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[PMID]:29399876
[Au] Autor:Martínez-García S; Rodríguez-Martínez S; Cancino-Diaz ME; Cancino-Diaz JC
[Ad] Endereço:Departamento de Microbiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Ciudad de México, Mexico.
[Ti] Título:Extracellular proteases of Staphylococcus epidermidis: roles as virulence factors and their participation in biofilm.
[So] Source:APMIS;126(3):177-185, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Staphylococci produce a large number of extracellular proteases, some of which are considered as potential virulence factors. Staphylococcus epidermidis is a causative agent of nosocomial infections in medical devices by the formation of biofilms. It has been proposed that proteases contribute to the different stages of biofilm formation. S. epidermidis secretes a small number of extracellular proteases, such as serine protease Esp, cysteine protease EcpA, and metalloprotease SepA that have a relatively low substrate specificity. Recent findings indicate a significant contribution of extracellular proteases in biofilm formation through the proteolytic inactivation of adhesion molecules. The objective of this work is to provide an overview of the current knowledge of S. epidermidis' extracellular proteases during pathogenicity, especially in the different stages of biofilm formation.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Biofilmes/crescimento & desenvolvimento
Cisteína Proteases/metabolismo
Metaloendopeptidases/metabolismo
Serina Proteases/metabolismo
Staphylococcus epidermidis/enzimologia
[Mh] Termos MeSH secundário: Moléculas de Adesão Celular/metabolismo
Infecção Hospitalar/microbiologia
Infecção Hospitalar/patologia
Seres Humanos
Infecções Estafilocócicas/microbiologia
Infecções Estafilocócicas/patologia
Staphylococcus epidermidis/metabolismo
Staphylococcus epidermidis/patogenicidade
Fatores de Virulência/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Cell Adhesion Molecules); 0 (Virulence Factors); EC 3.4.- (Cysteine Proteases); EC 3.4.- (Serine Proteases); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.- (SepA protein, Staphylococcus epidermidis)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180206
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12805


  2 / 13350 MEDLINE  
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[PMID]:29413990
[Au] Autor:Kelly J; Murphy JE
[Ad] Endereço:Mitochondrial Biology & Radiation Research Centre, Dept. of Life Sciences, Institute of Technology Sligo, Ash Lane, Sligo, Ireland. Electronic address: janiskelly@mail.itsligo.ie.
[Ti] Título:Mitochondrial gene expression changes in cultured human skin cells following simulated sunlight irradiation.
[So] Source:J Photochem Photobiol B;179:167-174, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Exposure of skin to simulated sunlight irradiation (SSI) has being extensively researched and shown to be the main cause for changes in the skin including changes in cellular function and generation of reactive oxygen species (ROS). This oxidative stress can subsequently exert downstream effects and the subcellular compartments most affected by this oxidative stress are mitochondria. The importance of functional mitochondrial morphology is apparent as morphological defects are related to many human diseases including diabetes mellitus, liver disease, neurodegenerative diseases, aging and cancer. OBJECTIVE: The main objective of this study was to evaluate solar radiation-induced changes in mitochondrial gene expression in human skin cells using a Q-Sun solar simulator to deliver a close match to the intensity of summer sunlight. METHODS: Spontaneously immortalised human skin epidermal keratinocytes (HaCaT) and Human Dermal Fibroblasts (HDFn) were divided into two groups. Group A were irradiated once and Group B twice 7days apart; following irradiation, mitochondrial gene expression was evaluated 1, 4 and 7days post primary exposure for group A and 1, 4, 7 and 14days post-secondary exposure for group B. RESULTS: Both the epidermal and dermal cells displayed significant reduced expression of the genes analysed for mitochondrial morphology and function; however, epidermal cells displayed this reduction post SSI earlier then dermal cells at multiple time points. CONCLUSION: The data presented here reinforces the fact that epidermal cells, while displaying a heightened sensitivity to sunlight, are less prone to changes in gene expression, while dermal cells, which appear to be more resilient are possibly more prone to genomic instability and mitochondrial damage.
