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[PMID]:29377929
[Au] Autor:Allard D; Charlebois R; Gilbert L; Stagg J; Chrobak P
[Ad] Endereço:Centre de Recherche du Centre Hospitalier l'Université de Montréal (CRCHUM), Faculté de Pharmacie de l'Université de Montréal et Institut du Cancer de Montréal, Montréal, Quebec, Canada.
[Ti] Título:CD73-A2a adenosine receptor axis promotes innate B cell antibody responses to pneumococcal polysaccharide vaccination.
[So] Source:PLoS One;13(1):e0191973, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many individuals at risk of streptococcal infection respond poorly to the pneumococcal polysaccharide vaccine Pneumovax 23. Identification of actionable pathways able to enhance Pneumovax responsiveness is highly relevant. We investigated the contribution of the extracellular adenosine pathway regulated by the ecto-nucleotidase CD73 in Pneumovax-induced antibody responses. Using gene-targeted mice, we demonstrated that CD73-or A2a adenosine receptor deficiency significantly delayed isotype switching. Nevertheless, CD73- or A2aR- deficient adult mice ultimately produced antigen-specific IgG3 and controlled Streptococcus pneumoniae infection as efficiently as wild type (WT) mice. Compared to adults, young WT mice failed to control S. pneumoniae infection after vaccination and this was associated with lower levels of CD73 on innate B cells. We hypothesized that pharmacological activation of A2a receptor may improve Pneumovax 23 immunization in young WT mice. Remarkably, administration of the A2a adenosine receptor agonist CGS 21680 significantly increased IgG3 responses and significantly enhanced survival after S. pneumoniae challenge. Our study thus suggests that pharmacological activation of the A2a adenosine receptor could improve the efficacy of Pneumovax 23 vaccination in individuals at risk of streptococcal infection.
[Mh] Termos MeSH primário: 5´-Nucleotidase/metabolismo
Linfócitos B/imunologia
Imunidade Inata
Vacinas Pneumocócicas/imunologia
Receptor A2A de Adenosina/metabolismo
[Mh] Termos MeSH secundário: 5'-Nucleotidase/genética
Animais
Ensaio de Imunoadsorção Enzimática
Imunofluorescência
Imunoglobulina G/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptor A2A de Adenosina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunoglobulin G); 0 (Pneumococcal Vaccines); 0 (Receptor, Adenosine A2A); EC 3.1.3.5 (5'-Nucleotidase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191973


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[PMID]:28464916
[Au] Autor:Xie M; Qin H; Luo Q; Huang Q; He X; Yang Z; Lan P; Lian L
[Ad] Endereço:Department of Colorectal Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, 26 Yuancun Erheng Rd, Guangzhou, Guangdong, 510655, People's Republic of China.
[Ti] Título:MicroRNA-30a regulates cell proliferation and tumor growth of colorectal cancer by targeting CD73.
[So] Source:BMC Cancer;17(1):305, 2017 May 02.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: MicroRNAs are non-coding RNAs which regulate a variety of cellular functions in the development of tumors. Among the numerous microRNAs, microRNA-30a (miR-30a) is thought to play an important role in the processes of various human tumors. In this study, we aimed to explore the role of miR-30a in the process of colorectal cancer (CRC). METHODS: The quantitative real-time PCR and western blot analysis were used to detect the expressions of miR-30a and CD73 in CRC cell lines and clinical tissues. The luciferase reporter assay was conducted to validate the association between miR-30a and CD73. The CCK-8, terminal deoxynucleotidyl transferase dUTP -biotin nick end labeling (TUNEL) assays and cell cycle flow cytometry were carried out to verify the biological functions of miR-30a in vitro. The nude mouse tumorigenicity experiment was used to clarify the biological role of miR-30a in vivo. RESULTS: The expression of miR-30a was significantly reduced in tumor cells and tissues of CRC. The proliferation ability of CRC cells was suppressed and the apoptosis of cells was promoted when miR-30a is over-regulated, however, the biological effects would be inverse since the miR-30a is down-regulated. CD73 is thought to be a target binding gene of miR-30a because miR-30a can bind directly to the 3'-UTR of CD73 mRNA, subsequently reducing its expression. The proliferation suppression of the CRC cells mediated by miR-30a could be rescued after up-regulating the expression of CD73. CONCLUSIONS: MiR-30a plays an important role on regulating the cell proliferation and apoptosis, thus affecting the growth of the tumor in CRC. And it may participate in the disease process of CRC by regulating the expression of CD73.
