Base de dados : MEDLINE
Pesquisa : D08.811.399.325.500.400.300.500 [Categoria DeCS]
Referências encontradas : 761 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 77 ir para página                         

  1 / 761 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28767697
[Au] Autor:Burse M; Shi J; Aiken C
[Ad] Endereço:Department of Pathology, Immunology and Microbiology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
[Ti] Título:Cyclophilin A potentiates TRIM5α inhibition of HIV-1 nuclear import without promoting TRIM5α binding to the viral capsid.
[So] Source:PLoS One;12(8):e0182298, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The host immunophilin cyclophilin A (CypA) binds to the capsid protein (CA) of HIV-1 and regulates its infectivity. Depending on the target cell type, CypA can either promote or inhibit HIV-1 infection. The ability of CypA to promote HIV-1 infection has been extensively studied and linked to several steps in early replication including uncoating, reverse transcription and nuclear import. By contrast, the mechanism by which CypA inhibits infection is less well understood. We investigated the mechanism by which CypA potentiates restriction of HIV-1 by the tripartite motif-containing protein 5 (TRIM5α). Depletion of TRIM5α in the African green monkey cell line Vero, resulted in a loss of inhibition of infection by CypA, demonstrating that inhibition by CypA is mediated by TRIM5α. Complementary genetic and biochemical assays failed to demonstrate an ability of CypA to promote binding of TRIM5α to the viral capsid. TRIM5α inhibits HIV-1 reverse transcription in a proteasome-dependent manner; however, we observed that inhibition of proteasome activity did not reduce the ability of CypA to inhibit infection, suggesting that CypA acts at a step after reverse transcription. Accordingly, we observed a CypA-dependent reduction in the accumulation of nuclear HIV-1 DNA, indicating that CypA specifically promotes TRIM5α inhibition of HIV-1 nuclear import. We also observed that the ability of CypA to inhibit HIV-1 infection is abolished by amino acid substitutions within the conserved CPSF6-binding surface in CA. Our results indicate that CypA inhibits HIV-1 infection in Vero cells not by promoting TRIM5α binding to the capsid but by blocking nuclear import of the HIV-1 preintegration complex.
[Mh] Termos MeSH primário: Proteínas do Capsídeo/metabolismo
Ciclofilina A/metabolismo
HIV-1/patogenicidade
Proteínas com Motivo Tripartido/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Cercopithecus aethiops
Ciclofilina A/genética
HIV-1/genética
HIV-1/metabolismo
RNA Viral/genética
Transcrição Genética
Proteínas com Motivo Tripartido/genética
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Capsid Proteins); 0 (RNA, Viral); 0 (Tripartite Motif Proteins); EC 5.2.1.- (Cyclophilin A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182298


  2 / 761 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28739738
[Au] Autor:Gong Z; Chi C; Huang X; Chu H; Wang J; Du F; Jiang L; Chen J
[Ad] Endereço:Department of Oncology, the Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, P.R. China.
[Ti] Título:Cyclophilin A Is Overexpressed in Hepatocellular Carcinoma and Is Associated with the Cell Cycle.
[So] Source:Anticancer Res;37(8):4443-4447, 2017 08.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:AIM: To investigate the expression of cyclophilin A (CypA) in human hepatocellular carcinoma (HCC) and explore the effects of CypA on the cell cycle in HCC. MATERIALS AND METHODS: CypA expression was assessed by immunohistochemistry in 48 cases of HCC tissues and paired adjacent tissues. CypA plasmid was transfected into HCC cells and the cell cycle was analyzed. RESULTS: Positivity for CypA was higher in HCC tissues than in adjacent tissues (79.1% vs. 12.5%, p<0.05). Positivity for CypA was significantly higher in stage III and IV HCC than in stage I and II (p<0.05). Elevated CypA induced an increase of the percentage of S-phase cells (from 34.79% to 42.14%) and a decrease of G -G phase cells (from 58.10% to 50.64%). CONCLUSION: CypA is overexpressed in HCC and is associated with TNM stage. CypA also appears to promote the transition of the cell cycle from G to S phase.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/patologia
Ciclofilina A/metabolismo
Neoplasias Hepáticas/patologia
Regulação para Cima
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/metabolismo
Ciclo Celular
Linhagem Celular Tumoral
Proliferação Celular
Progressão da Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias Hepáticas/metabolismo
Masculino
Estadiamento de Neoplasias
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 5.2.1.- (Cyclophilin A)
[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:170726
[St] Status:MEDLINE