[Mh] Termos MeSH primário: Expressão Gênica/efeitos da radiação
Mitocôndrias/genética
Luz Solar
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares/genética
ATPases Associadas a Diversas Atividades Celulares/metabolismo
Linhagem Celular
Derme/citologia
Epiderme/citologia
GTP Fosfo-Hidrolases/genética
GTP Fosfo-Hidrolases/metabolismo
Seres Humanos
Queratinócitos/citologia
Queratinócitos/metabolismo
Queratinócitos/efeitos da radiação
Metaloendopeptidases/genética
Metaloendopeptidases/metabolismo
Mitocôndrias/efeitos da radiação
Proteínas de Transporte da Membrana Mitocondrial/genética
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitochondrial Membrane Transport Proteins); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (superoxide dismutase 2); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.- (YME1L1 protein, human); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (MFN2 protein, human); EC 3.6.1.- (OPA1 protein, human); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities); EC 3.6.5.- (Mfn1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


  3 / 13350 MEDLINE  
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[PMID]:27774687
[Au] Autor:Clark KM; Jenkins JL; Fedoriw N; Dumont ME
[Ad] Endereço:Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, 14642.
[Ti] Título:Human CaaX protease ZMPSTE24 expressed in yeast: Structure and inhibition by HIV protease inhibitors.
[So] Source:Protein Sci;26(2):242-257, 2017 Feb.
[Is] ISSN:1469-896X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The function and localization of proteins and peptides containing C-terminal "CaaX" (Cys-aliphatic-aliphatic-anything) sequence motifs are modulated by post-translational attachment of isoprenyl groups to the cysteine sulfhydryl, followed by proteolytic cleavage of the aaX amino acids. The zinc metalloprotease ZMPSTE24 is one of two enzymes known to catalyze this cleavage. The only identified target of mammalian ZMPSTE24 is prelamin A, the precursor to the nuclear scaffold protein lamin A. ZMPSTE24 also cleaves prelamin A at a second site 15 residues upstream from the CaaX site. Mutations in ZMPSTE24 result in premature-aging diseases and inhibition of ZMPSTE24 activity has been reported to be an off-target effect of HIV protease inhibitors. We report here the expression (in yeast), purification, and crystallization of human ZMPSTE24 allowing determination of the structure to 2.0 Å resolution. Compared to previous lower resolution structures, the enhanced resolution provides: (1) a detailed view of the active site of ZMPSTE24, including water coordinating the catalytic zinc; (2) enhanced visualization of fenestrations providing access from the exterior to the interior cavity of the protein; (3) a view of the C-terminus extending away from the main body of the protein; (4) localization of ordered lipid and detergent molecules at internal and external surfaces and also projecting through fenestrations; (5) identification of water molecules associated with the surface of the internal cavity. We also used a fluorogenic assay of the activity of purified ZMPSTE24 to demonstrate that HIV protease inhibitors directly inhibit the human enzyme in a manner indicative of a competitive mechanism.
[Mh] Termos MeSH primário: Inibidores da Protease de HIV/química
Proteínas de Membrana/antagonistas & inibidores
Proteínas de Membrana/química
Metaloendopeptidases/antagonistas & inibidores
Metaloendopeptidases/química
[Mh] Termos MeSH secundário: Domínio Catalítico
Seres Humanos
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Metaloendopeptidases/genética
Metaloendopeptidases/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIV Protease Inhibitors); 0 (Membrane Proteins); 0 (Recombinant Proteins); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.84 (ZMPSTE24 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/pro.3074


  4 / 13350 MEDLINE  
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[PMID]:28902287
[Au] Autor:Sutter A; Antunes D; Silva-Almeida M; Costa MGS; Caffarena ER
[Ad] Endereço:Grupo de Biofísica Computacional e Modelagem Molecular, Programa de Computação Científica, Rio de Janeiro, RJ, Brasil.
[Ti] Título:Structural insights into leishmanolysins encoded on chromosome 10 of Leishmania (Viannia) braziliensis.
[So] Source:Mem Inst Oswaldo Cruz;112(9):617-625, 2017 Sep.