[Mh] Termos MeSH primário: 5´-Nucleotidase/metabolismo
Apoptose/genética
Proliferação Celular/genética
Neoplasias Colorretais/metabolismo
MicroRNAs/genética
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Neoplasias Colorretais/genética
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Camundongos
Camundongos Nus
MicroRNAs/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (MIRN30 microRNA, human); 0 (MicroRNAs); EC 3.1.3.5 (5'-Nucleotidase); EC 3.1.3.5 (NT5E protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3291-8


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[PMID]:29305710
[Au] Autor:Dietrich F; Figueiró F; Filippi-Chiela EC; Cappellari AR; Rockenbach L; Tremblay A; de Paula PB; Roesler R; Filho AB; Sévigny J; Morrone FB; Battastini AMO
[Ad] Endereço:Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, UFRGS, Porto Alegre, RS, CEP 90035-003, Brazil.
[Ti] Título:Ecto-5'-nucleotidase/CD73 contributes to the radiosensitivity of T24 human bladder cancer cell line.
[So] Source:J Cancer Res Clin Oncol;144(3):469-482, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Trimodal therapy is a reasonable bladder-preserving option to radical cystectomy. However, many tumors are radioresistive. In this sense, the identification of new prognostic and predictive biomarkers that allow the selection of patients with better responses to radiation therapy would improve outcomes. With the aim of using ecto-5'-nucleotidase/CD73 as a predictive biomarker, the role of this enzyme in the context of radiotherapy in T24 human bladder cancer cell line was investigated. METHODS: T24 cell line was exposure to a single dose of radiation (4 Gray) and trypan blue assay (pharmacological assays of viability/cumulative population doubling), flow cytometry (cell cycle/cell death/active caspase-3/ecto-5'-nucleotidase/CD73 protein staining), DAPI staining (nuclear morphometric assay), RT-PCR and real-time PCR, malachite green method (ectonucleotidase enzymatic assay), and HPLC (analysis of AMP metabolism) were carried out. T24 cell line in which ecto-5'-nucleotidase/CD73 has been completely silenced (5'KO) was also used. RESULTS: The exposure of T24 cell line to a single dose (4 Gray) of radiation-induced cell death and triggered a transitory increase in ecto-5'-nucleotidase/CD73 expression, increased ectonucleotidase activity, and led to adenosine and inosine accumulation in the extracellular medium. Pharmacological inhibition or knocking out ecto-5'-nucleotidase/CD73 rescued cells' proliferative capacity, reducing their sensitivity to radiation. CONCLUSION: Our findings show that the induction of ecto-5'-nucleotidase/CD73 by radiation contributes to the radiosensitivity of T24 cell line.
[Mh] Termos MeSH primário: 5´-Nucleotidase/fisiologia
Tolerância a Radiação/genética
Neoplasias da Bexiga Urinária/patologia
Neoplasias da Bexiga Urinária/radioterapia
[Mh] Termos MeSH secundário: 5'-Nucleotidase/genética
5'-Nucleotidase/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/genética
Proliferação Celular/efeitos da radiação
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Proteínas Ligadas por GPI/fisiologia
Regulação Enzimológica da Expressão Gênica/efeitos da radiação
Regulação Neoplásica da Expressão Gênica/efeitos da radiação
Técnicas de Silenciamento de Genes
Seres Humanos
Dose de Radiação
Neoplasias da Bexiga Urinária/genética
Neoplasias da Bexiga Urinária/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPI-Linked Proteins); EC 3.1.3.5 (5'-Nucleotidase); EC 3.1.3.5 (NT5E protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2567-3


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[PMID]:28746783
[Au] Autor:D'Souza L; Gupta SL; Bal V; Rath S; George A
[Ad] Endereço:National Institute of Immunology, New Delhi, India.
