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[PMID]:29381830
[Au] Autor:Sioud M
[Ad] Endereço:Department of Cancer Immunology, Oslo University Hospital, The Norwegian Radium Hospital, Montebello, Oslo, Norway.
[Ti] Título:T-cell cross-reactivity may explain the large variation in how cancer patients respond to checkpoint inhibitors.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The therapeutic use of the immune system to specifically attack tumours has been a long-standing vision among tumour immunologists. Recently, the use of checkpoint inhibitors to turn-off immunosuppressive signals has proven to be effective in enhancing T-cell reactivity against patient-specific neoantigens, resulting from somatic mutations. Several of the identified T-cell epitopes share similarity with common bacterial and viral antigens, suggesting the involvement of pre-existing microbial cross-reactive T cells in rapid and durable tumour regression seen in some patients. This notion of T-cell cross-reactivity is further supported by the findings that intestinal bacteria can influence checkpoint-blockade therapy. Moreover, early data indicate the presence of such T cells in long-term survival breast cancer patients. This review highlights the main challenges for cancer immunotherapy and discusses the potential contribution of T-cell cross-reactivity in cancer immunotherapy and whether it can be used as a biomarker to predict the responsiveness to checkpoint inhibitors.
[Mh] Termos MeSH primário: Reações Cruzadas/imunologia
Imunoterapia/métodos
Neoplasias/imunologia
Neoplasias/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Antígenos de Bactérias/imunologia
Antígenos de Neoplasias/imunologia
Antígenos Virais/imunologia
Biomarcadores Tumorais/imunologia
Antígeno CTLA-4/antagonistas & inibidores
Células Dendríticas/imunologia
Epitopos de Linfócito T/imunologia
Seres Humanos
Ativação Linfocitária/imunologia
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Receptores Imunológicos/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Antigens, Neoplasm); 0 (Antigens, Viral); 0 (Biomarkers, Tumor); 0 (CTLA-4 Antigen); 0 (Epitopes, T-Lymphocyte); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Immunologic); 0 (TIGIT protein, human)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12643


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[PMID]:28449072
[Au] Autor:Vasta GR; Feng C; González-Montalbán N; Mancini J; Yang L; Abernathy K; Frost G; Palm C
[Ad] Endereço:Department of Microbiology and Immunology, University of Maryland School of Medicine, UMB, and Institute of Marine and Environmental Technology, Columbus Center, 701 East Pratt Street, Baltimore, MD 21202, USA.
[Ti] Título:Functions of galectins as 'self/non-self'-recognition and effector factors.
[So] Source:Pathog Dis;75(5), 2017 Jul 31.
[Is] ISSN:2049-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Carbohydrate structures on the cell surface encode complex information that through specific recognition by carbohydrate-binding proteins (lectins) modulates interactions between cells, cells and the extracellular matrix, or mediates recognition of potential microbial pathogens. Galectins are a family of ß-galactoside-binding lectins, which are evolutionary conserved and have been identified in most organisms, from fungi to invertebrates and vertebrates, including mammals. Since their discovery in the 1970s, their biological roles, initially understood as limited to recognition of endogenous carbohydrate ligands in embryogenesis and development, have expanded in recent years by the discovery of their roles in tissue repair and regulation of immune homeostasis. More recently, evidence has accumulated to support the notion that galectins can also bind glycans on the surface of potentially pathogenic microbes, and function as recognition and effector factors in innate immunity, thus establishing a new paradigm. Furthermore, some parasites 'subvert' the recognition roles of the vector/host galectins for successful attachment or invasion. These recent findings have revealed a striking functional diversification in this structurally conserved lectin family.
[Mh] Termos MeSH primário: Galectinas/metabolismo
Interações Hospedeiro-Patógeno
Evasão da Resposta Imune
Imunidade Inata
Receptores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Galectins); 0 (Receptors, Immunologic)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1093/femspd/ftx046


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[PMID]:28747428
[Au] Autor:Slootweg E; Koropacka K; Roosien J; Dees R; Overmars H; Lankhorst RK; van Schaik C; Pomp R; Bouwman L; Helder J; Schots A; Bakker J; Smant G; Goverse A
[Ad] Endereço:Laboratory of Nematology, Department of Plant Sciences, Wageningen University, 6708 PD Wageningen, The Netherlands.
[Ti] Título:Sequence Exchange between Homologous NB-LRR Genes Converts Virus Resistance into Nematode Resistance, and Vice Versa.
[So] Source:Plant Physiol;175(1):498-510, 2017 Sep.
[Is] ISSN:1532-2548
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plants have evolved a limited repertoire of NB-LRR disease resistance ( ) genes to protect themselves against myriad pathogens. This limitation is thought to be counterbalanced by the rapid evolution of NB-LRR proteins, as only a few sequence changes have been shown to be sufficient to alter resistance specificities toward novel strains of a pathogen. However, little is known about the flexibility of NB-LRR genes to switch resistance specificities between phylogenetically unrelated pathogens. To investigate this, we created domain swaps between the close homologs and , which confer resistance in potato ( ) to the cyst nematode and , respectively. The genetic fusion of the CC-NB-ARC of Gpa2 with the LRR of Rx1 (Gpa2 /Rx1 ) results in autoactivity, but lowering the protein levels restored its specific activation response, including extreme resistance to in potato shoots. The reciprocal chimera (Rx1 /Gpa2 ) shows a loss-of-function phenotype, but exchange of the first three LRRs of Gpa2 by the corresponding region of Rx1 was sufficient to regain a wild-type resistance response to in the roots. These data demonstrate that exchanging the recognition moiety in the LRR is sufficient to convert extreme virus resistance in the leaves into mild nematode resistance in the roots, and vice versa. In addition, we show that the CC-NB-ARC can operate independently of the recognition specificities defined by the LRR domain, either aboveground or belowground. These data show the versatility of NB-LRR genes to generate resistance to unrelated pathogens with completely different lifestyles and routes of invasion.
[Mh] Termos MeSH primário: Resistência à Doença/genética
Doenças das Plantas/imunologia
Proteínas de Plantas/metabolismo
Potexvirus/fisiologia
Solanum tuberosum/genética
Tylenchoidea/fisiologia
[Mh] Termos MeSH secundário: Animais
Mutação com Perda de Função
Fenótipo
Doenças das Plantas/parasitologia
Doenças das Plantas/virologia
Folhas de Planta/genética
Folhas de Planta/imunologia
Folhas de Planta/parasitologia
Folhas de Planta/virologia
Proteínas de Plantas/genética
Raízes de Plantas/genética
Raízes de Plantas/imunologia
Raízes de Plantas/parasitologia
Raízes de Plantas/virologia
Brotos de Planta/genética
Brotos de Planta/imunologia
Brotos de Planta/parasitologia
Brotos de Planta/virologia
Domínios Proteicos
Proteínas/genética
Proteínas/metabolismo
Receptores Imunológicos/genética
Receptores Imunológicos/metabolismo
Proteínas Recombinantes de Fusão
Solanum tuberosum/imunologia
Solanum tuberosum/parasitologia
Solanum tuberosum/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Proteins); 0 (Proteins); 0 (Receptors, Immunologic); 0 (Recombinant Fusion Proteins); 0 (leucine-rich repeat proteins)
[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:170728
[St] Status:MEDLINE
[do] DOI:10.1104/pp.17.00485


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[PMID]:29261670
[Au] Autor:Jeffery HC; McDowell P; Lutz P; Wawman RE; Roberts S; Bagnall C; Birtwistle J; Adams DH; Oo YH
[Ad] Endereço:Centre for Liver Research and National Institute for Health Research Birmingham Biomedical Research Centre, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
[Ti] Título:Human intrahepatic ILC2 are IL-13positive amphiregulinpositive and their frequency correlates with model of end stage liver disease score.
[So] Source:PLoS One;12(12):e0188649, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Innate lymphoid cells (ILC) have been implicated in the initiation of inflammation and fibrosis in mice. However, ILC have not been characterized in inflamed human liver tissue. METHODS: Human intrahepatic lymphocytes were isolated by mechanical digestion and phenotyped by flow cytometry. Conditioned medium from cultures of primary human biliary epithelial cells, stellate cells, fibroblasts and inflamed human liver tissue was used to model the effects of the inflammatory liver environment of ILC phenotype and function. RESULTS: All three ILC subsets were present in the human liver, with the ILC1 (CRTH2negCD117neg) subset constituting around 70% of intrahepatic ILCs. Both NCRpos (NKp44+) and NCRneg ILC3 (CRTH2negCD117pos) subsets were also detected. ILC2 (CRTH2pos) frequency correlated with disease severity measured by model of end stage liver disease (MELD) scoring leading us to study this subset in more detail. ILC2 displayed a tissue resident CD69+ CD161++ phenotype and expressed chemokine receptor CCR6 allowing them to respond to CCL20 secreted by cholangiocytes and stellate cells. ILC2 expressed integrins VLA-5 and VLA-6 and the IL-2 and IL-7 cytokine receptors CD25 and CD127 although IL-2 and IL-7 were barely detectable in inflamed liver tissue. Although biliary epithelial cells secrete IL-33, intrahepatic ILC2 had low expression of the ST2 receptor. Intrahepatic ILC2 secreted the immunoregulatory and repair cytokines IL-13 and amphiregulin. CONCLUSIONS: Intrahepatic ILC2 express receptors allowing them to be recruited to bile ducts in inflamed portal tracts. Their frequencies increased with worsening liver function. Their secretion of IL-13 and amphiregulin suggests they may be recruited to promote resolution and repair and thereby they may contribute to ongoing fibrogenesis in liver disease.
[Mh] Termos MeSH primário: Anfirregulina/metabolismo
Doença Hepática Terminal/imunologia
Imunidade Inata
Interleucina-13/metabolismo
Fígado/metabolismo
Linfócitos/metabolismo
Modelos Biológicos
[Mh] Termos MeSH secundário: Células Epiteliais/metabolismo
Seres Humanos
Inflamação/patologia
Integrinas/genética
Integrinas/metabolismo
Interleucina-2/metabolismo
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Interleucina-7/metabolismo
Fígado/patologia
Contagem de Linfócitos
Subfamília B de Receptores Semelhantes a Lectina de Células NK/metabolismo
Fenótipo
Receptores de Quimiocinas/genética
Receptores de Quimiocinas/metabolismo
Receptores Imunológicos/metabolismo
Receptores de Prostaglandina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amphiregulin); 0 (Integrins); 0 (Interleukin-13); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-7); 0 (NK Cell Lectin-Like Receptor Subfamily B); 0 (Receptors, Chemokine); 0 (Receptors, Immunologic); 0 (Receptors, Prostaglandin); 0 (prostaglandin D2 receptor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188649


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[PMID]:29221729
[Au] Autor:Alcántara-Hernández M; Leylek R; Wagar LE; Engleman EG; Keler T; Marinkovich MP; Davis MM; Nolan GP; Idoyaga J
[Ad] Endereço:Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA; Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
[Ti] Título:High-Dimensional Phenotypic Mapping of Human Dendritic Cells Reveals Interindividual Variation and Tissue Specialization.
[So] Source:Immunity;47(6):1037-1050.e6, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Given the limited efficacy of clinical approaches that rely on ex vivo generated dendritic cells (DCs), it is imperative to design strategies that harness specialized DC subsets in situ. This requires delineating the expression of surface markers by DC subsets among individuals and tissues. Here, we performed a multiparametric phenotypic characterization and unbiased analysis of human DC subsets in blood, tonsil, spleen, and skin. We uncovered previously unreported phenotypic heterogeneity of human cDC2s among individuals, including variable expression of functional receptors such as CD172a. We found marked differences in DC subsets localized in blood and lymphoid tissues versus skin, and a striking absence of the newly discovered Axl DCs in the skin. Finally, we evaluated the capacity of anti-receptor monoclonal antibodies to deliver vaccine components to skin DC subsets. These results offer a promising path for developing DC subset-specific immunotherapies that cannot be provided by transcriptomic analysis alone.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/imunologia
Variação Biológica Individual
Células Dendríticas/imunologia
Fenótipo
Proteínas Proto-Oncogênicas/imunologia
Receptores Proteína Tirosina Quinases/imunologia
Receptores Imunológicos/imunologia
Pele/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/química
Anticorpos Monoclonais/metabolismo
Anticorpos Monoclonais/farmacocinética
Antígenos CD/genética
Antígenos CD/imunologia
Antígenos de Diferenciação/genética
Biomarcadores/análise
Vacinas Anticâncer/administração & dosagem
Vacinas Anticâncer/biossíntese
Citofotometria/métodos
Células Dendríticas/citologia
Feminino
Expressão Gênica
Seres Humanos
Imunofenotipagem
Imunoterapia
Linfonodos/citologia
Linfonodos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Terapia de Alvo Molecular
Neoplasias/genética
Neoplasias/imunologia
Neoplasias/patologia
Neoplasias/terapia
Especificidade de Órgãos
Tonsila Palatina/citologia
Tonsila Palatina/imunologia
Proteínas Proto-Oncogênicas/deficiência
Proteínas Proto-Oncogênicas/genética
Receptores Proteína Tirosina Quinases/deficiência
Receptores Proteína Tirosina Quinases/genética
Receptores Imunológicos/genética
Pele/citologia
Baço/citologia
Baço/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, CD); 0 (Antigens, Differentiation); 0 (Biomarkers); 0 (Cancer Vaccines); 0 (Proto-Oncogene Proteins); 0 (Receptors, Immunologic); 0 (SIRPA protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (axl receptor tyrosine kinase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:29202958
[Au] Autor:Jiang T; Wang Y; Zhu M; Wang Y; Huang M; Jin G; Guo X; Sha J; Dai J; Hu Z
[Ad] Endereço:State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, People's Republic of China; Department of Epidemiology and Biostatistics, School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China.
[Ti] Título:Transcriptome-wide association study revealed two novel genes associated with nonobstructive azoospermia in a Chinese population.
[So] Source:Fertil Steril;108(6):1056-1062.e4, 2017 Dec.
[Is] ISSN:1556-5653
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate the associations between genetically cis-regulated gene expression levels and nonobstructive azoospermia (NOA) susceptibility. DESIGN: Transcriptome-wide association study (TWAS). SETTING: Medical university. INTERVENTIONS: None. MAIN OUTCOME MEASURE(S): The cis-hg values for each gene were estimated with GCTA software. The effect sizes of cis-single-nucleotide polymorphisms (SNPs) on gene expression were measured using GEMMA software. Gene expression levels were entered into our existing NOA GWAS cohort using GEMMA software. The TWAS P-values were calculated using logistic regression models. RESULT(S): Expression levels of 1,296 cis-heritable genes were entered into our existing NOA GWAS data. The TWAS results identified two novel genes as statistically significantly associated with NOA susceptibility: PILRA and ZNF676. In addition, 6p21.32, previously reported in NOA GWAS, was further validated to be a susceptible region to NOA risk. CONCLUSION(S): Analysis with TWAS provides fruitful targets for follow-up functional studies.
[Mh] Termos MeSH primário: Azoospermia/genética
Proteínas de Ligação a DNA/genética
Fertilidade/genética
Glicoproteínas de Membrana/genética
Polimorfismo de Nucleotídeo Único
Receptores Imunológicos/genética
Transcriptoma
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
Azoospermia/diagnóstico
Azoospermia/etnologia
Azoospermia/fisiopatologia
Estudos de Casos e Controles
China
Biologia Computacional
Bases de Dados Genéticas
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Modelos Logísticos
Masculino
Razão de Chances
Fenótipo
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Membrane Glycoproteins); 0 (PILRA protein, human); 0 (Receptors, Immunologic); 0 (ZNF676 protein, human)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:28747319
[Au] Autor:Sudworth A; Vaage JT; Inngjerdingen M; Kveberg L
[Ad] Endereço:Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
[Ti] Título:Frontline Science: A hyporesponsive subset of rat NK cells negative for Ly49s3 and NKR-P1B are precursors to the functionally mature NKR-P1B subset.
[So] Source:J Leukoc Biol;102(6):1289-1298, 2017 Dec.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rat NK cells are divided into major subsets expressing either Ly49 receptors or the inhibitory NKR-P1B receptor in conjunction with NKG2A/C/E receptors. A minor subset of NKp46 cells lacking expression of both Ly49 receptors and NKR-P1B is present in blood and spleen and is associated with decreased functional competence. We hypothesized that this subset may represent precursors to Ly49 and/or NKR-P1B NK cells. When cultured in vitro in IL-2 and IL-15 or adoptively transferred to syngeneic hosts, a portion of NKR-P1B Ly49s3 cells transformed to express NKR-P1B, but very little Ly49s3. Acquisition of NKR-P1B by NKR-P1B Ly49s3 cells coincided with increased degranulation. In addition, although NKR-P1B Ly49s3 cells highly proliferate, proliferative activity was reduced upon acquisition of NKR-P1B at comparable levels to bona fide NKR-P1B NK cells. A fraction of NKR-P1B Ly49s3 cells remained negative for NKR-P1B, both in vitro and after adoptive transfer in vivo. Most NKR-P1B Ly49s3 cells expressed the transcription factor Eomesodermin and NK cell markers, indicating that these cells represent conventional NK cells. Our findings suggest that the NKR-P1B Ly49s3 NK cells are precursors to NKR-P1B single-positive cells and that functional competence is acquired upon expression of NKR-P1B.
[Mh] Termos MeSH primário: Diferenciação Celular
Células Matadoras Naturais/citologia
Células Matadoras Naturais/metabolismo
Subfamília A de Receptores Semelhantes a Lectina de Células NK/metabolismo
Receptores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Antígeno CD11b/metabolismo
Degranulação Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Interleucina-15/farmacologia
Interleucina-2/farmacologia
Células Matadoras Naturais/efeitos dos fármacos
Células Matadoras Naturais/fisiologia
Fenótipo
Ratos
Baço/citologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Interleukin-15); 0 (Interleukin-2); 0 (Ly49s3 protein, rat); 0 (NK Cell Lectin-Like Receptor Subfamily A); 0 (NKR-P1B protein, rat); 0 (Receptors, Immunologic)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.1HI0517-177RR


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[PMID]:27770832
[Au] Autor:Bjorke B; Shoja-Taheri F; Kim M; Robinson GE; Fontelonga T; Kim KT; Song MR; Mastick GS
[Ad] Endereço:Department of Biology, University of Nevada, Reno, NV, 89557, USA.
[Ti] Título:Contralateral migration of oculomotor neurons is regulated by Slit/Robo signaling.
[So] Source:Neural Dev;11(1):18, 2016 10 22.
[Is] ISSN:1749-8104
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oculomotor neurons develop initially like typical motor neurons, projecting axons out of the ventral midbrain to their ipsilateral targets, the extraocular muscles. However, in all vertebrates, after the oculomotor nerve (nIII) has reached the extraocular muscle primordia, the cell bodies that innervate the superior rectus migrate to join the contralateral nucleus. This motor neuron migration represents a unique strategy to form a contralateral motor projection. Whether migration is guided by diffusible cues remains unknown. METHODS: We examined the role of Slit chemorepellent signals in contralateral oculomotor migration by analyzing mutant mouse embryos. RESULTS: We found that the ventral midbrain expresses high levels of both Slit1 and 2, and that oculomotor neurons express the repellent Slit receptors Robo1 and Robo2. Therefore, Slit signals are in a position to influence the migration of oculomotor neurons. In Slit 1/2 or Robo1/2 double mutant embryos, motor neuron cell bodies migrated into the ventral midbrain on E10.5, three days prior to normal migration. These early migrating neurons had leading projections into and across the floor plate. In contrast to the double mutants, embryos which were mutant for single Slit or Robo genes did not have premature migration or outgrowth on E10.5, demonstrating a cooperative requirement of Slit1 and 2, as well as Robo1 and 2. To test how Slit/Robo midline repulsion is modulated, we found that the normal migration did not require the receptors Robo3 and CXCR4, or the chemoattractant, Netrin 1. The signal to initiate contralateral migration is likely autonomous to the midbrain because oculomotor neurons migrate in embryos that lack either nerve outgrowth or extraocular muscles, or in cultured midbrains that lacked peripheral tissue. CONCLUSION: Overall, our results demonstrate that a migratory subset of motor neurons respond to floor plate-derived Slit repulsion to properly control the timing of contralateral migration.
[Mh] Termos MeSH primário: Orientação de Axônios
Movimento Celular
Peptídeos e Proteínas de Sinalização Intercelular/fisiologia
Neurônios Motores/fisiologia
Proteínas do Tecido Nervoso/fisiologia
Nervo Oculomotor/crescimento & desenvolvimento
Receptores Imunológicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Membrana/fisiologia
Mesencéfalo/fisiologia
Camundongos
Fatores de Crescimento Neural/fisiologia
Netrina-1
Receptores CXCR4/fisiologia
Transdução de Sinais
Proteínas Supressoras de Tumor/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCR4 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Nerve Growth Factors); 0 (Nerve Tissue Proteins); 0 (Ntn1 protein, mouse); 0 (Receptors, CXCR4); 0 (Receptors, Immunologic); 0 (Robo2 protein, mouse); 0 (Robo3 protein, mouse); 0 (Slit homolog 2 protein); 0 (Slit1 protein, mouse); 0 (Tumor Suppressor Proteins); 0 (roundabout protein); 158651-98-0 (Netrin-1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28465241
[Au] Autor:Kizuka Y; Kitazume S; Taniguchi N
[Ad] Endereço:Disease Glycomics Team, Systems Glycobiology Research Group, Global Research Cluster, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan. Electronic address: y.kizuka@riken.jp.
[Ti] Título:N-glycan and Alzheimer's disease.
[So] Source:Biochim Biophys Acta;1861(10):2447-2454, 2017 10.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Alzheimer's disease (AD) is a major form of dementia. Many evidence-based clinical trials have been performed, but no effective treatment has yet been developed. This suggests that our understanding of AD patho-mechanisms is still insufficient. In particular, the pathological roles of posttranslational modifications including glycosylation have remained poorly understood, but recent advances in glycobiology technology have gradually revealed that sugar modifications of AD-related molecules are profoundly involved in the onset and progression of this disease. SCOPE OF REVIEW: We summarize the roles of N-glycans in AD pathogenesis and progression, particularly focusing on key AD-related molecules, including amyloid precursor protein (APP), α-, ß-, and γ-secretases, and tau. MAJOR CONCLUSIONS: Biochemical, genetic and pharmacological studies have gradually revealed how N-glycans regulate AD development and progression through functional modulation of the key glycoproteins. These findings suggest that further glycobiology approaches in AD research will reveal novel glycan-based drug targets and early biomarkers of AD. However, N-glycan structures of these molecules in physiological and disease conditions and their precise functions are still largely unclear. Deeper glycobiology studies will be needed to reveal how AD pathology is regulated by glycosylation. GENERAL SIGNIFICANCE: It is now known that N-glycans play significant roles in AD development. However, specific pathological functions of particular glycan epitopes on each AD-related glycoprotein are still poorly understood. Future glycobiology studies with more sensitive glycoproteomic techniques and a wider variety of chemical glycosylation inhibitors could contribute to the development of novel glycan-based AD therapeutics. This article is part of a Special Issue entitled Neuro-glycoscience, edited by Kenji Kadomatsu and Hiroshi Kitagawa.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Precursor de Proteína beta-Amiloide/metabolismo
Polissacarídeos/metabolismo
Processamento de Proteína Pós-Traducional
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/genética
Doença de Alzheimer/patologia
Secretases da Proteína Precursora do Amiloide/genética
Precursor de Proteína beta-Amiloide/genética
Sequência de Carboidratos
Glicosilação
Seres Humanos
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Neprilisina/genética
Neprilisina/metabolismo
Polissacarídeos/química
Proteólise
Receptores Imunológicos/genética
Receptores Imunológicos/metabolismo
Transdução de Sinais
Proteínas tau/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (APP protein, human); 0 (Amyloid beta-Protein Precursor); 0 (MAPT protein, human); 0 (Membrane Glycoproteins); 0 (Polysaccharides); 0 (Receptors, Immunologic); 0 (TREM2 protein, human); 0 (tau Proteins); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171130
[Lr] Data última revisão:
171130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:28981752
[Au] Autor:Yui A; Akiba H; Kudo S; Nakakido M; Nagatoishi S; Tsumoto K
[Ad] Endereço:Department of Bioengineering, School of Engineering, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8656, Japan.
[Ti] Título:Thermodynamic analyses of amino acid residues at the interface of an antibody B2212A and its antigen roundabout homolog 1.
[So] Source:J Biochem;162(4):255-258, 2017 Oct 01.
[Is] ISSN:1756-2651
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Artificial affinity maturation of antibodies is promising but often shows difficulties because the roles of each amino acid residue are not well known. To elucidate their roles in affinity against the antigen and thermal stability, interface residues in single-chain Fv of an antibody B2212A with its antigen roundabout homolog 1 were mutated and analyzed. Some amino acids played important roles in the affinity while others contributed to thermal stability.
[Mh] Termos MeSH primário: Aminoácidos/química
Anticorpos/química
Anticorpos/imunologia
Antígenos/química
Proteínas do Tecido Nervoso/química
Proteínas do Tecido Nervoso/imunologia
Receptores Imunológicos/química
Receptores Imunológicos/imunologia
Termodinâmica
[Mh] Termos MeSH secundário: Aminoácidos/imunologia
Antígenos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Antibodies); 0 (Antigens); 0 (Nerve Tissue Proteins); 0 (Receptors, Immunologic); 0 (roundabout protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1093/jb/mvx050



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