[Is] ISSN:1678-8060
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Leishmanolysins have been described as important parasite virulence factors because of their roles in the infection of promastigotes and resistance to host's defenses. Leishmania (Viannia) braziliensis contains several leishmanolysin genes in its genome, especially in chromosome 10. However, the functional impact of such diversity is not understood, but may be attributed partially to the lack of structural data for proteins from this parasite. OBJECTIVES: This works aims to compare leishmanolysin sequences from L. (V.) braziliensis and to understand how the diversity impacts in their structural and dynamic features. METHODS: Leishmanolysin sequences were retrieved from GeneDB. Subsequently, 3D models were built using comparative modeling methods and their dynamical behavior was studied using molecular dynamic simulations. FINDINGS: We identified three subgroups of leishmanolysins according to sequence variations. These differences directly affect the electrostatic properties of leishmanolysins and the geometry of their active sites. We identified two levels of structural heterogeneity that might be related to the ability of promastigotes to interact with a broad range of substrates. MAIN CONCLUSION: Altogether, the structural plasticity of leishmanolysins may constitute an important evolutionary adaptation rarely explored when considering the virulence of L. (V.) braziliensis parasites.
[Mh] Termos MeSH primário: Variação Genética
Leishmania braziliensis/genética
Metaloendopeptidases/genética
Conformação Proteica
[Mh] Termos MeSH secundário: Cromossomos
Seres Humanos
Modelos Moleculares
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.- (glycoprotein gp63, Leishmania)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE


  5 / 13350 MEDLINE  
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[PMID]:28805828
[Au] Autor:Braun DA; Rao J; Mollet G; Schapiro D; Daugeron MC; Tan W; Gribouval O; Boyer O; Revy P; Jobst-Schwan T; Schmidt JM; Lawson JA; Schanze D; Ashraf S; Ullmann JFP; Hoogstraten CA; Boddaert N; Collinet B; Martin G; Liger D; Lovric S; Furlano M; Guerrera IC; Sanchez-Ferras O; Hu JF; Boschat AC; Sanquer S; Menten B; Vergult S; De Rocker N; Airik M; Hermle T; Shril S; Widmeier E; Gee HY; Choi WI; Sadowski CE; Pabst WL; Warejko JK; Daga A; Basta T; Matejas V; Scharmann K; Kienast SD; Behnam B; Beeson B; Begtrup A; Bruce M; Ch'ng GS; Lin SP
[Ad] Endereço:Department of Medicine, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Título:Mutations in KEOPS-complex genes cause nephrotic syndrome with primary microcephaly.
[So] Source:Nat Genet;49(10):1529-1538, 2017 Oct.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Galloway-Mowat syndrome (GAMOS) is an autosomal-recessive disease characterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain anomalies. Here we identified recessive mutations in OSGEP, TP53RK, TPRKB, and LAGE3, genes encoding the four subunits of the KEOPS complex, in 37 individuals from 32 families with GAMOS. CRISPR-Cas9 knockout in zebrafish and mice recapitulated the human phenotype of primary microcephaly and resulted in early lethality. Knockdown of OSGEP, TP53RK, or TPRKB inhibited cell proliferation, which human mutations did not rescue. Furthermore, knockdown of these genes impaired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-response signaling, and ultimately induced apoptosis. Knockdown of OSGEP or TP53RK induced defects in the actin cytoskeleton and decreased the migration rate of human podocytes, an established intermediate phenotype of SRNS. We thus identified four new monogenic causes of GAMOS, describe a link between KEOPS function and human disease, and delineate potential pathogenic mechanisms.
