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Pesquisa : D08.811.399.325.500.400.300 [Categoria DeCS]
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[PMID]:28450114
[Au] Autor:Xie L; Cheng L; Xu G; Zhang J; Ji X; Song E
[Ad] Endereço:Department of Ophthalmology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
[Ti] Título:The novel cyclophilin D inhibitor compound 19 protects retinal pigment epithelium cells and retinal ganglion cells from UV radiation.
[So] Source:Biochem Biophys Res Commun;487(4):807-812, 2017 06 10.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excessive Ultra violet (UV) radiation induces injuries to retinal pigment epithelium (RPE) cells (RPEs) and retinal ganglion cells (RGCs), causing retinal degeneration. Cyclophilin D (Cyp-D)-dependent mitochondrial permeability transition pore (mPTP) opening mediates UV-induced cell death. In this study, we show that a novel Cyp-D inhibitor compound 19 efficiently protected RPEs and RGCs from UV radiation. Compound 19-mediated cytoprotection requires Cyp-D, as it failed to further protect RPEs/RGCs from UV when Cyp-D was silenced by targeted shRNAs. Compound 19 almost blocked UV-induced p53-Cyp-D mitochondrial association, mPTP opening and subsequent cytochrome C release. Further studies showed that compound 19 inhibited UV-induced reactive oxygen species (ROS) production, lipid peroxidation and DNA damage. Together, compound 19 protects RPEs and RGCs from UV radiation, possibly via silencing Cyp-D-regulated intrinsic mitochondrial death pathway. Compound 19 could a lead compound for treating UV-associated retinal degeneration diseases.
[Mh] Termos MeSH primário: Pirrolidinas/farmacologia
Células Ganglionares da Retina/efeitos dos fármacos
Células Ganglionares da Retina/efeitos da radiação
Epitélio Pigmentado da Retina/efeitos dos fármacos
Epitélio Pigmentado da Retina/efeitos da radiação
Raios Ultravioleta
Ureia/análogos & derivados
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Ciclofilinas/antagonistas & inibidores
Dano ao DNA
Relação Dose-Resposta a Droga
Seres Humanos
Peroxidação de Lipídeos/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Estrutura Molecular
Pirrolidinas/síntese química
Pirrolidinas/química
Espécies Reativas de Oxigênio/metabolismo
Epitélio Pigmentado da Retina/citologia
Relação Estrutura-Atividade
Ureia/síntese química
Ureia/química
Ureia/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1-(4-aminobenzyl)-3-(4-(methylthio)-1-(2-(2-(methylthio)phenyl)pyrrolidin-1-yl)-1-oxobutan-2-yl)urea); 0 (Pyrrolidines); 0 (Reactive Oxygen Species); 8W8T17847W (Urea); EC 5.2.1.- (Cyclophilins); EC 5.2.1.8 (PPID protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:28789840
[Au] Autor:Huang ZL; Pandya D; Banta DK; Ansari MS; Oh U
[Ad] Endereço:Department of Neurology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA.
[Ti] Título:Cyclophilin inhibitor NIM811 ameliorates experimental allergic encephalomyelitis.
[So] Source:J Neuroimmunol;311:40-48, 2017 Oct 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cyclophilins have diverse functions that may affect the course of central nervous system (CNS) inflammatory disorders. Anti-inflammatory and neuroprotective mechanisms may be targeted by inhibition of cyclophilin A-dependent and cyclophilin D-dependent functions, respectively. We tested the effect of cyclophilin inhibition on CNS inflammation by administering N-methyl-4-isoleucine-cyclosporin (NIM811) to mice undergoing experimental allergic encephalomyelitis (EAE). Treatment with NIM811 resulted in significant reduction of EAE clinical severity. Analysis of mitochondrial calcium retention capacity and the course of EAE in cyclophilin D knockout mice indicated that the effect of NIM811 on EAE was not entirely cyclophilin D-dependent. NIM811-treated EAE animals showed reduction in interleukin-2 expression and reduction in CNS inflammatory infiltrates. These results indicate that anti-inflammatory rather than neuroprotective mechanisms associated with cyclophilins are likely involved in the mechanism of NIM811 in EAE.
