
[Ti] Título:Immunoprotective responses of T helper type 1 stimulatory protein-S-adenosyl-L-homocysteine hydrolase against experimental visceral leishmaniasis.
[So] Source:Clin Exp Immunol;185(2):165-79, 2016 Aug.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:It is well known that a patient in clinical remission of visceral leishmaniasis (VL) remains immune to reinfection, which provides a rationale for the feasibility of a vaccine against this deadly disease. In earlier studies, observation of significant cellular responses in treated Leishmania patients as well as in hamsters against leishmanial antigens from different fractions led to its further proteomic characterization, wherein S-adenosyl-L-homocysteine hydrolase (AdoHcy) was identified as a helper type 1 (Th1) stimulatory protein. The present study includes immunological characterization of this protein, its cellular responses [lymphoproliferation, nitric oxide (NO) production and cytokine responses] in treated Leishmania-infected hamsters and patients as well as prophylactic efficacy against Leishmania challenge in hamsters and the immune responses generated thereof. Significantly higher cellular responses were noticed against recombinant L. donovani S-adenosyl-L-homocysteine hydrolase (rLdAdoHcy) compared to soluble L. donovani antigen in treated samples. Moreover, stimulation of peripheral blood mononuclear cells with rLdAdoHcy up-regulated the levels of interferon (IFN)-γ, interleukin (IL)-12 and down-regulated IL-10. Furthermore, vaccination with rLdAdoHcy generated perceptible delayed-type hypersensitivity response and exerted considerably good prophylactic efficacy (∼70% inhibition) against L. donovani challenge. The efficacy was confirmed by the increased expression levels of inducible NO synthase and Th1-type cytokines, IFN-γ and IL-12 and down-regulation of IL-4, IL-10 and transforming growth factor (TGF)-ß. The results indicate the potentiality of rLdAdoHcy protein as a suitable vaccine candidate against VL.
[Mh] Termos MeSH primário: Adenosil-Homocisteinase/imunologia
Adenosil-Homocisteinase/metabolismo
Vacinas contra Leishmaniose/imunologia
Leishmaniose Visceral/imunologia
Células Th1/enzimologia
[Mh] Termos MeSH secundário: Adenosil-Homocisteinase/administração & dosagem
Adenosil-Homocisteinase/genética
Adolescente
Adulto
Animais
Antígenos de Protozoários/imunologia
Criança
Pré-Escolar
Cricetinae
Citocinas/genética
Feminino
Seres Humanos
Leishmania donovani/imunologia
Leishmania donovani/isolamento & purificação
Leishmaniose Visceral/prevenção & controle
Leucócitos Mononucleares/imunologia
Ativação Linfocitária
Masculino
Óxido Nítrico/biossíntese
Proteômica
Proteínas de Protozoários/imunologia
Células Th1/imunologia
Vacinação
Vacinas Sintéticas/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Protozoan); 0 (Cytokines); 0 (Leishmaniasis Vaccines); 0 (Protozoan Proteins); 0 (Vaccines, Synthetic); 31C4KY9ESH (Nitric Oxide); EC 3.3.1.1 (Adenosylhomocysteinase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160223
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12780


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[PMID]:26750250
[Au] Autor:Liu C; Chen Q; Schneller SW
[Ad] Endereço:Molette Laboratory for Drug Discovery, Department of Chemistry and Biochemistry, Auburn University, Auburn, AL 36849-5312, United States.
[Ti] Título:Enantiomeric 3-deaza-1',6'-isoneplanocin and its 3-bromo analogue: Synthesis by the Ullmann reaction and their antiviral properties.
[So] Source:Bioorg Med Chem Lett;26(3):928-930, 2016 Feb 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The 1',6'-isomer of neplanocin A possesses biological properties that have not been optimised through rationally conceived analogues. In that direction, this Letter reports the use of the Ullmann reaction to achieve enantiomeric 3-deaza-1',6'-isoneplanocin and 3-bromo-3-deaza-1',6'-isoneplanocin. These four compounds showed significant Ebola activity that is not specifically due to their inhibition of S-adenonosylhomocysteine hydrolase, as might have been expected for 3-deazaadenine carbocyclic nucleosides. For some members of this group, antiviral activity was also found against human cytomegalovirus, hepatitis B, norovirus, and measles.
[Mh] Termos MeSH primário: Adenosina/análogos & derivados
Antivirais/química
[Mh] Termos MeSH secundário: Adenina/análogos & derivados
Adenina/química
Adenosina/síntese química
Adenosina/química
Adenosina/farmacologia
Adenosil-Homocisteinase/antagonistas & inibidores
Adenosil-Homocisteinase/metabolismo
Antivirais/síntese química
Antivirais/farmacologia
Citomegalovirus/efeitos dos fármacos
Ebolavirus/efeitos dos fármacos
Seres Humanos
Morbillivirus/efeitos dos fármacos
Norovirus/efeitos dos fármacos
Nucleosídeos/química
Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Nucleosides); 6811-77-4 (3-deazaadenine); 72877-50-0 (neplanocin A); EC 3.3.1.1 (Adenosylhomocysteinase); JAC85A2161 (Adenine); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160112
[St] Status:MEDLINE