[Mh] Termos MeSH primário: Hérnia Hiatal/genética
Microcefalia/genética
Complexos Multiproteicos/genética
Mutação
Nefrose/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Sistemas CRISPR-Cas
Proteínas de Transporte/genética
Movimento Celular
Citoesqueleto/ultraestrutura
Reparo do DNA/genética
Estresse do Retículo Endoplasmático/genética
Técnicas de Inativação de Genes
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/deficiência
Peptídeos e Proteínas de Sinalização Intracelular/genética
Metaloendopeptidases/deficiência
Metaloendopeptidases/genética
Camundongos
Modelos Moleculares
Síndrome Nefrótica/genética
Síndrome Nefrótica/patologia
Podócitos/metabolismo
Podócitos/ultraestrutura
Conformação Proteica
Proteínas Serina-Treonina Quinases/deficiência
Proteínas Serina-Treonina Quinases/genética
Processamento Pós-Transcricional do RNA/genética
RNA de Transferência/metabolismo
Homeostase do Telômero/genética
Peixe-Zebra
Proteínas de Peixe-Zebra/deficiência
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Intracellular Signaling Peptides and Proteins); 0 (LAGE3 protein, human); 0 (Multiprotein Complexes); 0 (TPRKB protein, human); 0 (Zebrafish Proteins); 9014-25-9 (RNA, Transfer); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (TP53RK protein, human); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.57 (O-sialoglycoprotein endopeptidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3933


  6 / 13350 MEDLINE  
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[PMID]:28800585
[Au] Autor:Cohen JE; Wang R; Shen RF; Wu WW; Keller JE
[Ad] Endereço:Laboratory of Respiratory and Special Pathogens, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, Maryland, United States of America.
[Ti] Título:Comparative pathogenomics of Clostridium tetani.
[So] Source:PLoS One;12(8):e0182909, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Clostridium tetani and Clostridium botulinum produce two of the most potent neurotoxins known, tetanus neurotoxin and botulinum neurotoxin, respectively. Extensive biochemical and genetic investigation has been devoted to identifying and characterizing various C. botulinum strains. Less effort has been focused on studying C. tetani likely because recently sequenced strains of C. tetani show much less genetic diversity than C. botulinum strains and because widespread vaccination efforts have reduced the public health threat from tetanus. Our aim was to acquire genomic data on the U.S. vaccine strain of C. tetani to better understand its genetic relationship to previously published genomic data from European vaccine strains. We performed high throughput genomic sequence analysis on two wild-type and two vaccine C. tetani strains. Comparative genomic analysis was performed using these and previously published genomic data for seven other C. tetani strains. Our analysis focused on single nucleotide polymorphisms (SNP) and four distinct constituents of the mobile genome (mobilome): a hypervariable flagellar glycosylation island region, five conserved bacteriophage insertion regions, variations in three CRISPR (clustered regularly interspaced short palindromic repeats)-Cas (CRISPR-associated) systems, and a single plasmid. Intact type IA and IB CRISPR/Cas systems were within 10 of 11 strains. A type IIIA CRISPR/Cas system was present in two strains. Phage infection histories derived from CRISPR-Cas sequences indicate C. tetani encounters phages common among commensal gut bacteria and soil-borne organisms consistent with C. tetani distribution in nature. All vaccine strains form a clade distinct from currently sequenced wild type strains when considering variations in these mobile elements. SNP, flagellar glycosylation island, prophage content and CRISPR/Cas phylogenic histories provide tentative evidence suggesting vaccine and wild type strains share a common ancestor.
[Mh] Termos MeSH primário: Proteínas de Bactérias/genética
Sistemas CRISPR-Cas
Clostridium tetani/genética
Genoma Bacteriano
Filogenia
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Bacteriófagos/genética
Sequência de Bases
Mapeamento Cromossômico
Clostridium tetani/classificação
Clostridium tetani/patogenicidade
Ilhas Genômicas
Glicosilação
Metaloendopeptidases/biossíntese
Metaloendopeptidases/genética
Plasmídeos/química
Plasmídeos/metabolismo
Análise de Sequência de DNA
Toxina Tetânica/biossíntese
Toxina Tetânica/genética
Toxoide Tetânico/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Tetanus Toxin); 0 (Tetanus Toxoid); 11032-48-7 (tetanospasmin); EC 3.4.24.- (Metalloendopeptidases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182909


  7 / 13350 MEDLINE  
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[PMID]:28738346
[Au] Autor:Li Y; Huang J; Li L; Liu L
[Ad] Endereço:State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
[Ti] Título:Synergistic Activity of Berberine with Azithromycin against Pseudomonas Aeruginosa Isolated from Patients with Cystic Fibrosis of Lung In Vitro and In Vivo.
[So] Source:Cell Physiol Biochem;42(4):1657-1669, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Pseudomonas aeruginosa (PA) is one of the major opportunistic pathogens which can cause chronic lung infection of cystic fibrosis (CF). The formation of PA biofilm promotes CF development and restricts the antimicrobial efficacies of current antibiotics. METHODS: The antimicrobial effects of azithromycin (AZM) and berberine (BER) alone and in combination were evaluated using microdilution method, checkerboard assay, time-kill test, qRT-PCR analysis and absorption method. The treatments of AZM and/or BER were further evaluated in an animal lung infection model via observing survival rate, bacterial burden and histopathology of lung, the levels of pro-/anti-inflammatory cytokines. RESULTS: AZM-BER were demonstrated to be synergistic against ten clinical PA isolates as well as the standard reference PA ATCC27853, in which PA03 was the most susceptible isolate to AZM-BER with FICI of 0.13 and chosen for subsequent experiments. The synergism of AZM-BER was further confirmed against PA03 in time-kill test and scanning electron microscope (SEM) at their concentrations showing synergism. In PA03, we found that AZM-BER could significantly attenuate productions of a series of virulence factors including alginate, LasA protease, LasB protease, pyoverdin, pyocyanin, chitinase as well as extracellular DNA, and remarkably inhibit the levels of quorum sensing (QS) molecules and the expressions of lasI, lasR, rhlI, rhlR at 1/2×MIC, 1×MIC and 2×MIC. In the infection model, the mice survival were increased markedly, the inflammations of infected lungs were improved greatly along with reduced IL-6, IL-8 and ascended IL-10 at 0.8 mg/kg of AZM combined with 3.2 mg/kg of BER. CONCLUSION: BER might be a promising synergist to enhance the antimicrobial activity of AZM in vitro and in vivo.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Azitromicina/farmacologia
Berberina/farmacologia
Biofilmes/efeitos dos fármacos
Infecções por Pseudomonas/tratamento farmacológico
Pseudomonas aeruginosa/efeitos dos fármacos
[Mh] Termos MeSH secundário: Alginatos
Animais
Proteínas de Bactérias/antagonistas & inibidores
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Biofilmes/crescimento & desenvolvimento
Quitinases/antagonistas & inibidores
Quitinases/genética
Quitinases/metabolismo
Ciclofosfamida
Fibrose Cística/microbiologia
DNA Bacteriano/antagonistas & inibidores
DNA Bacteriano/biossíntese
Combinação de Medicamentos
Sinergismo Farmacológico
Ácido Glucurônico/antagonistas & inibidores
Ácido Glucurônico/biossíntese
Ácidos Hexurônicos/antagonistas & inibidores
Seres Humanos
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Pulmão/microbiologia
Metaloendopeptidases/antagonistas & inibidores
Metaloendopeptidases/genética
Metaloendopeptidases/metabolismo
Metaloproteases/antagonistas & inibidores
Metaloproteases/genética
Metaloproteases/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Testes de Sensibilidade Microbiana
Neutropenia/induzido quimicamente
Neutropenia/tratamento farmacológico
Neutropenia/genética
Neutropenia/patologia
Oligopeptídeos/antagonistas & inibidores
Oligopeptídeos/biossíntese
Infecções por Pseudomonas/induzido quimicamente
Infecções por Pseudomonas/genética
Infecções por Pseudomonas/patologia
Pseudomonas aeruginosa/crescimento & desenvolvimento
Pseudomonas aeruginosa/patogenicidade
Piocianina/antagonistas & inibidores
Piocianina/biossíntese
Fatores de Virulência/antagonistas & inibidores
Fatores de Virulência/genética
Fatores de Virulência/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alginates); 0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (DNA, Bacterial); 0 (Drug Combinations); 0 (Hexuronic Acids); 0 (Oligopeptides); 0 (Virulence Factors); 0I8Y3P32UF (Berberine); 8062-00-8 (pyoverdin); 83905-01-5 (Azithromycin); 8A5D83Q4RW (Glucuronic Acid); 8C3Z4148WZ (alginic acid); 8N3DW7272P (Cyclophosphamide); 9OQM399341 (Pyocyanine); EC 3.2.1.14 (Chitinases); EC 3.4.- (LasA protein, Pseudomonas aeruginosa); EC 3.4.- (Metalloproteases); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.26 (pseudolysin, Pseudomonas aeruginosa)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.1159/000479411


  8 / 13350 MEDLINE  
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[PMID]:28694294
[Au] Autor:Ko SH; Jeon JI; Myung HS; Kim YJ; Kim JM
[Ad] Endereço:Department of Microbiology and Department of Biomedical Science, Hanyang University College of Medicine and Graduate School of Biomedical Science and Engineering, Seoul, South Korea.
[Ti] Título:Bacteroides fragilis Enterotoxin Induces Formation of Autophagosomes in Endothelial Cells but Interferes with Fusion with Lysosomes for Complete Autophagic Flux through a Mitogen-Activated Protein Kinase-, AP-1-, and C/EBP Homologous Protein-Dependent Pathway.
[So] Source:Infect Immun;85(10), 2017 Oct.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:enterotoxin (BFT), a virulence factor of enterotoxigenic (ETBF), plays an essential role in mucosal inflammation. Although autophagy contributes to the pathogenesis of diverse infectious diseases, little is known about autophagy in ETBF infection. This study was conducted to investigate the role of BFT in the autophagic process in endothelial cells (ECs). Stimulation of human umbilical vein ECs (HUVECs) with BFT increased light chain 3 protein II (LC3-II) conversion from LC3-I and protein expression of p62, Atg5, and Atg12. In addition, BFT-exposed ECs showed increased indices of autophagosomal fusion with lysosomes such as LC3-lysosome-associated protein 2 (LAMP2) colocalization and the percentage of red vesicles monitored by the expression of dual-tagged LC3B. BFT also upregulated expression of C/EBP homologous protein (CHOP), and inhibition of CHOP significantly increased indices of autophagosomal fusion with lysosomes. BFT activated an AP-1 transcription factor, in which suppression of AP-1 activity significantly downregulated CHOP and augmented autophagosomal fusion with lysosomes. Furthermore, suppression of Jun N-terminal protein kinase (JNK) mitogen-activated protein kinase (MAPK) significantly inhibited the AP-1 and CHOP signals, leading to an increase in autophagosomal fusion with lysosomes in BFT-stimulated ECs. These results suggest that BFT induced accumulation of autophagosomes in ECs, but activation of a signaling pathway involving JNK, AP-1, and CHOP may interfere with complete autophagy.
[Mh] Termos MeSH primário: Autofagossomos/fisiologia
Autofagia
Bacteroides fragilis/metabolismo
Lisossomos/fisiologia
Metaloendopeptidases/metabolismo
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fator de Transcrição AP-1/metabolismo
Fator de Transcrição CHOP/metabolismo
[Mh] Termos MeSH secundário: Autofagossomos/microbiologia
Bacteroides fragilis/patogenicidade
Células Cultivadas
Regulação para Baixo
Células Endoteliais/metabolismo
Células Endoteliais/microbiologia
Células Endoteliais/ultraestrutura
Seres Humanos
Lisossomos/microbiologia
NF-kappa B/metabolismo
Transdução de Sinais
Veias Umbilicais/citologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DDIT3 protein, human); 0 (NF-kappa B); 0 (Transcription Factor AP-1); 147336-12-7 (Transcription Factor CHOP); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.74 (fragilysin)
[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:170712
[St] Status:MEDLINE


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[PMID]:28594571
[Au] Autor:Li S; Fu B; Wang L; Dorf ME
[Ad] Endereço:1 Department of Physiological Sciences, Oklahoma State University , Stillwater, Oklahoma.
[Ti] Título:ZMPSTE24 Is Downstream Effector of Interferon-Induced Transmembrane Antiviral Activity.
[So] Source:DNA Cell Biol;36(7):513-517, 2017 Jul.
[Is] ISSN:1557-7430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The zinc metalloprotease ZMPSTE24 is a constitutively and ubiquitously expressed host restriction factor that is responsible for limiting infection by a broad spectrum of enveloped viruses, including influenza A, vesicular stomatitis, zika, ebola, Sindbis, cowpox, and vaccinia viruses, but not murine leukemia or adenovirus. Antiviral function is independent of ZMPSTE24 enzymatic activity. Protein interaction and genetic complementation studies indicate that ZMPSTE24 is a component of a common antiviral pathway that is associated with interferon-induced transmembrane proteins. In vivo studies with zmpste24-deficient mice demonstrate the importance of ZMPSTE24 for antiviral defense.
[Mh] Termos MeSH primário: Membrana Celular/imunologia
Endossomos/imunologia
Interações Hospedeiro-Patógeno
Proteínas de Membrana/genética
Metaloendopeptidases/genética
Proteínas de Ligação a RNA/genética
[Mh] Termos MeSH secundário: Animais
Membrana Celular/efeitos dos fármacos
Membrana Celular/virologia
Endossomos/efeitos dos fármacos
Endossomos/virologia
Regulação da Expressão Gênica
Teste de Complementação Genética
Células HEK293
Seres Humanos
Imunidade Inata
Vírus da Influenza A/efeitos dos fármacos
Vírus da Influenza A/imunologia
Interferon gama/farmacologia
Proteínas de Membrana/imunologia
Metaloendopeptidases/imunologia
Camundongos
Camundongos Knockout
Ligação Proteica
Mapeamento de Interação de Proteínas
Proteínas de Ligação a RNA/imunologia
Transdução de Sinais
Internalização do Vírus/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IFITM3 protein, human); 0 (Membrane Proteins); 0 (RNA-Binding Proteins); 82115-62-6 (Interferon-gamma); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.84 (ZMPSTE24 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1089/dna.2017.3791


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[PMID]:28581479
[Au] Autor:Campos CA; Bowen AJ; Han S; Wisse BE; Palmiter RD; Schwartz MW
[Ad] Endereço:Department of Biochemistry, Howard Hughes Medical Institute, University of Washington, Seattle, Washington, USA.
[Ti] Título:Cancer-induced anorexia and malaise are mediated by CGRP neurons in the parabrachial nucleus.
[So] Source:Nat Neurosci;20(7):934-942, 2017 Jul.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Anorexia is a common manifestation of chronic diseases, including cancer. Here we investigate the contribution to cancer anorexia made by calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus (PBN) that transmit anorexic signals. We show that CGRP neurons are activated in mice implanted with Lewis lung carcinoma cells. Inactivation of CGRP neurons before tumor implantation prevents anorexia and loss of lean mass, and their inhibition after symptom onset reverses anorexia. CGRP neurons are also activated in Apc mice, which develop intestinal cancer and lose weight despite the absence of reduced food intake. Inactivation of CGRP neurons in Apc mice permits hyperphagia that counteracts weight loss, revealing a role for these neurons in a 'nonanorexic' cancer model. We also demonstrate that inactivation of CGRP neurons prevents lethargy, anxiety and malaise associated with cancer. These findings establish CGRP neurons as key mediators of cancer-induced appetite suppression and associated behavioral changes.
[Mh] Termos MeSH primário: Anorexia/fisiopatologia
Peptídeo Relacionado com Gene de Calcitonina/fisiologia
Carcinoma Pulmonar de Lewis/fisiopatologia
Comportamento de Doença/fisiologia
Neoplasias/fisiopatologia
Núcleos Parabraquiais/fisiologia
[Mh] Termos MeSH secundário: Proteína da Polipose Adenomatosa do Colo/genética
Animais
Comportamento Animal/fisiologia
Peso Corporal
Caquexia/fisiopatologia
Peptídeo Relacionado com Gene de Calcitonina/antagonistas & inibidores
Peptídeo Relacionado com Gene de Calcitonina/genética
Clozapina/análogos & derivados
Clozapina/farmacologia
Metabolismo Energético/fisiologia
Feminino
Masculino
Metaloendopeptidases/farmacologia
Camundongos
Camundongos Transgênicos
Núcleos Parabraquiais/efeitos dos fármacos
Toxina Tetânica/farmacologia
Células Tumorais Cultivadas/transplante
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenomatous Polyposis Coli Protein); 0 (Calca protein, mouse); 0 (Tetanus Toxin); 0 (adenomatous polyposis coli protein, mouse); 83652-28-2 (Calcitonin Gene-Related Peptide); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.- (zinc-endopeptidase, tetanus neurotoxin); J60AR2IKIC (Clozapine); MZA8BK588J (clozapine N-oxide)
[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:170606
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4574



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