[Mh] Termos MeSH primário: Ciclosporina/uso terapêutico
Encefalomielite Autoimune Experimental/tratamento farmacológico
Imunossupressores/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Encéfalo/ultraestrutura
Calcineurina/metabolismo
Cálcio/metabolismo
Ciclofilinas/deficiência
Ciclofilinas/genética
Ciclosporina/metabolismo
Ciclosporina/farmacologia
Citocinas/genética
Citocinas/metabolismo
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/patologia
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Imunossupressores/farmacologia
Leucócitos/efeitos dos fármacos
Leucócitos/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microglia/efeitos dos fármacos
Microglia/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Glicoproteína Mielina-Oligodendrócito/imunologia
Glicoproteína Mielina-Oligodendrócito/toxicidade
Fragmentos de Peptídeos/imunologia
Fragmentos de Peptídeos/toxicidade
Baço/metabolismo
Baço/ultraestrutura
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Immunosuppressive Agents); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (myelin oligodendrocyte glycoprotein (35-55)); 83HN0GTJ6D (Cyclosporine); 96262S4I14 ((melle-4)cyclosporin); EC 3.1.3.16 (Calcineurin); EC 5.2.1.- (Cyclophilins); EC 5.2.1.8 (cyclophilin D); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE


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[PMID]:28739742
[Au] Autor:Gong Z; Mu Y; Chen J; Chu H; Lian P; Wang C; Wang J; Jiang L
[Ad] Endereço:Department of Oncology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, P.R. China.
[Ti] Título:Expression and Significance of Cyclophilin J in Primary Gastric Adenocarcinoma.
[So] Source:Anticancer Res;37(8):4475-4481, 2017 08.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Biomarkers are essential in early diagnosis and understanding of the molecular mechanism of human cancer. The expression of cyclophilin J, a novel member of the cyclophilin family, was investigated in primary gastric adenocarcinoma. MATERIALS AND METHODS: Western blot analysis was carried out on 36 paired tumor and normal tissue samples; immunohistochemical analysis was carried out on 120 gastric carcinoma tissues and normal adjacent tissue. RESULTS: Cyclophilin J protein was overexpressed in 72.2% of gastric carcinoma tissues compared to adjacent normal tissues. Immunohistochemical analysis revealed that cyclophilin J was overexpressed in 49.2% (59/120) and 23.3% (28/120) of gastric carcinoma tissues and adjacent tissues, respectively (p<0.05). Expression of cyclophilin J was associated with the degree of differentiation, but not with lymph node metastasis, gender or depth of tumor infiltration. The overall survival of patients showed no association with the overexpression of cyclophilin J protein. CONCLUSION: Cyclophilin J expression was up-regulated in gastric carcinoma compared to normal gastric tissues. However, in order to confirm its association with the survival of patients with gastric cancer, more cases need to be studied.
[Mh] Termos MeSH primário: Adenocarcinoma/metabolismo
Ciclofilinas/metabolismo
Neoplasias Gástricas/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/mortalidade
Adenocarcinoma/patologia
Adulto
Idoso
Biomarcadores Tumorais
Western Blotting
Ciclofilinas/genética
Feminino
Mucosa Gástrica/metabolismo
Mucosa Gástrica/patologia
Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Metástase Linfática
Masculino
Meia-Idade
Gradação de Tumores
Invasividade Neoplásica
Prognóstico
Neoplasias Gástricas/genética
Neoplasias Gástricas/mortalidade
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 5.2.1.- (Cyclophilins); EC 5.2.1.- (cyclophilin J, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28700644
[Au] Autor:Moretti ML; Alárcon-Reverte R; Pearce S; Morran S; Hanson BD
[Ad] Endereço:Department of Plant Sciences, University of California, Davis, California, United States of America.
[Ti] Título:Transcription of putative tonoplast transporters in response to glyphosate and paraquat stress in Conyza bonariensis and Conyza canadensis and selection of reference genes for qRT-PCR.
[So] Source:PLoS One;12(7):e0180794, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herbicide resistance is a challenge for modern agriculture further complicated by cases of resistance to multiple herbicides. Conyza bonariensis and Conyza canadensis are invasive weeds of field crops, orchards, and non-cropped areas in many parts of the world. In California, USA, Conyza populations resistant to the herbicides glyphosate and paraquat have recently been described. Although the mechanism conferring resistance to glyphosate and paraquat in these species was not elucidated, reduced translocation of these herbicides was observed under experimental conditions in both species. Glyphosate and paraquat resistance associated with reduced translocation are hypothesized to be a result of sequestration of herbicides into the vacuole, with the possible involvement of over-expression of genes encoding tonoplast transporters of ABC-transporter families in cases of glyphosate resistance or cationic amino acid transporters (CAT) in cases of paraquat resistance. However, gene expression in response to herbicide treatment has not been studied in glyphosate and paraquat resistant populations. In the current study, we evaluated the transcript levels of genes possibly involved in resistance using real-time PCR. First, we evaluated eight candidate reference genes following herbicide treatment and selected three genes that exhibited stable expression profiles; ACTIN, HEAT-SHOCK-PROTEIN-70, and CYCLOPHILIN. The reference genes identified here can be used for further studies related to plant-herbicide interactions. We used these reference genes to assay the transcript levels of EPSPS, ABC transporters, and CAT in response to herbicide treatment in susceptible and resistant Conyza spp. lines. No transcription changes were observed in EPSPS or CAT genes after glyphosate or paraquat treatment, suggesting that these genes are not involved in the resistance mechanism. Transcription of the two ABC transporter genes increased following glyphosate treatment in all Conyza spp. lines. Transcription of ABC transporters also increased after paraquat treatment in all three lines of C. bonariensis. However, in C. canadensis, paraquat treatment increased transcription of only one ABC transporter gene in the susceptible line. The increase in transcription of ABC transporters after herbicide treatment is likely a stress response based on similar response observed across all Conyza lines regardless of resistance or sensitivity to glyphosate or paraquat, thus these genes do not appear to be directly involved in the mechanism of resistance in Conyza spp.
[Mh] Termos MeSH primário: Conyza/efeitos dos fármacos
Conyza/metabolismo
Glicina/análogos & derivados
Paraquat/farmacologia
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Sistemas de Transporte de Aminoácidos Básicos/genética
Sistemas de Transporte de Aminoácidos Básicos/metabolismo
Conyza/genética
Ciclofilinas/genética
Ciclofilinas/metabolismo
Glicina/farmacologia
Proteínas de Choque Térmico HSP70/genética
Proteínas de Choque Térmico HSP70/metabolismo
Proteínas de Plantas/genética
Proteínas de Plantas/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Amino Acid Transport Systems, Basic); 0 (HSP70 Heat-Shock Proteins); 0 (Plant Proteins); 4632WW1X5A (glyphosate); EC 5.2.1.- (Cyclophilins); PLG39H7695 (Paraquat); TE7660XO1C (Glycine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180794


  5 / 1257 MEDLINE  
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[PMID]:28673552
[Au] Autor:Georgiou C; McNae I; Wear M; Ioannidis H; Michel J; Walkinshaw M
[Ad] Endereço:University of Edinburgh, Michael Swann Building, Max Born Crescent, Edinburgh, Scotland, EH9 3BF, UK; University of Edinburgh, Joseph Black Building, David Brewster Road, Edinburgh, Scotland, EH9 3FJ, UK.
[Ti] Título:Pushing the Limits of Detection of Weak Binding Using Fragment-Based Drug Discovery: Identification of New Cyclophilin Binders.
[So] Source:J Mol Biol;429(16):2556-2570, 2017 Aug 04.
[Is] ISSN:1089-8638
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fragment-based drug discovery is an increasingly popular method to identify novel small-molecule drug candidates. One of the limitations of the approach is the difficulty of accurately characterizing weak binding events. This work reports a combination of X-ray diffraction, surface plasmon resonance experiments and molecular dynamics simulations for the characterization of binders to different isoforms of the cyclophilin (Cyp) protein family. Although several Cyp inhibitors have been reported in the literature, it has proven challenging to achieve high binding selectivity for different isoforms of this protein family. The present studies have led to the identification of several structurally novel fragments that bind to diverse Cyp isoforms in distinct pockets with low millimolar dissociation constants. A detailed comparison of the merits and drawbacks of the experimental and computational techniques is presented, and emerging strategies for designing ligands with enhanced isoform specificity are described.
[Mh] Termos MeSH primário: Ciclofilinas/antagonistas & inibidores
Ciclofilinas/metabolismo
Descoberta de Drogas/métodos
Limite de Detecção
[Mh] Termos MeSH secundário: Simulação de Dinâmica Molecular
Ligação Proteica
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/metabolismo
Ressonância de Plasmônio de Superfície/métodos
Difração de Raios X/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Isoforms); EC 5.2.1.- (Cyclophilins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE


  6 / 1257 MEDLINE  
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[PMID]:28671258
[Au] Autor:Auler PA; Benitez LC; do Amaral MN; Vighi IL; Rodrigues GS; da Maia LC; Braga EJB
[Ad] Endereço:Departamento de Botânica, Instituto de Biologia, , , Brasil pri_auler@hotmail.com.
[Ti] Título:Selection of candidate reference genes and validation for real-time PCR studies in rice plants exposed to low temperatures.
[So] Source:Genet Mol Res;16(2), 2017 Jun 29.
[Is] ISSN:1676-5680
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Rice is a cereal that presents a great ability to adapt to different soil and climate conditions. However, as it is a tropical crop with C3 metabolism, it performs better in warm temperatures with high solar radiation. Tolerance to stress caused by low temperatures is a highly complex process that involves various metabolic pathways and cellular compartments, resulting in general or specific effects on plant growth and development. In order to observe the true effect of a particular stress on genetic expression, reference genes need to be chosen for real-time PCRs, the expression levels of which should remain stable independent of the situation imposed. In this paper, the expression stability was evaluated of the actin 11 (ACT11), ubiquitin-conjugating enzyme 2 (UBC-E2), glyceraldehyde 3-phosphate dehydrogenase (GAPDH), beta tubilin (ß-Tubulin), eukaryotic initiation factor 4α (eIF-4-α), eukaryotic initiation factor 1α (eIF-1-α), ubiquitin 10 (UBQ10), ubiquitin 5 (UBQ5), aquaporin (TIP41), and cyclophilin genes, in two rice genotypes cultivated in low temperature (13°C) conditions in vegetative stage (V4). The analysis material (leaves) was collected after 0, 6, 24, 48, and 72 h of exposure to the stress. In this study, the geNorm, BestKeeper, ΔCt, NormFinder, and RefFinder methods were used to evaluate the expression stability of the candidate reference genes. The results revealed that the most indicated genes for all the analysis methods were UBQ10 and UBQ5 for BRS Bojuru and BRS Pampa, respectively. On the other hand, the eIF-1-α gene presents the least expression stability and is not indicated for studies of rice plants subjected to low temperatures. The validation with the antioxidant system genes SODCc1-Cu/Zn, CATC, APX2, and GR2 confirmed the importance of using previously tested normalizing genes for adequate real-time PCR results.
[Mh] Termos MeSH primário: Resposta ao Choque Frio/genética
Genes de Plantas
Oryza/genética
Reação em Cadeia da Polimerase em Tempo Real/normas
[Mh] Termos MeSH secundário: Actinas/genética
Aquaporinas/genética
Ciclofilinas/genética
Fator de Iniciação 4A em Eucariotos/genética
Gliceraldeído-3-Fosfato Desidrogenase (Fosforiladora)/genética
Proteínas de Plantas/genética
Reação em Cadeia da Polimerase em Tempo Real/métodos
Padrões de Referência
Tubulina (Proteína)/genética
Ubiquitinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Actins); 0 (Aquaporins); 0 (Plant Proteins); 0 (Tubulin); 0 (Ubiquitins); EC 1.2.1.12 (Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)); EC 2.7.7.- (Eukaryotic Initiation Factor-4A); EC 5.2.1.- (Cyclophilins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.4238/gmr16029695


  7 / 1257 MEDLINE  
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[PMID]:28663253
[Au] Autor:Choo HJ; Kholmukhamedov A; Zhou C; Jobe S
[Ad] Endereço:From the BloodCenter of Wisconsin, Milwaukee (A.K., S.J.); Emory University School of Medicine, Department of Pediatrics and Children's Healthcare of Atlanta, GA (H.-J.C., C.Z., S.J.); Emory University, School of Medicine, Department of Cell Biology, Atlanta, GA (H.-J.C.); and Medical College of Wis
[Ti] Título:Inner Mitochondrial Membrane Disruption Links Apoptotic and Agonist-Initiated Phosphatidylserine Externalization in Platelets.
[So] Source:Arterioscler Thromb Vasc Biol;37(8):1503-1512, 2017 Aug.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Phosphatidylserine exposure mediates platelet procoagulant function and regulates platelet life span. Apoptotic, necrotic, and integrin-mediated mechanisms have been implicated as intracellular determinants of platelet phosphatidylserine exposure. Here, we investigate (1) the role of mitochondrial events in platelet phosphatidylserine exposure initiated by these distinct stimuli and (2) the cellular interactions of the procoagulant platelet in vitro and in vivo. APPROACH AND RESULTS: Key mitochondrial events were examined, including cytochrome c release and inner mitochondrial membrane (IMM) disruption. In both ABT-737 (apoptotic) and agonist (necrotic)-treated platelets, phosphatidylserine externalization was temporally correlated with IMM disruption. Agonist stimulation resulted in rapid cyclophilin D-dependent IMM disruption that coincided with phosphatidylserine exposure. ABT-737 treatment caused rapid cytochrome c release, eventually followed by caspase-dependent IMM disruption that again closely coincided with phosphatidylserine exposure. A nonmitochondrial and integrin-mediated mechanism has been implicated in the formation of a novel phosphatidylserine-externalizing platelet subpopulation. Using image cytometry, this subpopulation is demonstrated to be the result of the interaction of an aggregatory platelet and a procoagulant platelet rather than indicative of a novel intracellular mechanism regulating platelet phosphatidylserine externalization. Using electron microscopy, similar interactions between aggregatory and procoagulant platelets are demonstrated in vitro and in vivo within a mesenteric vein hemostatic thrombus. CONCLUSIONS: Platelet phosphatidylserine externalization is closely associated with the mitochondrial event of IMM disruption identifying a common pathway in phosphatidylserine-externalizing platelets. The limited interaction of procoagulant platelets and integrin-active aggregatory platelets identifies a potential mechanism for procoagulant platelet retention within the hemostatic thrombus.
[Mh] Termos MeSH primário: Apoptose
Plaquetas/metabolismo
Mitocôndrias/metabolismo
Membranas Mitocondriais/metabolismo
Fosfatidilserinas/sangue
Agregação Plaquetária
Trombose Venosa/sangue
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Compostos de Bifenilo/farmacologia
Coagulação Sanguínea/efeitos dos fármacos
Plaquetas/efeitos dos fármacos
Plaquetas/ultraestrutura
Caspases/sangue
Venenos de Crotalídeos/farmacologia
Ciclofilinas/sangue
Ciclofilinas/genética
Citocromos c/sangue
Modelos Animais de Doenças
Genótipo
Integrinas/sangue
Cinética
Lectinas Tipo C
Camundongos Knockout
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/ultraestrutura
Membranas Mitocondriais/efeitos dos fármacos
Necrose
Nitrofenóis/farmacologia
Fenótipo
Piperazinas/farmacologia
Agregação Plaquetária/efeitos dos fármacos
Transdução de Sinais
Sulfonamidas/farmacologia
Trombina/farmacologia
Trombose Venosa/genética
Trombose Venosa/patologia
Proteína Killer-Antagonista Homóloga a bcl-2/sangue
Proteína Killer-Antagonista Homóloga a bcl-2/genética
Proteína X Associada a bcl-2/sangue
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABT-737); 0 (Bak1 protein, mouse); 0 (Bax protein, mouse); 0 (Biphenyl Compounds); 0 (Crotalid Venoms); 0 (Integrins); 0 (Lectins, C-Type); 0 (Nitrophenols); 0 (Phosphatidylserines); 0 (Piperazines); 0 (Sulfonamides); 0 (bcl-2 Homologous Antagonist-Killer Protein); 0 (bcl-2-Associated X Protein); 37206-04-5 (convulxin); 9007-43-6 (Cytochromes c); EC 3.4.21.5 (Thrombin); EC 3.4.22.- (Caspases); EC 5.2.1.- (Cyclophilins); EC 5.2.1.8 (cyclophilin D)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170819
[Lr] Data última revisão:
170819
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309473


  8 / 1257 MEDLINE  
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[PMID]:28654636
[Au] Autor:Baker JD; Shelton LB; Zheng D; Favretto F; Nordhues BA; Darling A; Sullivan LE; Sun Z; Solanki PK; Martin MD; Suntharalingam A; Sabbagh JJ; Becker S; Mandelkow E; Uversky VN; Zweckstetter M; Dickey CA; Koren J; Blair LJ
[Ad] Endereço:Department of Molecular Medicine and Byrd Alzheimer's Institute, University of South Florida, Tampa, Florida, United States of America.
[Ti] Título:Human cyclophilin 40 unravels neurotoxic amyloids.
[So] Source:PLoS Biol;15(6):e2001336, 2017 Jun.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The accumulation of amyloidogenic proteins is a pathological hallmark of neurodegenerative disorders. The aberrant accumulation of the microtubule associating protein tau (MAPT, tau) into toxic oligomers and amyloid deposits is a primary pathology in tauopathies, the most common of which is Alzheimer's disease (AD). Intrinsically disordered proteins, like tau, are enriched with proline residues that regulate both secondary structure and aggregation propensity. The orientation of proline residues is regulated by cis/trans peptidyl-prolyl isomerases (PPIases). Here we show that cyclophilin 40 (CyP40), a PPIase, dissolves tau amyloids in vitro. Additionally, CyP40 ameliorated silver-positive and oligomeric tau species in a mouse model of tau accumulation, preserving neuronal health and cognition. Nuclear magnetic resonance (NMR) revealed that CyP40 interacts with tau at sites rich in proline residues. CyP40 was also able to interact with and disaggregate other aggregating proteins that contain prolines. Moreover, CyP40 lacking PPIase activity prevented its capacity for disaggregation in vitro. Finally, we describe a unique structural property of CyP40 that may permit disaggregation to occur in an energy-independent manner. This study identifies a novel human protein disaggregase and, for the first time, demonstrates its capacity to dissolve intracellular amyloids.
[Mh] Termos MeSH primário: Amiloide/metabolismo
Ciclofilinas/metabolismo
Doenças Neurodegenerativas/metabolismo
alfa-Sinucleína/metabolismo
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/genética
Doença de Alzheimer/metabolismo
Amiloide/genética
Amiloide/ultraestrutura
Animais
Western Blotting
Encéfalo/metabolismo
Encéfalo/patologia
Encéfalo/fisiopatologia
Transtornos Cognitivos/genética
Transtornos Cognitivos/metabolismo
Transtornos Cognitivos/fisiopatologia
Ciclofilinas/genética
Ciclosporina/farmacologia
Modelos Animais de Doenças
Feminino
Células HEK293
Seres Humanos
Masculino
Camundongos Transgênicos
Microscopia Eletrônica de Transmissão
Doenças Neurodegenerativas/genética
Agregados Proteicos/efeitos dos fármacos
Agregação Patológica de Proteínas
Tauopatias/genética
Tauopatias/metabolismo
alfa-Sinucleína/genética
Proteínas tau/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid); 0 (Protein Aggregates); 0 (alpha-Synuclein); 0 (tau Proteins); 83HN0GTJ6D (Cyclosporine); EC 5.2.1.- (Cyclophilins); EC 5.2.1.8 (cyclophilin D)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2001336


  9 / 1257 MEDLINE  
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[PMID]:28619996
[Au] Autor:Unsworth AJ; Bye AP; Tannetta DS; Desborough MJR; Kriek N; Sage T; Allan HE; Crescente M; Yaqoob P; Warner TD; Jones CI; Gibbins JM
[Ad] Endereço:From the Institute of Cardiovascular and Metabolic Research, School of Biological Sciences (A.J.U., A.P.B., N.K., T.S., M.C., C.I.J., J.M.G.) and Department of Food and Nutritional Sciences (D.S.T., P.Y.), University of Reading, United Kingdom; Oxford Haemophilia and Thrombosis Centre, Oxford Biomed
[Ti] Título:Farnesoid X Receptor and Liver X Receptor Ligands Initiate Formation of Coated Platelets.
[So] Source:Arterioscler Thromb Vasc Biol;37(8):1482-1493, 2017 Aug.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The liver X receptors (LXRs) and farnesoid X receptor (FXR) have been identified in human platelets. Ligands of these receptors have been shown to have nongenomic inhibitory effects on platelet activation by platelet agonists. This, however, seems contradictory with the platelet hyper-reactivity that is associated with several pathological conditions that are associated with increased circulating levels of molecules that are LXR and FXR ligands, such as hyperlipidemia, type 2 diabetes mellitus, and obesity. APPROACH AND RESULTS: We, therefore, investigated whether ligands for the LXR and FXR receptors were capable of priming platelets to the activated state without stimulation by platelet agonists. Treatment of platelets with ligands for LXR and FXR converted platelets to the procoagulant state, with increases in phosphatidylserine exposure, platelet swelling, reduced membrane integrity, depolarization of the mitochondrial membrane, and microparticle release observed. Additionally, platelets also displayed features associated with coated platelets such as P-selectin exposure, fibrinogen binding, fibrin generation that is supported by increased serine protease activity, and inhibition of integrin αIIbß3. LXR and FXR ligand-induced formation of coated platelets was found to be dependent on both reactive oxygen species and intracellular calcium mobilization, and for FXR ligands, this process was found to be dependent on cyclophilin D. CONCLUSIONS: We conclude that treatment with LXR and FXR ligands initiates coated platelet formation, which is thought to support coagulation but results in desensitization to platelet stimuli through inhibition of αIIbß3 consistent with their ability to inhibit platelet function and stable thrombus formation in vivo.
[Mh] Termos MeSH primário: Benzoatos/farmacologia
Benzilaminas/farmacologia
Coagulação Sanguínea/efeitos dos fármacos
Plaquetas/efeitos dos fármacos
Isoxazóis/farmacologia
Receptores X do Fígado/agonistas
Ativação Plaquetária/efeitos dos fármacos
Inibidores da Agregação de Plaquetas/farmacologia
Receptores Citoplasmáticos e Nucleares/agonistas
[Mh] Termos MeSH secundário: Plaquetas/metabolismo
Sinalização do Cálcio/efeitos dos fármacos
Micropartículas Derivadas de Células/efeitos dos fármacos
Micropartículas Derivadas de Células/metabolismo
Ciclofilinas/sangue
Relação Dose-Resposta a Droga
Fibrina/metabolismo
Fibrinogênio/metabolismo
Seres Humanos
Ligantes
Receptores X do Fígado/sangue
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Selectina-P/sangue
Fosfatidilserinas/sangue
Complexo Glicoproteico GPIIb-IIIa de Plaquetas/antagonistas & inibidores
Complexo Glicoproteico GPIIb-IIIa de Plaquetas/metabolismo
Espécies Reativas de Oxigênio/sangue
Receptores Citoplasmáticos e Nucleares/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoates); 0 (Benzylamines); 0 (GW 3965); 0 (Isoxazoles); 0 (Ligands); 0 (Liver X Receptors); 0 (P-Selectin); 0 (Phosphatidylserines); 0 (Platelet Aggregation Inhibitors); 0 (Platelet Glycoprotein GPIIb-IIIa Complex); 0 (Reactive Oxygen Species); 0 (Receptors, Cytoplasmic and Nuclear); 0 (SELP protein, human); 0 (farnesoid X-activated receptor); 9001-31-4 (Fibrin); 9001-32-5 (Fibrinogen); EC 5.2.1.- (Cyclophilins); EC 5.2.1.8 (PPID protein, human); SR225WUZ0H (GW 4064)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309135


  10 / 1257 MEDLINE  
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[PMID]:28506462
[Au] Autor:Gustafson CL; Parsley NC; Asimgil H; Lee HW; Ahlbach C; Michael AK; Xu H; Williams OL; Davis TL; Liu AC; Partch CL
[Ad] Endereço:Department of Chemistry and Biochemistry, University of California, Santa Cruz, Santa Cruz, CA 95064, USA.
[Ti] Título:A Slow Conformational Switch in the BMAL1 Transactivation Domain Modulates Circadian Rhythms.
[So] Source:Mol Cell;66(4):447-457.e7, 2017 May 18.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The C-terminal transactivation domain (TAD) of BMAL1 (brain and muscle ARNT-like 1) is a regulatory hub for transcriptional coactivators and repressors that compete for binding and, consequently, contributes to period determination of the mammalian circadian clock. Here, we report the discovery of two distinct conformational states that slowly exchange within the dynamic TAD to control timing. This binary switch results from cis/trans isomerization about a highly conserved Trp-Pro imide bond in a region of the TAD that is required for normal circadian timekeeping. Both cis and trans isomers interact with transcriptional regulators, suggesting that isomerization could serve a role in assembling regulatory complexes in vivo. Toward this end, we show that locking the switch into the trans isomer leads to shortened circadian periods. Furthermore, isomerization is regulated by the cyclophilin family of peptidyl-prolyl isomerases, highlighting the potential for regulation of BMAL1 protein dynamics in period determination.
[Mh] Termos MeSH primário: Fatores de Transcrição ARNTL/metabolismo
Relógios Circadianos
Ritmo Circadiano
[Mh] Termos MeSH secundário: Fatores de Transcrição ARNTL/química
Fatores de Transcrição ARNTL/genética
Animais
Linhagem Celular Tumoral
Ciclofilinas/genética
Ciclofilinas/metabolismo
Proteínas de Drosophila/química
Proteínas de Drosophila/metabolismo
Seres Humanos
Isomerismo
Camundongos
Mutação
Proteínas Circadianas Period/genética
Proteínas Circadianas Period/metabolismo
Filogenia
Prolina
Domínios Proteicos
Transdução de Sinais
Relação Estrutura-Atividade
Fatores de Tempo
Transfecção
Triptofano
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ARNTL Transcription Factors); 0 (ARNTL protein, human); 0 (Arntl protein, mouse); 0 (CYCLE protein, Drosophila); 0 (Drosophila Proteins); 0 (PER2 protein, human); 0 (Per2 protein, mouse); 0 (Period Circadian Proteins); 8DUH1N11BX (Tryptophan); 9DLQ4CIU6V (Proline); EC 5.2.1.- (Cyclophilins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE



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