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[PMID]:26439876
[Au] Autor:Borth H; Weber N; Meyer D; Wartenberg A; Arlt E; Zierler S; Breit A; Wennemuth G; Gudermann T; Boekhoff I
[Ad] Endereço:Walther Straub Institute of Pharmacology and Toxicology, Ludwig-Maximilians-Universit, ä, t M, ü, nchen, München, Germany.
[Ti] Título:The IP3 R Binding Protein Released With Inositol 1,4,5-Trisphosphate Is Expressed in Rodent Reproductive Tissue and Spermatozoa.
[So] Source:J Cell Physiol;231(5):1114-29, 2016 May.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Besides its capacity to inhibit the 1,4,5-trisphosphate (IP3) receptor, the regulatory protein IRBIT (IP3 receptor binding protein released with IP3) is also able to control the activity of numerous ion channels and electrolyte transporters and thereby creates an optimal electrolyte composition of various biological fluids. Since a reliable execution of spermatogenesis and sperm maturation critically depends on the establishment of an adequate microenvironment, the expression of IRBIT in male reproductive tissue was examined using immunohistochemical approaches combined with biochemical fractionation methods. The present study documents that IRBIT is expressed in Leydig and Sertoli cells. In addition, pronounced IRBIT expression was detected in sperm precursors during early stages of spermatogenesis as well as in spermatozoa. Analyzing tissue sections of rodent epididymides, IRBIT was found to co-localize with the proton pumping V-ATPase and the cystic fibrosis transmembrane conductance regulator (CFTR) at the apical surface of narrow and clear cells. A similar co-localization of IRBIT with CFTR was also observed for Sertoli cells and developing germ cells. Remarkably, assaying caudal sperm in immunogold electron microscopy, IRBIT was found to localize to the acrosomal cap and the flagellum as well as to the sperm nucleus; moreover, a prominent oligomerization was observed for spermatozoa. The pronounced occurrence of IRBIT in the male reproductive system and mature spermatozoa indicates a potential role for IRBIT in establishing the essential luminal environment for a faithful execution of spermatogenesis and epididymal sperm maturation, and suggest a participation of IRBIT during maturation steps after ejaculation and/or the final fertilization process.
[Mh] Termos MeSH primário: Adenosil-Homocisteinase/metabolismo
Inositol 1,4,5-Trifosfato/metabolismo
Reprodução
Espermatozoides/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Epididimo/citologia
Epididimo/metabolismo
Células Epiteliais/metabolismo
Immunoblotting
Imuno-Histoquímica
Receptores de Inositol 1,4,5-Trifosfato/metabolismo
Células Intersticiais do Testículo/citologia
Células Intersticiais do Testículo/metabolismo
Masculino
Ratos Sprague-Dawley
Células de Sertoli/citologia
Células de Sertoli/metabolismo
Espermatozoides/citologia
Testículo/citologia
Testículo/ultraestrutura
ATPases Vacuolares Próton-Translocadoras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Inositol 1,4,5-Trisphosphate Receptors); 85166-31-0 (Inositol 1,4,5-Trisphosphate); EC 3.3.1.1 (Adenosylhomocysteinase); EC 3.3.1.1 (IRBIT protein, rat); EC 3.6.1.- (Vacuolar Proton-Translocating ATPases)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:160126
[Lr] Data última revisão:
160126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151007
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25209



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