  3 / 761 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28729360
[Au] Autor:Dawar FU; Xiong Y; Khattak MNK; Li J; Lin L; Mei J
[Ad] Endereço:College of Fisheries, Huazhong Agricultural University, Wuhan, Hubei, China.
[Ti] Título:Potential role of cyclophilin A in regulating cytokine secretion.
[So] Source:J Leukoc Biol;102(4):989-992, 2017 Oct.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cyclophilin A (CypA), a peptidylprolyl - isomerase, is a ubiquitous and multifunctional protein. In addition to its role as a host-cell receptor for cyclosporine A, CypA has diverse functions in inflammatory conditions and diseases. CypA secreted in response to inflammatory stimuli binds to the cell surface via its receptor CD147 and induces secretion of various inflammatory cytokines. However, silencing and inhibition of either CypA or CD147 inhibits inflammatory cytokine expression and inflammation. This report reviews the literature related to the mechanism of CypA-dependent cytokine secretion and discusses this factor as a possible therapeutic target in inflammatory diseases.
[Mh] Termos MeSH primário: Basigina/imunologia
Ciclofilina A/imunologia
Citocinas/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Inflamação/imunologia
Inflamação/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (BSG protein, human); 0 (Cytokines); 136894-56-9 (Basigin); EC 5.2.1.- (Cyclophilin A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3RU0317-090RR


  4 / 761 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28394340
[Au] Autor:Lu W; Cheng F; Yan W; Li X; Yao X; Song W; Liu M; Shen X; Jiang H; Chen J; Li J; Huang J
[Ad] Endereço:Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, China.
[Ti] Título:Selective targeting p53 lung cancer cells harboring homozygous p53 Arg72 by an inhibitor of CypA.
[So] Source:Oncogene;36(33):4719-4731, 2017 Aug 17.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:TP53 plays essential roles in tumor initiation and progression, and is frequently mutated in cancer. However, pharmacological stabilization and reactivation of p53 have not been actively explored for targeted cancer therapies. Herein, we identify a novel Cyclophilin A (CypA) small molecule inhibitor (HL001) that induces non-small cell lung cancer (NSCLC) cell cycle arrest and apoptosis via restoring p53 expression. We find that HL001 stabilizes p53 through inhibiting the MDM2-mediated p53 ubiquitination. Further mechanistic studies reveal that the downregulation of G3BP1 and the induction of reactive oxygen species and DNA damage by HL001 contribute to p53 stabilization. Surprisingly, HL001 selectively suppresses tumor growth in p53 wild-type NSCLC harboring Arg72 homozygous alleles (p53-72R) through disrupting interaction between MDM2 and p53-72R in a CypA-dependent manner. Moreover, combining HL001 with cisplatin synergistically enhance tumor regression in orthotopic NSCLC mouse model. Collectively, this study demonstrates that pharmacologic inhibition of CypA offers a potential therapeutic strategy via specific activation of p53-72R in NSCLC.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Ciclofilina A/antagonistas & inibidores
Inibidores Enzimáticos/uso terapêutico
Fluorenos/uso terapêutico
Neoplasias Pulmonares/tratamento farmacológico
Terapia de Alvo Molecular
Proteína Supressora de Tumor p53/metabolismo
Ureia/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Carcinoma Pulmonar de Células não Pequenas/genética
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Cisplatino/uso terapêutico
DNA Helicases
Inibidores Enzimáticos/química
Inibidores Enzimáticos/farmacologia
Fluorenos/química
Fluorenos/farmacologia
Homozigoto
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Pulmonares/genética
Camundongos
Camundongos Nus
Proteínas de Ligação a Poli-ADP-Ribose
Estabilidade Proteica/efeitos dos fármacos
Proteólise/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-mdm2/metabolismo
RNA Helicases
Proteínas com Motivo de Reconhecimento de RNA
Proteína Supressora de Tumor p53/genética
Ureia/química
Ureia/farmacologia
Ureia/uso terapêutico
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Carrier Proteins); 0 (Enzyme Inhibitors); 0 (Fluorenes); 0 (HL001 compound); 0 (Poly-ADP-Ribose Binding Proteins); 0 (RNA Recognition Motif Proteins); 0 (Tumor Suppressor Protein p53); 8W8T17847W (Urea); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2); EC 3.6.4.- (DNA Helicases); EC 3.6.4.12 (G3BP1 protein, human); EC 3.6.4.13 (RNA Helicases); EC 5.2.1.- (Cyclophilin A); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.41


