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[PMID]:28470667
[Au] Autor:Tanaka T; Zhang W; Sun Y; Shuai Z; Chida AS; Kenny TP; Yang GX; Sanz I; Ansari A; Bowlus CL; Ippolito GC; Coppel RL; Okazaki K; He XS; Leung PSC; Gershwin ME
[Ad] Endereço:Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, Davis, CA.
[Ti] Título:Autoreactive monoclonal antibodies from patients with primary biliary cholangitis recognize environmental xenobiotics.
[So] Source:Hepatology;66(3):885-895, 2017 09.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A major problem in autoimmunity has been identification of the earliest events that lead to breach of tolerance. Although there have been major advances in dissecting effector pathways and the multilineage immune responses to mitochondrial self-antigens in primary biliary cholangitis, the critical links between environmental factors and tolerance remain elusive. We hypothesized that environmental xenobiotic modification of the E2 subunit of the pyruvate dehydrogenase (PDC-E2) inner lipoyl domain can lead to loss of tolerance to genetically susceptible hosts. Previously we demonstrated that serum anti-PDC-E2 autoantibodies cross-react with the chemical xenobiotics 2-octynoic acid and 6,8-bis (acetylthio) octanoic acid and further that there is a high frequency of PDC-E2-specific peripheral plasmablasts. Herein we generated 104 recombinant monoclonal antibodies (mAbs) based on paired heavy-chain and light-chain variable regions of individual plasmablasts derived from primary biliary cholangitis patients. We identified 32 mAbs reactive with native PDC-E2, including 20 specific for PDC-E2 and 12 cross-reactive with both PDC-E2 and 2-octynoic acid and 6,8-bis (acetylthio) octanoic acid. A lower frequency of replacement somatic hypermutations, indicating a lower level of affinity maturation, was observed in the complementarity-determining regions of the cross-reactive mAbs in comparison to mAbs exclusively recognizing PDC-E2 or those for irrelevant antigens. In particular, when the highly mutated heavy-chain gene of a cross-reactive mAb was reverted to the germline sequence, the PDC-E2 reactivity was reduced dramatically, whereas the xenobiotic reactivity was retained. Importantly, cross-reactive mAbs also recognized lipoic acid, a mitochondrial fatty acid that is covalently bound to PDC-E2. CONCLUSION: Our data reflect that chemically modified lipoic acid or lipoic acid itself, through molecular mimicry, is the initial target that leads to the development of primary biliary cholangitis. (Hepatology 2017;66:885-895).
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Autoantígenos/imunologia
Autoimunidade/genética
Colangite/imunologia
Colangite/patologia
Xenobióticos/imunologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/metabolismo
Autoantígenos/genética
Autoimunidade/imunologia
Feminino
Amplificação de Genes
Seres Humanos
Immunoblotting
Masculino
Mimetismo Molecular/genética
Reação em Cadeia da Polimerase em Tempo Real
Sensibilidade e Especificidade
Ácido Tióctico/imunologia
Ácido Tióctico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Autoantigens); 0 (Xenobiotics); 73Y7P0K73Y (Thioctic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29245


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[PMID]:29370185
[Au] Autor:Kim H; Kimoto T; Sakai S; Takahashi E; Kido H
[Ad] Endereço:Division of Enzyme Chemistry, Institute for Enzyme Research, Tokushima University, Tokushima, Japan.
[Ti] Título:Adjuvanting influenza hemagglutinin vaccine with a human pulmonary surfactant-mimicking synthetic compound SF-10 induces local and systemic cell-mediated immunity in mice.
[So] Source:PLoS One;13(1):e0191133, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We reported previously that intranasal instillation of a synthetic human pulmonary surfactant with a carboxy vinyl polymer as a viscosity improver, named SF-10, shows potent adjuvanticity for humoral immunity in mice and cynomolgus monkeys. SF-10 effectively induces influenza hemagglutinin vaccine (HAv)-specific IgA in nasal and lung washes and IgG in sera with their neutralizing activities. Since CD8+ T cell-mediated protection is an important requirement for adaptive immunity, we investigated in this study the effects of SF-10 with antigen on local and systemic cell-mediated immunity. Nasal instillation of ovalbumin, a model antigen, combined with SF-10 efficiently delivered antigen to mucosal dendritic and epithelial cells and promoted cross-presentation in antigen presenting cells, yielding a high percentage of ovalbumin-specific cytotoxic T lymphocytes in the nasal mucosa, compared with ovalbumin alone. Nasal immunization of HAv-SF-10 also induced HAv-specific cytotoxic T lymphocytes and upregulated granzyme B expression in splenic CD8+ T cells with their high cytotoxicity against target cells pulsed with HA peptide. Furthermore, nasal vaccination of HAv-SF-10 significantly induced higher cytotoxic T lymphocytes-mediated cytotoxicity in the lungs and cervical lymph nodes in the early phase of influenza virus infection compared with HAv alone. Protective immunity induced by HAv-SF-10 against lethal influenza virus infection was partially and predominantly suppressed after depletion of CD8+ and CD4+ T cells (induced by intraperitoneal injection of the corresponding antibodies), respectively, suggesting that CD4+ T cells predominantly and CD8+ T cells partially contribute to the protective immunity in the advanced stage of influenza virus infection. These results suggest that SF-10 promotes effective antigen delivery to antigen presenting cells, activates CD8+ T cells via cross-presentation, and induces cell-mediated immune responses against antigen.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/administração & dosagem
Hemaglutinação por Vírus/imunologia
Imunidade Celular
Vacinas contra Influenza/administração & dosagem
Mimetismo Molecular
Surfactantes Pulmonares/química
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Feminino
Vacinas contra Influenza/imunologia
Depleção Linfocítica
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Mucosa Nasal/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Influenza Vaccines); 0 (Pulmonary Surfactants)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191133


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[PMID]:29191386
[Au] Autor:Xue H; Tian GY
[Ad] Endereço:Department of Pathology, Jinhua People's Hospital, Jinhua City, Zhejiang Province, 321000, China.
[Ti] Título:MiR-429 regulates the metastasis and EMT of HCC cells through targeting RAB23.
[So] Source:Arch Biochem Biophys;637:48-55, 2018 01 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Accumulating documents have revealed that microRNAs (miRNAs) play critical roles in the development and progression of tumors. MiR-429 has been reported to be involved in regulating various cellular processes. However, its biological role and underlying mechanism in hepatocellular carcinoma (HCC) still need to be further studied. The present study aimed to investigate the function of miR-429 in the progression of HCC. In terms of this paper, it was found that miR-429 was down-regulated in HCC tissues and cells. After being transfected with miR-429 mimics, miR-429 decreased the migratory capacity and reversed the EMT to MET in HCC cells. RAB23 was confirmed as a target of miR-429. Rescue assays further verified that the function of miR-429 in HCC cells was exerted through targeting RAB23. In general, it was concluded that the signal pathway miR-429/RAB23 might be a potential target for HCC treatment.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Neoplasias Hepáticas/genética
MicroRNAs/genética
Proteínas rab de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/patologia
Carcinoma Hepatocelular/secundário
Linhagem Celular Tumoral
Movimento Celular
Regulação para Baixo
Transição Epitelial-Mesenquimal/genética
Regulação Neoplásica da Expressão Gênica
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
MicroRNAs/metabolismo
Mimetismo Molecular
Transdução de Sinais
Transfecção
Regulação para Cima
Proteínas rab de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MIRN429 microRNA, human); 0 (MicroRNAs); EC 3.6.1.- (RAB23 protein, human); EC 3.6.5.2 (rab GTP-Binding Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


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[PMID]:29220372
[Au] Autor:Huang MF; Lin SJ; Ko TP; Liao YT; Hsu KC; Wang HC
[Ad] Endereço:Graduate Institute of Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
[Ti] Título:The monomeric form of Neisseria DNA mimic protein DMP19 prevents DNA from binding to the histone-like HU protein.
[So] Source:PLoS One;12(12):e0189461, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA mimicry is a direct and effective strategy by which the mimic competes with DNA for the DNA binding sites on other proteins. Until now, only about a dozen proteins have been shown to function via this strategy, including the DNA mimic protein DMP19 from Neisseria meningitides. We have shown previously that DMP19 dimer prevents the operator DNA from binding to the transcription factor NHTF. Here, we provide new evidence that DMP19 monomer can also interact with the Neisseria nucleoid-associated protein HU. Using BS3 crosslinking, gel filtration and isothermal titration calorimetry assays, we found that DMP19 uses its monomeric form to interact with the Neisseria HU dimer. Crosslinking conjugated mass spectrometry was used to investigate the binding mode of DMP19 monomer and HU dimer. Finally, an electrophoretic mobility shift assay (EMSA) confirmed that the DNA binding affinity of HU is affected by DMP19. These results showed that DMP19 is bifunctional in the gene regulation of Neisseria through its variable oligomeric forms.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Histonas/metabolismo
Mimetismo Molecular
Neisseria/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Dimerização
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Histones)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189461


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[PMID]:29053971
[Au] Autor:Hebbandi Nanjundappa R; Ronchi F; Wang J; Clemente-Casares X; Yamanouchi J; Sokke Umeshappa C; Yang Y; Blanco J; Bassolas-Molina H; Salas A; Khan H; Slattery RM; Wyss M; Mooser C; Macpherson AJ; Sycuro LK; Serra P; McKay DM; McCoy KD; Santamaria P
[Ad] Endereço:Julia McFarlane Diabetes Research Centre (JMDRC), University of Calgary, Calgary AB T2N 4N1, Canada; Department of Microbiology, Immunology, and Infectious Diseases, Snyder Institute for Chronic Diseases, University of Calgary, Calgary AB T2N 4N1, Canada.
[Ti] Título:A Gut Microbial Mimic that Hijacks Diabetogenic Autoreactivity to Suppress Colitis.
[So] Source:Cell;171(3):655-667.e17, 2017 Oct 19.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The gut microbiota contributes to the development of normal immunity but, when dysregulated, can promote autoimmunity through various non-antigen-specific effects on pathogenic and regulatory lymphocytes. Here, we show that an integrase expressed by several species of the gut microbial genus Bacteroides encodes a low-avidity mimotope of the pancreatic ß cell autoantigen islet-specific glucose-6-phosphatase-catalytic-subunit-related protein (IGRP ). Studies in germ-free mice monocolonized with integrase-competent, integrase-deficient, and integrase-transgenic Bacteroides demonstrate that the microbial epitope promotes the recruitment of diabetogenic CD8+ T cells to the gut. There, these effectors suppress colitis by targeting microbial antigen-loaded, antigen-presenting cells in an integrin ß7-, perforin-, and major histocompatibility complex class I-dependent manner. Like their murine counterparts, human peripheral blood T cells also recognize Bacteroides integrase. These data suggest that gut microbial antigen-specific cytotoxic T cells may have therapeutic value in inflammatory bowel disease and unearth molecular mimicry as a novel mechanism by which the gut microbiota can regulate normal immune homeostasis. PAPERCLIP.
[Mh] Termos MeSH primário: Autoantígenos/imunologia
Bacteroides/imunologia
Colite/imunologia
Microbioma Gastrointestinal
Glucose-6-Fosfatase/imunologia
[Mh] Termos MeSH secundário: Adulto
Animais
Bacteroides/classificação
Bacteroides/enzimologia
Colite/microbiologia
Feminino
Glucose-6-Fosfatase/genética
Seres Humanos
Tecido Linfoide/imunologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos NOD
Meia-Idade
Mimetismo Molecular
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantigens); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 3.1.3.9. (G6PC2 protein, human); EC 3.1.3.9. (G6pc2 protein, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE


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[PMID]:29040286
[Au] Autor:Mousa AA; Roche DB; Terkawi MA; Kameyama K; Kamyingkird K; Vudriko P; Salama A; Cao S; Orabi S; Khalifa H; Ahmed M; Attia M; Elkirdasy A; Nishikawa Y; Xuan X; Cornillot E
[Ad] Endereço:Institut de Biologie Computationnelle (IBC), LIRMM, CNRS, Université de Montpellier, Montpellier, France.
[Ti] Título:Human babesiosis: Indication of a molecular mimicry between thrombospondin domains from a novel Babesia microti BmP53 protein and host platelets molecules.
[So] Source:PLoS One;12(10):e0185372, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human babesiosis is caused by the apicomplexan parasite Babesia microti, which is of major public health concern in the United States and elsewhere, resulting in malaise and fatigue, followed by a fever and hemolytic anemia. In this paper we focus on the characterization of a novel B. microti thrombospondin domain (TSP1)-containing protein (BmP53) from the new annotation of the B. microti genome (locus 'BmR1_04g09041'). This novel protein (BmP53) had a single TSP1 and a transmembrane domain, with a short cytoplasmic tail containing a sub-terminal glutamine residue, but no signal peptide and Von Willebrand factor type A domains (VWA), which are found in classical thrombospondin-related adhesive proteins (TRAP). Co-localization assays of BmP53 and Babesia microti secreted antigen 1 (BmSA1) suggested that BmP53 might be a non-secretory membranous protein. Molecular mimicry between the TSP1 domain from BmP53 and host platelets molecules was indicated through different measures of sequence homology, phylogenetic analysis, 3D structure and shared epitopes. Indeed, hamster isolated platelets cross-reacted with mouse anti-BmP53-TSP1. Molecular mimicry are used to help parasites to escape immune defenses, resulting in immune evasion or autoimmunity. Furthermore, specific host reactivity was also detected against the TSP1-free part of BmP53 in infected hamster sera. In conclusion, the TSP1 domain mimicry might help in studying the mechanisms of parasite-induced thrombocytopenia, with the TSP1-free truncate of the protein representing a potential safe candidate for future vaccine studies.
[Mh] Termos MeSH primário: Antígenos de Protozoários/imunologia
Babesia microti/imunologia
Babesiose/parasitologia
Plaquetas/parasitologia
Evasão da Resposta Imune
Proteínas de Protozoários/imunologia
Trombospondina 1/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Antígenos de Protozoários/química
Antígenos de Protozoários/genética
Babesia microti/genética
Babesia microti/isolamento & purificação
Babesiose/imunologia
Sítios de Ligação
Clonagem Molecular
Cricetulus
Eritrócitos/parasitologia
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Glutationa Transferase/genética
Glutationa Transferase/metabolismo
Seres Humanos
Camundongos
Modelos Moleculares
Mimetismo Molecular
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Estrutura Secundária de Proteína
Proteínas de Protozoários/química
Proteínas de Protozoários/genética
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Trombospondina 1/química
Trombospondina 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Protozoan); 0 (Protozoan Proteins); 0 (Recombinant Fusion Proteins); 0 (Thrombospondin 1); EC 2.5.1.18 (Glutathione Transferase)
[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:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185372


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[PMID]:29023448
[Au] Autor:Guven-Maiorov E; Tsai CJ; Nussinov R
[Ad] Endereço:Cancer and Inflammation Program, Leidos Biomedical Research, Inc. Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, MD, United States of America.
[Ti] Título:Structural host-microbiota interaction networks.
[So] Source:PLoS Comput Biol;13(10):e1005579, 2017 Oct.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hundreds of different species colonize multicellular organisms making them "metaorganisms". A growing body of data supports the role of microbiota in health and in disease. Grasping the principles of host-microbiota interactions (HMIs) at the molecular level is important since it may provide insights into the mechanisms of infections. The crosstalk between the host and the microbiota may help resolve puzzling questions such as how a microorganism can contribute to both health and disease. Integrated superorganism networks that consider host and microbiota as a whole-may uncover their code, clarifying perhaps the most fundamental question: how they modulate immune surveillance. Within this framework, structural HMI networks can uniquely identify potential microbial effectors that target distinct host nodes or interfere with endogenous host interactions, as well as how mutations on either host or microbial proteins affect the interaction. Furthermore, structural HMIs can help identify master host cell regulator nodes and modules whose tweaking by the microbes promote aberrant activity. Collectively, these data can delineate pathogenic mechanisms and thereby help maximize beneficial therapeutics. To date, challenges in experimental techniques limit large-scale characterization of HMIs. Here we highlight an area in its infancy which we believe will increasingly engage the computational community: predicting interactions across kingdoms, and mapping these on the host cellular networks to figure out how commensal and pathogenic microbiota modulate the host signaling and broadly cross-species consequences.
[Mh] Termos MeSH primário: Microbiota/fisiologia
Modelos Moleculares
Mimetismo Molecular
Mapas de Interação de Proteínas/fisiologia
Simbiose/fisiologia
[Mh] Termos MeSH secundário: Animais
Biologia Computacional
Seres Humanos
Camundongos
Receptores Toll-Like
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Toll-Like Receptors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171105
[Lr] Data última revisão:
171105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005579


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[PMID]:28981852
[Au] Autor:Feng G; Luo C; Yi H; Yuan L; Lin B; Luo X; Hu X; Wang H; Lei C; Nie Z; Yao S
[Ad] Endereço:State Key Laboratory of Chemo/Biosensing and Chemometrics, College of Chemistry and Chemical Engineering, Hunan University, Changsha 410082, PR China.
[Ti] Título:DNA mimics of red fluorescent proteins (RFP) based on G-quadruplex-confined synthetic RFP chromophores.
[So] Source:Nucleic Acids Res;45(18):10380-10392, 2017 Oct 13.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Red fluorescent proteins (RFPs) have emerged as valuable biological markers for biomolecule imaging in living systems. Developing artificial fluorogenic systems that mimic RFPs remains an unmet challenge. Here, we describe the design and synthesis of six new chromophores analogous to the chromophores in RFPs. We demonstrate, for the first time, that encapsulating RFP chromophore analogues in canonical DNA G-quadruplexes (G4) can activate bright fluorescence spanning red and far-red spectral regions (Em = 583-668 nm) that nearly match the entire RFP palette. Theoretical calculations and molecular dynamics simulations reveal that DNA G4 greatly restricts radiationless deactivation of chromophores induced by a twisted intramolecular charge transfer (TICT). These DNA mimics of RFP exhibit attractive photophysical properties comparable or superior to natural RFPs, including high quantum yield, large Stokes shifts, excellent anti-photobleaching properties, and two-photon fluorescence. Moreover, these RFP chromophore analogues are a novel and distinctive type of topology-selective G4 probe specific to parallel G4 conformation. The DNA mimics of RFP have been further exploited for imaging of target proteins. Using cancer-specific cell membrane biomarkers as targets, long-term real-time monitoring in single live cell and two-photon fluorescence imaging in tissue sections have been achieved without the need for genetic coding.
[Mh] Termos MeSH primário: DNA/química
Corantes Fluorescentes/química
Quadruplex G
Proteínas Luminescentes/química
Mimetismo Molecular
[Mh] Termos MeSH secundário: Fluorescência
Corantes Fluorescentes/metabolismo
Seres Humanos
Proteínas Luminescentes/metabolismo
Modelos Moleculares
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (Luminescent Proteins); 0 (red fluorescent protein); 9007-49-2 (DNA)
[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:171006
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx803


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[PMID]:28973477
[Au] Autor:Einarson OJ; Sen D
[Ad] Endereço:Department of Chemistry, Simon Fraser University, Burnaby, British Columbia V5A 1S6, Canada.
[Ti] Título:Self-biotinylation of DNA G-quadruplexes via intrinsic peroxidase activity.
[So] Source:Nucleic Acids Res;45(17):9813-9822, 2017 Sep 29.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The striking and ubiquitous in vitro affinity between hemin and DNA/RNA G-quadruplexes raises the intriguing possibility of its relevance to biology. To date, no satisfactory experimental framework has been reported for investigating such a possibility. Complexation by G-quadruplexes leads to activation of the bound hemin toward catalysis of 1- and 2-electron oxidative reactions, with phenolic compounds being particularly outstanding substrates. We report here a strategy for exploiting that intrinsic peroxidase activity of hemin•G-quadruplex complexes for self-biotinylation of their G-quadruplex component. Such self-biotinylation occurs with good efficiency and high discrimination in vitro, being specific for G-quadruplexes and not for duplexes. The biotinylated DNA, moreover, remains amenable to polymerase chain reaction amplification, rendering it suitable for analysis by ChIP-Seq and related methods. We anticipate that this self-biotinylation methodology will also serve as a sensitive tool, orthogonal to existing ones, for identifying, labeling and pulling down cellular RNA and DNA G-quadruplexes in general, as well as proteins bound to or proximal to such quadruplexes.
[Mh] Termos MeSH primário: DNA Catalítico/química
Quadruplex G
Hemina/química
Oligonucleotídeos/química
Peroxidases/química
[Mh] Termos MeSH secundário: Biocatálise
Técnicas Biossensoriais/métodos
Biotina/química
Biotinilação
Peróxido de Hidrogênio/química
Cinética
Mimetismo Molecular
Oxirredução
Fenóis/química
Reação em Cadeia da Polimerase
Estreptavidina/química
Tiramina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Catalytic); 0 (Oligonucleotides); 0 (Phenols); 0 (biotin tyramine); 6SO6U10H04 (Biotin); 743LRP9S7N (Hemin); 9013-20-1 (Streptavidin); BBX060AN9V (Hydrogen Peroxide); EC 1.11.1.- (Peroxidases); X8ZC7V0OX3 (Tyramine)
[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:171004
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx765


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[PMID]:28972997
[Au] Autor:Jahandideh F; Chakrabarti S; Davidge ST; Wu J
[Ad] Endereço:Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada.
[Ti] Título:Egg white hydrolysate shows insulin mimetic and sensitizing effects in 3T3-F442A pre-adipocytes.
[So] Source:PLoS One;12(10):e0185653, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Insulin resistance and inflammation in adipose tissue is a key mechanism underlying metabolic syndrome, a growing health problem characterized by diabetes, obesity and hypertension. Previous work from our research group has demonstrated the potential of egg white ovotransferrin derived bioactive peptides against hypertension, oxidative stress and inflammation in vitro and in vivo. Egg white hydrolysate (EWH) has also shown anti-hypertensive effects in spontaneously hypertensive rats. Given the interplay among hypertension, inflammation, oxidative stress and metabolic syndrome, the objective of the study was to test the EWH on differentiation, insulin signaling and inflammatory responses in 3T3-F442A pre-adipocytes. Our study suggested that EWH could promote adipocyte differentiation as shown by increased lipid accumulation, increased release of adiponectin and upregulation of peroxisome proliferator associated receptor gamma (PPARγ) and CCAAT/ enhancer binding protein alpha (C/EBP-α). In addition to enhanced insulin effects on the upregulation of protein kinase B/Akt phosphorylation, EWH treatment increased extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation to a level similar to that of insulin, indicating insulin sensitizing and mimetic properties of the EWH. EWH further attenuated cytokine induced inflammatory marker; cyclooxygenase -2 (COX-2) by 48.78%, possibly through the AP-1 pathway by down regulating c-Jun phosphorylation in adipocytes. Given the critical role of adipose in the pathogenesis of insulin resistance and metabolic syndrome, EWH may have potential applications in the prevention and management of metabolic syndrome and its complications.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Clara de Ovo
Insulina/metabolismo
Mimetismo Molecular
[Mh] Termos MeSH secundário: Células 3T3
Adipócitos/citologia
Adiponectina/metabolismo
Animais
Western Blotting
Diferenciação Celular
Relação Dose-Resposta a Droga
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Camundongos
PPAR gama/metabolismo
Fosforilação
Receptor de Insulina/metabolismo
Transdução de Sinais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Insulin); 0 (PPAR gamma); EC 2.7.10.1 (Receptor, Insulin); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[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:171004
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185653



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