[Ti] Título:CD73 expression identifies a subset of IgM antigen-experienced cells with memory attributes that is T cell and CD40 signalling dependent.
[So] Source:Immunology;152(4):602-612, 2017 12.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:B-cell memory was long characterized as isotype-switched, somatically mutated and germinal centre (GC)-derived. However, it is now clear that the memory pool is a complex mixture that includes unswitched and unmutated cells. Further, expression of CD73, CD80 and CD273 has allowed the categorization of B-cell memory into multiple subsets, with combinatorial expression of the markers increasing with GC progression, isotype-switching and acquisition of somatic mutations. We have extended these findings to determine whether these markers can be used to identify IgM memory phenotypically as arising from T-dependent versus T-independent responses. We report that CD73 expression identifies a subset of antigen-experienced IgM cells that share attributes of functional B-cell memory. This subset is reduced in the spleens of T-cell-deficient and CD40-deficient mice and in mixed marrow chimeras made with mutant and wild-type marrow, the proportion of CD73 IgM memory is restored in the T-cell-deficient donor compartment but not in the CD40-deficient donor compartment, indicating that CD40 ligation is involved in its generation. We also report that CD40 signalling supports optimal expression of CD73 on splenic T cells and age-associated B cells (ABCs), but not on other immune cells such as neutrophils, marginal zone B cells, peritoneal cavity B-1 B cells and regulatory T and B cells. Our data indicate that in addition to promoting GC-associated memory generation during B-cell differentiation, CD40-signalling can influence the composition of the unswitched memory B-cell pool. They also raise the possibility that a fraction of ABCs may represent T-cell-dependent IgM memory.
[Mh] Termos MeSH primário: 5´-Nucleotidase/imunologia
Antígenos CD40/imunologia
Regulação da Expressão Gênica/imunologia
Imunoglobulina M/imunologia
Memória Imunológica
Transdução de Sinais/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: 5'-Nucleotidase/genética
Animais
Linfócitos B/imunologia
Antígenos CD40/genética
Imunoglobulina M/genética
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Neutrófilos/imunologia
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD40 Antigens); 0 (Immunoglobulin M); EC 3.1.3.5 (5'-Nucleotidase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12800


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[PMID]:28461573
[Au] Autor:Ratiu JJ; Racine JJ; Hasham MG; Wang Q; Branca JA; Chapman HD; Zhu J; Donghia N; Philip V; Schott WH; Wasserfall C; Atkinson MA; Mills KD; Leeth CM; Serreze DV
[Ad] Endereço:The Jackson Laboratory, Bar Harbor, ME 04609.
[Ti] Título:Genetic and Small Molecule Disruption of the AID/RAD51 Axis Similarly Protects Nonobese Diabetic Mice from Type 1 Diabetes through Expansion of Regulatory B Lymphocytes.
[So] Source:J Immunol;198(11):4255-4267, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:B lymphocytes play a key role in type 1 diabetes (T1D) development by serving as a subset of APCs preferentially supporting the expansion of autoreactive pathogenic T cells. As a result of their pathogenic importance, B lymphocyte-targeted therapies have received considerable interest as potential T1D interventions. Unfortunately, the B lymphocyte-directed T1D interventions tested to date failed to halt ß cell demise. IgG autoantibodies marking humans at future risk for T1D indicate that B lymphocytes producing them have undergone the affinity-maturation processes of class switch recombination and, possibly, somatic hypermutation. This study found that CRISPR/Cas9-mediated ablation of the activation-induced cytidine deaminase gene required for class switch recombination/somatic hypermutation induction inhibits T1D development in the NOD mouse model. The activation-induced cytidine deaminase protein induces genome-wide DNA breaks that, if not repaired through RAD51-mediated homologous recombination, result in B lymphocyte death. Treatment with the RAD51 inhibitor 4,4'-diisothiocyanatostilbene-2, 2'-disulfonic acid also strongly inhibited T1D development in NOD mice. The genetic and small molecule-targeting approaches expanded CD73 B lymphocytes that exert regulatory activity suppressing diabetogenic T cell responses. Hence, an initial CRISPR/Cas9-mediated genetic modification approach has identified the AID/RAD51 axis as a target for a potentially clinically translatable pharmacological approach that can block T1D development by converting B lymphocytes to a disease-inhibitory CD73 regulatory state.
[Mh] Termos MeSH primário: Linfócitos B Reguladores/imunologia
Proteínas de Transporte/antagonistas & inibidores
Citidina Desaminase/antagonistas & inibidores
Diabetes Mellitus Tipo 1/imunologia
Diabetes Mellitus Tipo 1/prevenção & controle
Ativação Linfocitária
Proteínas Nucleares/antagonistas & inibidores
[Mh] Termos MeSH secundário: Ácido 4,4'-Di-Isotiocianoestilbeno-2,2'-Dissulfônico/farmacologia
5'-Nucleotidase/imunologia
Animais
Autoanticorpos/imunologia
Sistemas CRISPR-Cas
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Citidina Desaminase/genética
Citidina Desaminase/metabolismo
Diabetes Mellitus Experimental
Switching de Imunoglobulina
Camundongos
Camundongos Endogâmicos NOD
Proteínas Nucleares/deficiência
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Hipermutação Somática de Imunoglobulina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Carrier Proteins); 0 (Nuclear Proteins); 0 (Rad51ap1 protein, mouse); EC 3.1.3.5 (5'-Nucleotidase); EC 3.5.4.- (AICDA (activation-induced cytidine deaminase)); EC 3.5.4.5 (Cytidine Deaminase); Q1O6DSW23R (4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700024


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[PMID]:29195795
[Au] Autor:Kozarski M; Kubacka D; Wojtczak BA; Kasprzyk R; Baranowski MR; Kowalska J
[Ad] Endereço:University of Warsaw, Faculty of Physics, Institute of Experimental Physics, Division of Biophysics, Pasteura 5, 02-093 Warsaw, Poland.
[Ti] Título:7-Methylguanosine monophosphate analogues with 5'-(1,2,3-triazoyl) moiety: Synthesis and evaluation as the inhibitors of cNIIIB nucleotidase.
[So] Source:Bioorg Med Chem;26(1):191-199, 2018 01 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The hydrolysis of nucleoside 5'-monophosphates to the corresponding nucleosides and inorganic phosphate is catalysed by 5'-nucleotidases, thereby contributing to the control of endogenous nucleotide turnover and affecting the fate of exogenously delivered nucleotide- and nucleoside-derived therapeutics in cells. A recently identified nucleotidase cNIIIB shows preference towards 7-methylguanosine monophosphate (m GMP) as a substrate, which suggests its potential involvement in mRNA degradation. However, the extent of biological functions and the significance of cNIIIB remains to be elucidated. Here, we synthesised a series of m GMP analogues carrying a 1,2,3-triazole moiety at the 5' position as the potential inhibitors of human cNIIIB. The compounds were synthesised by using the copper-catalysed azide-alkyne cycloaddition (CuAAC) between 5'-azido-5'-deoxy-7-methylguanosine and different phosphate or phosphonate derivatives carrying terminal alkyne. The analogues were evaluated as cNIIIB inhibitors using HPLC and malachite green assays, demonstrating that compound 1a, carrying a 1,2,3-triazoylphosphonate moiety, inhibits cNIIIB activity at micromolar concentrations (IC 87.8 ±â€¯7.5 µM), while other analogues showed no activity. In addition, compound 1d was identified as an artifical substrate for cNIIIB. Further characterization of inhibitor 1a revealed that it is poorly recognised by other m G-binding proteins, eIF4E and DcpS, indicating its selectivity towards cNIIIB. The first inhibitor (1a) and unnatural substrate (1d) of cNIIIB, identified here, can be used as molecular probes for the elucidation of biological roles of cNIIIB, including the verification of its proposed function in mRNA metabolism.
[Mh] Termos MeSH primário: 5´-Nucleotidase/antagonistas & inibidores
Inibidores Enzimáticos/farmacologia
Análogos de Capuz de RNA/farmacologia
Triazóis/farmacologia
[Mh] Termos MeSH secundário: 5'-Nucleotidase/metabolismo
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Seres Humanos
Estrutura Molecular
Análogos de Capuz de RNA/síntese química
Análogos de Capuz de RNA/química
Relação Estrutura-Atividade
Triazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (RNA Cap Analogs); 0 (Triazoles); 10162-58-0 (7-methylguanosine-5'-monophosphate); EC 3.1.3.5 (5'-Nucleotidase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180106
[Lr] Data última revisão:
180106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE


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[PMID]:28855210
[Au] Autor:Turcotte M; Allard D; Mittal D; Bareche Y; Buisseret L; José V; Pommey S; Delisle V; Loi S; Joensuu H; Kellokumpu-Lehtinen PL; Sotiriou C; Smyth MJ; Stagg J
[Ad] Endereço:Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Québec, Canada.
[Ti] Título:CD73 Promotes Resistance to HER2/ErbB2 Antibody Therapy.
[So] Source:Cancer Res;77(20):5652-5663, 2017 Oct 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Expression of the ectonucleotidase CD73 by tumor cells, stromal cells, and immune cells is associated in cancer with immune suppression. In this study, we investigated the role of CD73 on the activity of the anti-HER2/ErbB2 monoclonal antibody (mAb) trastuzumab. In a prospective, randomized phase III clinical trial evaluating the activity of trastuzumab, high levels of CD73 gene expression were associated significantly with poor clinical outcome. In contrast, high levels of PD-1 and PD-L1 were associated with improved clinical outcome. In immunocompetent mouse models of HER2/ErbB2-driven breast cancer, CD73 expression by tumor cells and host cells significantly suppressed immune-mediated responses mediated by anti-ErbB2 mAb. Furthermore, anti-CD73 mAb therapy enhanced the activity of anti-ErbB2 mAb to treat engrafted or spontaneous tumors as well as lung metastases. Gene ontology enrichment analysis from gene-expression data revealed a positive association of CD73 expression with extracellular matrix organization, TGFß genes, epithelial-to-mesenchymal transition (EMT) transcription factors and hypoxia-inducible-factor (HIF)-1 gene signature. Human mammary cells treated with TGFß or undergoing EMT upregulated CD73 cell-surface expression, confirming roles for these pathways. In conclusion, our findings establish CD73 in mediating resistance to trastuzumab and provide new insights into how CD73 is regulated in breast cancer. .
[Mh] Termos MeSH primário: 5´-Nucleotidase/imunologia
Anticorpos Monoclonais/fisiologia
Antígenos CD/imunologia
Antígenos de Neoplasias/imunologia
Neoplasias da Mama/terapia
Receptor ErbB-2/imunologia
Tetraspaninas/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/imunologia
Neoplasias da Mama/imunologia
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Modelos Animais de Doenças
Resistência a Medicamentos Antineoplásicos
Feminino
Proteínas Ligadas por GPI/imunologia
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Transgênicos
Terapia de Alvo Molecular
Distribuição Aleatória
Transdução de Sinais
Trastuzumab/imunologia
Trastuzumab/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (Cd37 protein, mouse); 0 (GPI-Linked Proteins); 0 (Tetraspanins); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Erbb2 protein, mouse); EC 2.7.10.1 (Receptor, ErbB-2); EC 3.1.3.5 (5'-Nucleotidase); EC 3.1.3.5 (NT5E protein, human); P188ANX8CK (Trastuzumab)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0707


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[PMID]:28717030
[Au] Autor:Kao DJ; Saeedi BJ; Kitzenberg D; Burney KM; Dobrinskikh E; Battista KD; Vázquez-Torres A; Colgan SP; Kominsky DJ
[Ad] Endereço:Mucosal Inflammation Program, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
[Ti] Título:Intestinal Epithelial Ecto-5'-Nucleotidase (CD73) Regulates Intestinal Colonization and Infection by Nontyphoidal Salmonella.
[So] Source:Infect Immun;85(10), 2017 Oct.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ecto-5'-nucleotidase (CD73) is expressed abundantly on the apical surface of intestinal epithelial cells (IECs) and functions as the terminal enzyme in the generation of extracellular adenosine. Previous work demonstrated that adenosine signaling in IECs results in a number of tissue-protective effects during inflammation; however, a rationale for its apical expression has been lacking. We hypothesized that the highly polarized expression of CD73 is indicative of an important role for extracellular adenosine as a mediator of host-microbe interactions. We show that adenosine harbors bacteriostatic activity against serovar Typhimurium that is not shared by the related purine metabolite 5'-AMP, inosine, or hypoxanthine. Analysis of colonization in IEC-specific CD73 knockout mice ( ) revealed a nearly 10-fold increase in colonization compared to that in controls. Despite the increased luminal colonization by , mice were protected against colitis and showed reduced burdens in viscera, suggesting that adenosine promotes dissemination. The knockdown of CD73 expression in cultured IECs resulted in dramatic defects in intraepithelial localization and replication as well as defective transepithelial translocation by In conclusion, we define a novel antimicrobial activity of adenosine in the gastrointestinal tract and unveil an important role for adenosine as a regulator of host-microbe interactions. These findings have broad implications for the development of new therapeutic agents for infectious disease.
[Mh] Termos MeSH primário: 5´-Nucleotidase/metabolismo
Adenosina/metabolismo
Interações Hospedeiro-Patógeno
Mucosa Intestinal/microbiologia
Salmonella enterica/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: 5'-Nucleotidase/deficiência
5'-Nucleotidase/genética
Adenosina/imunologia
Animais
Carga Bacteriana
Linhagem Celular
Células Epiteliais/microbiologia
Inflamação
Camundongos
Camundongos Knockout
Nucleotidases/metabolismo
Salmonella enterica/fisiologia
Salmonella typhimurium/crescimento & desenvolvimento
Salmonella typhimurium/fisiologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.3.- (Nucleotidases); EC 3.1.3.31 (nucleotidase); EC 3.1.3.5 (5'-Nucleotidase); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE


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[PMID]:28710007
[Au] Autor:Doleski PH; Ten Caten MV; Passos DF; Castilhos LG; Leal DBR; Machado VS; Bottari NB; Vogel FF; Mendes RE; da Silva AS
[Ad] Endereço:Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Brazil; Department of Biochemistry and Molecular Biology, Universidade Federal de Santa Maria (UFSM), Brazil.
[Ti] Título:Toxoplasmosis treatment with diphenyl diselenide in infected mice modulates the activity of purinergic enzymes and reduces inflammation in spleen.
[So] Source:Exp Parasitol;181:7-13, 2017 Oct.
[Is] ISSN:1090-2449
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Toxoplasma gondii, an intracellular protozoan, may cause chronic infection in the brain tissue of the host inducing a systemic pro-inflammatory profile. Chronic infections can induce numerous physiological changes, such as alterations in the immune and oxidative profiles. Diphenyl diselenide (PhSe) , an organoselenium compound, has shown antioxidant and immunomodulatory activities in recent studies. So, the aim of this study was to investigate the activity of purinergic enzymes and reactive oxygen species (ROS) in serum and spleen of mice chronically infected by T. gondii, untreated and treated with (PhSe) . For this experiment, were divided into four groups: Group A (healthy mice), Group B (healthy mice treated with (PhSe) ), Group C (infected mice) and Group D (infected mice treated with (PhSe) ). Group C and group D were infected via oral route with ME49 Toxoplasma gondii strain. Groups B and D were treated subcutaneously with 5 µmol kg of (PhSe) . Chronic T. gondii infection induced splenomegaly and physiological changes in the spleen and raised histologic inflammatory markers, ROS levels and the activity of purinergic enzymes activity such as NTPDase, 5´nucleotidase and ADA. In serum, the infection increased 5´nucleotidase and ADA activities. (PhSe) per se has managed to decrease ROS levels and ADA activity and increase NTPDase and 5´nucleotidase in spleen. In infected mice, treatment with (PhSe) reversed splenomegaly, reduced histological inflammatory markers, ROS levels and ADA activity in the spleen. Our results prove that chronic toxoplasmosis can induce splenomegaly, heightens ROS levels and purinergic enzyme activity in mice. These results suggest that (PhSe) is a potential therapy for the alterations found in the spleen in chronic T. gondii infection.
[Mh] Termos MeSH primário: Derivados de Benzeno/uso terapêutico
Nucleotidases/sangue
Compostos Organosselênicos/uso terapêutico
Baço/patologia
Toxoplasmose Animal/tratamento farmacológico
[Mh] Termos MeSH secundário: 5'-Nucleotidase/sangue
5'-Nucleotidase/metabolismo
Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Derivados de Benzeno/farmacologia
Feminino
Inflamação/tratamento farmacológico
Camundongos
Nucleotidases/metabolismo
Compostos Organosselênicos/farmacologia
Espécies Reativas de Oxigênio/sangue
Espécies Reativas de Oxigênio/metabolismo
Baço/efeitos dos fármacos
Baço/enzimologia
Baço/metabolismo
Toxoplasmose Animal/enzimologia
Toxoplasmose Animal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzene Derivatives); 0 (Organoselenium Compounds); 0 (Reactive Oxygen Species); 1666-13-3 (diphenyldiselenide); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate); EC 3.1.3.- (Nucleotidases); EC 3.1.3.5 (5'-Nucleotidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE


  10 / 3556 MEDLINE  
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[PMID]:28652246
[Au] Autor:Reinhardt J; Landsberg J; Schmid-Burgk JL; Ramis BB; Bald T; Glodde N; Lopez-Ramos D; Young A; Ngiow SF; Nettersheim D; Schorle H; Quast T; Kolanus W; Schadendorf D; Long GV; Madore J; Scolyer RA; Ribas A; Smyth MJ; Tumeh PC; Tüting T; Hölzel M
[Ad] Endereço:Unit for RNA Biology, Department of Clinical Chemistry and Clinical Pharmacology, University of Bonn, Bonn, Germany.
[Ti] Título:MAPK Signaling and Inflammation Link Melanoma Phenotype Switching to Induction of CD73 during Immunotherapy.
[So] Source:Cancer Res;77(17):4697-4709, 2017 Sep 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Evolution of tumor cell phenotypes promotes heterogeneity and therapy resistance. Here we found that induction of CD73, the enzyme that generates immunosuppressive adenosine, is linked to melanoma phenotype switching. Activating MAPK mutations and growth factors drove CD73 expression, which marked both nascent and full activation of a mesenchymal-like melanoma cell state program. Proinflammatory cytokines like TNFα cooperated with MAPK signaling through the c-Jun/AP-1 transcription factor complex to activate CD73 transcription by binding to an intronic enhancer. In a mouse model of T-cell immunotherapy, CD73 was induced in relapse melanomas, which acquired a mesenchymal-like phenotype. We also detected CD73 upregulation in melanoma patients progressing under adoptive T-cell transfer or immune checkpoint blockade, arguing for an adaptive resistance mechanism. Our work substantiates CD73 as a target to combine with current immunotherapies, but its dynamic regulation suggests limited value of CD73 pretreatment expression as a biomarker to stratify melanoma patients. .
[Mh] Termos MeSH primário: 5´-Nucleotidase/metabolismo
Regulação Neoplásica da Expressão Gênica
Imunoterapia
Inflamação/complicações
Melanoma/patologia
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Linfócitos T/transplante
[Mh] Termos MeSH secundário: Adenosina/metabolismo
Transferência Adotiva
Animais
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Inflamação/patologia
Melanoma/imunologia
Melanoma/metabolismo
Melanoma/terapia
Camundongos
Camundongos Endogâmicos C57BL
Invasividade Neoplásica
Prognóstico
Estudos Retrospectivos
Fator de Transcrição AP-1/metabolismo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Transcription Factor AP-1); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 3.1.3.5 (5'-Nucleotidase); EC 3.1.3.5 (NT5E protein, human); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0395



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