  5 / 761 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28391416
[Au] Autor:Piechota-Polanczyk A; Wlodarczyk M; Sobolewska-Wlodarczyk A; Jonakowski M; Pilarczyk A; Stec-Michalska K; Wisniewska-Jarosinska M; Fichna J
[Ad] Endereço:Department of Biochemistry, Faculty of Medicine, Medical University of Lodz, Lodz, Poland. piechota.aleksandra@gmail.com.
[Ti] Título:Serum Cyclophilin A Correlates with Increased Tissue MMP-9 in Patients with Ulcerative Colitis, but Not with Crohn's Disease.
[So] Source:Dig Dis Sci;62(6):1511-1517, 2017 Jun.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cyclophilin A (CyPA) is an immunomodulatory protein, high expression of which correlates with poor outcome of patients with inflammatory diseases. However, its role in inflammatory bowel disease (IBD) has not been studied. AIM: This study analyzes the correlation between cyclophilin A, matrix metalloproteinase (MMP)-9, and tissue inhibitor of MMP (TIMP)/MMP-9 complexes in the inflamed and non-inflamed colon mucosa of UC and CD patients. METHODS: Serum and biopsy specimens from inflamed and non-inflamed colonic mucosa of 38 patients with IBD (19 with UC and 19 with CD) and 16 controls were included in our study. We measured serum and tissue level of CyPA, and tissue level of TNF-α, MMP-9, TIMP-1/MMP-9, and TIMP-2/MMP-9 using ELISA method. RESULTS: Our results indicated that serum, but not tissue CyPA is increased in UC, rather than in CD patients, compared to the control. The increase correlated with higher tissue concentration of MMP-9 and TNF-α, especially in the UC group. Moreover, we observed significantly higher level of TIMP-1/MMP-9 in UC and CD group, which overlapped with the change in MMP-9. There was no change in TIMP-2/MMP-9 in the analyzed groups. CONCLUSION: The current study suggests that serum CyPA may be an independent additional marker of IBD, especially of UC. Higher CyPA level may be followed by increased MMP-9 in those patients. However, further studies are necessary to verify the role of CyPA in IBD development.
[Mh] Termos MeSH primário: Colite Ulcerativa/metabolismo
Colite Ulcerativa/patologia
Doença de Crohn/metabolismo
Doença de Crohn/patologia
Ciclofilina A/sangue
Metaloproteinase 9 da Matriz/metabolismo
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Biópsia
Estudos de Casos e Controles
Colo/metabolismo
Colo/patologia
Ciclofilina A/metabolismo
Feminino
Seres Humanos
Mucosa Intestinal/metabolismo
Mucosa Intestinal/patologia
Masculino
Meia-Idade
Inibidor Tecidual de Metaloproteinase-1/metabolismo
Inibidor Tecidual de Metaloproteinase-2/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Tissue Inhibitor of Metalloproteinase-1); 0 (Tumor Necrosis Factor-alpha); 127497-59-0 (Tissue Inhibitor of Metalloproteinase-2); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 5.2.1.- (Cyclophilin A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170410
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4568-0


  6 / 761 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28317380
[Au] Autor:Vidotto A; Morais AT; Ribeiro MR; Pacca CC; Terzian AC; Gil LH; Mohana-Borges R; Gallay P; Nogueira ML
[Ad] Endereço:Laboratório de Virologia, Faculdade de Medicina de José do Rio Preto , São José do Rio Preto, São Paulo 15090-000, Brazil.
[Ti] Título:Systems Biology Reveals NS4B-Cyclophilin A Interaction: A New Target to Inhibit YFV Replication.
[So] Source:J Proteome Res;16(4):1542-1555, 2017 Apr 07.
[Is] ISSN:1535-3907
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Yellow fever virus (YFV) replication is highly dependent on host cell factors. YFV NS4B is reported to be involved in viral replication and immune evasion. Here interactions between NS4B and human proteins were determined using a GST pull-down assay and analyzed using 1-DE and LC-MS/MS. We present a total of 207 proteins confirmed using Scaffold 3 Software. Cyclophilin A (CypA), a protein that has been shown to be necessary for the positive regulation of flavivirus replication, was identified as a possible NS4B partner. 59 proteins were found to be significantly increased when compared with a negative control, and CypA exhibited the greatest difference, with a 22-fold change. Fisher's exact test was significant for 58 proteins, and the p value of CypA was the most significant (0.000000019). The Ingenuity Systems software identified 16 pathways, and this analysis indicated sirolimus, an mTOR pathway inhibitor, as a potential inhibitor of CypA. Immunofluorescence and viral plaque assays showed a significant reduction in YFV replication using sirolimus and cyclosporine A (CsA) as inhibitors. Furthermore, YFV replication was strongly inhibited in cells treated with both inhibitors using reporter BHK-21-rep-YFV17D-LucNeoIres cells. Taken together, these data suggest that CypA-NS4B interaction regulates YFV replication. Finally, we present the first evidence that YFV inhibition may depend on NS4B-CypA interaction.
[Mh] Termos MeSH primário: Ciclofilina A/metabolismo
Proteínas/genética
Replicação Viral/genética
Vírus da Febre Amarela/genética
[Mh] Termos MeSH secundário: Ciclofilina A/genética
Interações Hospedeiro-Patógeno/efeitos dos fármacos
Seres Humanos
Transdução de Sinais/efeitos dos fármacos
Sirolimo/administração & dosagem
Biologia de Sistemas
Serina-Treonina Quinases TOR/antagonistas & inibidores
Proteínas não Estruturais Virais/metabolismo
Replicação Viral/efeitos dos fármacos
Vírus da Febre Amarela/patogenicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NS4A protein, flavivirus); 0 (Proteins); 0 (Viral Nonstructural Proteins); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 5.2.1.- (Cyclophilin A); W36ZG6FT64 (Sirolimus)
[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:170321
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jproteome.6b00933


  7 / 761 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28261567
[Au] Autor:Pandey S; Tripathi D; Khubaib M; Kumar A; Sheikh JA; Sumanlatha G; Ehtesham NZ; Hasnain SE
[Ad] Endereço:Inflammation Biology and Cell Signaling Laboratory, National Institute of PathologyNew Delhi, India; Department of Biology, Dr. Reddy's Institute of Life Sciences, University of HyderabadHyderabad, India.
[Ti] Título: Peptidyl-Prolyl Isomerases Are Immunogenic, Alter Cytokine Profile and Aid in Intracellular Survival.
[So] Source:Front Cell Infect Microbiol;7:38, 2017.
[Is] ISSN:2235-2988
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:( ) has two peptidyl-prolyl isomerases (Ppiases) PpiA and PpiB, popularly known as cyclophilin A and cyclophilin B. The role of cyclophilins in processes such as signaling, cell surface recognition, chaperoning, and heat shock response has been well-documented. We present evidence that Ppiases modulate the host immune response. ELISA results revealed significant presence of antibodies to Ppiases in patient sera as compared to sera from healthy individuals. Treatment of THP-1 cells with increasing concentrations of rPpiA, induced secretion of pro-inflammatory cytokines TNF-α and IL-6. Alternatively, treatment with rPpiB inhibited secretion of TNF-α and induced secretion of IL-10. Furthermore, heterologous expression of PpiA and PpiB in increased bacterial survival in THP-1 cells as compared to those transformed with the vector control. Our results demonstrate that Ppiases are immunogenic proteins that can possibly modulate host immune response and enhance persistence of the pathogen within the host by subverting host cell generated stresses.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Ciclofilina A/metabolismo
Ciclofilinas/metabolismo
Interações Hospedeiro-Patógeno
Viabilidade Microbiana
Mycobacterium tuberculosis/enzimologia
Mycobacterium tuberculosis/imunologia
[Mh] Termos MeSH secundário: Anticorpos Antibacterianos/sangue
Citocinas/secreção
Ensaio de Imunoadsorção Enzimática
Expressão Gênica
Seres Humanos
Macrófagos/imunologia
Macrófagos/microbiologia
Mycobacterium smegmatis/enzimologia
Mycobacterium smegmatis/genética
Mycobacterium smegmatis/fisiologia
Tuberculose/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Bacterial); 0 (Cytokines); 137497-17-7 (cyclophilin B); EC 5.2.1.- (Cyclophilin A); EC 5.2.1.- (Cyclophilins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE
[do] DOI:10.3389/fcimb.2017.00038


  8 / 761 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28174352
[Au] Autor:Jin K; Vaziri ND
[Ad] Endereço:Division of Nephrology, Department of Internal Medicine, Keimyung University Dongsan Medical Center, Daegu, Korea. mdjin922@gmail.com.
[Ti] Título:Elevated Plasma Cyclophillin A in Hemodialysis and Peritoneal Dialysis Patients: a Novel Link to Systemic Inflammation.
[So] Source:Iran J Kidney Dis;11(1):44-49, 2017 01.
[Is] ISSN:1735-8604
[Cp] País de publicação:Iran
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Cyclophillin A has emerged as a novel mediator of oxidative stress and inflammation and a major player in cardiovascular disease, diabetes mellitus, viral infections, and neurodegenerative and thrombotic disorders. Cyclophillin A is released by certain cell types spontaneously or in response to inflammatory mediators, hypoxia, oxidative stress, and hyperglycemia. Many of these conditions are either present or frequently occur in patients with end-stage renal disease and can stimulate release of cyclophillin A, thereby amplifying systemic inflammation. To our knowledge, the effect of end-stage renal disease and dialysis modalities on circulating cyclophillin A has not been previously investigated. This study tested the hypothesis that extracellular cyclophillin A is elevated in patients maintained on hemodialysis and peritoneal dialysis. MATERIALS AND METHODS: Cyclophillin A, high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-α, and lipid levels were measured in the fasting plasma samples from 20 hemodialysis and 20 peritoneal dialysis patients, and 20 age- and sex-matched controls. RESULTS: Plasma cyclophillin A concentration in the patients on hemodialysis (105.3 ± 6.2 ng/mL) and peritoneal dialysis (106.8 ± 9.0 ng/mL) were significantly higher than that in the control group (29.7 ± 4.1 ng/mL). This was associated with significant elevation of high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-α. Plasma cyclophillin A concentration showed direct correlations with high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-α, and an inverse correlation with high-density lipoprotein cholesterol concentration. CONCLUSIONS: Plasma cyclophillin A concentration is markedly elevated and positively correlates with the markers of systemic inflammation in hemodialysis and peritoneal dialysis patients.
[Mh] Termos MeSH primário: Ciclofilina A/sangue
Inflamação/imunologia
Falência Renal Crônica
Diálise Peritoneal/métodos
Diálise Renal/métodos
[Mh] Termos MeSH secundário: Adulto
Proteína C-Reativa/análise
Feminino
Seres Humanos
Interleucina-6/sangue
Falência Renal Crônica/diagnóstico
Falência Renal Crônica/imunologia
Falência Renal Crônica/terapia
Masculino
Meia-Idade
Estresse Oxidativo/imunologia
Reprodutibilidade dos Testes
Estatística como Assunto
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 9007-41-4 (C-Reactive Protein); EC 5.2.1.- (Cyclophilin A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE


  9 / 761 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28153875
[Au] Autor:Ohtsuki T; Satoh K; Omura J; Kikuchi N; Satoh T; Kurosawa R; Nogi M; Sunamura S; Yaoita N; Aoki T; Tatebe S; Sugimura K; Takahashi J; Miyata S; Shimokawa H
[Ad] Endereço:From the Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
[Ti] Título:Prognostic Impacts of Plasma Levels of Cyclophilin A in Patients With Coronary Artery Disease.
[So] Source:Arterioscler Thromb Vasc Biol;37(4):685-693, 2017 Apr.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Cyclophilin A (CyPA) is secreted from vascular smooth muscle cells, inflammatory cells, and activated platelets in response to oxidative stress. We have recently demonstrated that plasma CyPA level is a novel biomarker for diagnosing coronary artery disease. However, it remains to be elucidated whether plasma CyPA levels also have a prognostic impact in such patients. APPROACH AND RESULTS: In 511 consecutive patients undergoing diagnostic coronary angiography, we measured the plasma levels of CyPA, high-sensitivity C-reactive protein (hsCRP), and brain natriuretic peptide and evaluated their prognostic impacts during the follow-up (42 months, interquartile range: 25-55 months). Higher CyPA levels (≥12 ng/mL) were significantly associated with all-cause death, rehospitalization, and coronary revascularization. Higher hsCRP levels (≥1 mg/L) were also significantly correlated with the primary end point and all-cause death, but not with rehospitalization or coronary revascularization. Similarly, higher brain natriuretic peptide levels (≥100 pg/mL) were significantly associated with all-cause death and rehospitalization, but not with coronary revascularization. Importantly, the combination of CyPA (≥12 ng/mL) and hsCRP (≥1 mg/L) was more significantly associated with all-cause death (hazard ratio, 21.2; 95% confidence interval, 4.9-92.3,; <0.001) than CyPA (≥12 ng/mL) or hsCRP (≥1 mg/L) alone. CONCLUSIONS: The results indicate that plasma CyPA levels can be used to predict all-cause death, rehospitalization, and coronary revascularization in patients with coronary artery disease and that when combined with other biomarkers (hsCRP and brain natriuretic peptide levels), the CyPA levels have further enhanced prognostic impacts in those patients.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/sangue
Ciclofilina A/sangue
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Proteína C-Reativa/análise
Causas de Morte
Angiografia Coronária
Doença da Artéria Coronariana/diagnóstico por imagem
Doença da Artéria Coronariana/mortalidade
Doença da Artéria Coronariana/terapia
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Revascularização Miocárdica
Peptídeo Natriurético Encefálico/sangue
Readmissão do Paciente
Fragmentos de Peptídeos/sangue
Valor Preditivo dos Testes
Prognóstico
Modelos de Riscos Proporcionais
Retratamento
Fatores de Risco
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Peptide Fragments); 0 (pro-brain natriuretic peptide (1-76)); 114471-18-0 (Natriuretic Peptide, Brain); 9007-41-4 (C-Reactive Protein); EC 5.2.1.- (Cyclophilin A)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.116.308986


  10 / 761 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28089447
[Au] Autor:Holliday MJ; Camilloni C; Armstrong GS; Vendruscolo M; Eisenmesser EZ
[Ad] Endereço:Department of Biochemistry and Molecular Genetics, University of Colorado Denver, 12801 East 17th Avenue, MS 8101, Aurora, CO 80045, USA.
[Ti] Título:Networks of Dynamic Allostery Regulate Enzyme Function.
[So] Source:Structure;25(2):276-286, 2017 Feb 07.
[Is] ISSN:1878-4186
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many protein systems rely on coupled dynamic networks to allosterically regulate function. However, the broad conformational space sampled by non-coherently dynamic systems has precluded detailed analysis of their communication mechanisms. Here, we have developed a methodology that combines the high sensitivity afforded by nuclear magnetic resonance relaxation techniques and single-site multiple mutations, termed RASSMM, to identify two allosterically coupled dynamic networks within the non-coherently dynamic enzyme cyclophilin A. Using this methodology, we discovered two key hotspot residues, Val6 and Val29, that communicate through these networks, the mutation of which altered active-site dynamics, modulating enzymatic turnover of multiple substrates. Finally, we utilized molecular dynamics simulations to identify the mechanism by which one of these hotspots is coupled to the larger dynamic networks. These studies confirm a link between enzyme dynamics and the catalytic cycle of cyclophilin A and demonstrate how dynamic allostery may be engineered to tune enzyme function.
[Mh] Termos MeSH primário: Ciclofilina A/química
Simulação de Dinâmica Molecular
Mutação
Valina/química
[Mh] Termos MeSH secundário: Regulação Alostérica
Motivos de Aminoácidos
Biocatálise
Domínio Catalítico
Ciclofilina A/genética
Ciclofilina A/metabolismo
Expressão Gênica
Seres Humanos
Ressonância Magnética Nuclear Biomolecular
Ligação Proteica
Conformação Proteica em alfa-Hélice
Domínios e Motivos de Interação entre Proteínas
Estrutura Secundária de Proteína
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Relação Estrutura-Atividade
Especificidade por Substrato
Valina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Recombinant Proteins); EC 5.2.1.- (Cyclophilin A); HG18B9YRS7 (Valine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170117
[St] Status:MEDLINE



página 1 de 77 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde