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[PMID]:29383769
[Au] Autor:Oldenburger IB; Wolters VM; Kardol-Hoefnagel T; Houwen RHJ; Otten HG
[Ad] Endereço:Department of Pediatric Gastroenterology, Wilhelmina Children's Hospital, Utrecht, The Netherlands.
[Ti] Título:Serum intestinal fatty acid-binding protein in the noninvasive diagnosis of celiac disease.
[So] Source:APMIS;126(3):186-190, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Current diagnostic guidelines for celiac disease (CD) in pediatric patients require a duodenal biopsy if the IgA anti-tissue transglutaminase (tTG) is below 10x the upper limit of normal (ULN). Additional markers may enable a noninvasive diagnosis in this group. Serum intestinal-fatty acid-binding protein (I-FABP), a marker for intestinal epithelial damage, could be useful in this respect. A total of 95 children with a clinical suspicion of CD and tTG 1-10x ULN were investigated. All had a duodenal biopsy and analysis of serum I-FABP. A control group of 161 children with familial short stature and normal tTG was included. I-FABP levels in the 71 patients with tTG 1-10x ULN and biopsy-proven CD (median 725 pg/mL) were not significantly different (p = 0.13) from the levels in the 24 patients with a tTG 1-10x ULN but a normal biopsy (median 497 pg/mL). However, when combining tTG and I-FABP levels, 11/24 patients could have been diagnosed noninvasively if tTG is ≥ 50 U/mL and I-FABP ≥880 pg/mL or in 12/19 patients if tTG is ≥ 60 U/mL and I-FABP ≥ 620 pg/mL. Therefore, addition of I-FABP to the diagnostic procedure of CD may provide a noninvasive diagnosis in patients with a tTG ≥ 50 U/mL.
[Mh] Termos MeSH primário: Doença Celíaca/diagnóstico
Doença Celíaca/patologia
Proteínas de Ligação a Ácido Graxo/sangue
Proteínas de Ligação ao GTP/imunologia
Imunoglobulina A/sangue
Transglutaminases/imunologia
[Mh] Termos MeSH secundário: Adolescente
Doença Celíaca/sangue
Criança
Pré-Escolar
Duodeno/patologia
Proteínas de Ligação a Ácido Graxo/metabolismo
Feminino
Antígenos HLA-DQ/sangue
Seres Humanos
Imunoglobulina A/imunologia
Lactente
Mucosa Intestinal/patologia
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FABP2 protein, human); 0 (Fatty Acid-Binding Proteins); 0 (HLA-DQ Antigens); 0 (HLA-DQ2 antigen); 0 (HLA-DQ8 antigen); 0 (Immunoglobulin A); EC 2.3.2.- (transglutaminase 2); EC 2.3.2.13 (Transglutaminases); EC 2.3.2.13 (transglutaminase 1); EC 3.6.1.- (GTP-Binding Proteins)
[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:180201
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12800


  2 / 27595 MEDLINE  
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[PMID]:28453723
[Au] Autor:Blanca Ramírez M; Lara Ordóñez AJ; Fdez E; Madero-Pérez J; Gonnelli A; Drouyer M; Chartier-Harlin MC; Taymans JM; Bubacco L; Greggio E; Hilfiker S
[Ad] Endereço:Institute of Parasitology and Biomedicine 'López-Neyra', Consejo Superior de Investigaciones Científicas (CSIC), 18016 Granada, Spain.
[Ti] Título:GTP binding regulates cellular localization of Parkinson's disease-associated LRRK2.
[So] Source:Hum Mol Genet;26(14):2747-2767, 2017 07 15.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mutations in leucine-rich repeat kinase 2 (LRRK2) comprise the most common cause of familial Parkinson's disease (PD), and sequence variants modify risk for sporadic PD. Previous studies indicate that LRRK2 interacts with microtubules (MTs) and alters MT-mediated vesicular transport processes. However, the molecular determinants within LRRK2 required for such interactions have remained unknown. Here, we report that most pathogenic LRRK2 mutants cause relocalization of LRRK2 to filamentous structures which colocalize with a subset of MTs, and an identical relocalization is seen upon pharmacological LRRK2 kinase inhibition. The pronounced colocalization with MTs does not correlate with alterations in LRRK2 kinase activity, but rather with increased GTP binding. Synthetic mutations which impair GTP binding, as well as LRRK2 GTP-binding inhibitors profoundly interfere with the abnormal localization of both pathogenic mutant as well as kinase-inhibited LRRK2. Conversely, addition of a non-hydrolyzable GTP analog to permeabilized cells enhances the association of pathogenic or kinase-inhibited LRRK2 with MTs. Our data elucidate the mechanism underlying the increased MT association of select pathogenic LRRK2 mutants or of pharmacologically kinase-inhibited LRRK2, with implications for downstream MT-mediated transport events.
[Mh] Termos MeSH primário: Guanosina Trifosfato/metabolismo
Serina-Treonina Proteína Quinase-2 com Repetições Ricas em Leucina/metabolismo
Doença de Parkinson/metabolismo
[Mh] Termos MeSH secundário: GTP Fosfo-Hidrolases/metabolismo
Proteínas de Ligação ao GTP/genética
Proteínas de Ligação ao GTP/metabolismo
Variação Genética
Guanosina Trifosfato/genética
Células HEK293
Seres Humanos
Serina-Treonina Proteína Quinase-2 com Repetições Ricas em Leucina/antagonistas & inibidores
Serina-Treonina Proteína Quinase-2 com Repetições Ricas em Leucina/genética
Microtúbulos/genética
Microtúbulos/metabolismo
Mutação
Doença de Parkinson/genética
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 86-01-1 (Guanosine Triphosphate); EC 2.7.11.1 (LRRK2 protein, human); EC 2.7.11.1 (Leucine-Rich Repeat Serine-Threonine Protein Kinase-2); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180225
[Lr] Data última revisão:
180225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx161


  3 / 27595 MEDLINE  
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[PMID]:29374703
[Au] Autor:Kang S; Oh SC; Min BW; Lee DH
[Ad] Endereço:Department of Surgery, Korea University Guro Hospital, Seoul, Republic of Korea.
[Ti] Título:Transglutaminase 2 Regulates Self-renewal and Stem Cell Marker of Human Colorectal Cancer Stem Cells.
[So] Source:Anticancer Res;38(2):787-794, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The aim of this study was to investigate the role of transglutaminase 2 (TGM2) in colorectal cancer stem cells (CCSCs). MATERIALS AND METHODS: We used the TU12 cell line possessing CD133-expressing CCSCs. After isolating CD133 (-) and CD133 (+) CCSCs, we overexpressed and knocked-down TGM2 to investigate its role in human CCSCs. RESULTS: The expression level of TGM2 was 25-fold higher in tumorigenic cells than non-tumorigenic cells. We found that knockdown of TGM2 by specific RNA interference markedly inhibited cell growth and caused down-regulation of the stemness markers, CD133, SOX2, and ß-catenin. We further demonstrated that knockdown of TGM2 inhibited cell metastatic abilities by down-regulating N-cadherin and vimentin and up-regulating E-cadherin. These findings revealed that TGM2 expression is markedly increased in human colorectal cancer and that down-regulation of TGM2 in tumors may serve as a treatment for colorectal cancer patients. Therefore, this study indicate that TGM2 affects the metastatic potential and stemness of CCSCs by regulating EMT- and stemness-related proteins. CONCLUSION: The metastatic potential of CSCs arises from highly expressed TGM2.
[Mh] Termos MeSH primário: Neoplasias Colorretais/enzimologia
Proteínas de Ligação ao GTP/biossíntese
Células-Tronco Neoplásicas/enzimologia
Transglutaminases/biossíntese
[Mh] Termos MeSH secundário: Antígeno AC133/biossíntese
Antígenos CD/metabolismo
Biomarcadores Tumorais
Caderinas/metabolismo
Linhagem Celular Tumoral
Movimento Celular/fisiologia
Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Regulação para Baixo
Transição Epitelial-Mesenquimal
Proteínas de Ligação ao GTP/genética
Proteínas de Ligação ao GTP/metabolismo
Técnicas de Silenciamento de Genes
Seres Humanos
Imuno-Histoquímica
Invasividade Neoplásica
Metástase Neoplásica
Células-Tronco Neoplásicas/patologia
Transglutaminases/genética
Transglutaminases/metabolismo
Células Tumorais Cultivadas
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Antigens, CD); 0 (Biomarkers, Tumor); 0 (CDH1 protein, human); 0 (CDH2 protein, human); 0 (Cadherins); 0 (PROM1 protein, human); 0 (Vimentin); EC 2.3.2.- (transglutaminase 2); EC 2.3.2.13 (Transglutaminases); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  4 / 27595 MEDLINE  
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[PMID]:29381915
[Au] Autor:Zhang S; Liu W; Liu X; Qi J; Deng C
[Ti] Título:Biomarkers identification for acute myocardial infarction detection via weighted gene co-expression network analysis.
[So] Source:Medicine (Baltimore);96(47):e8375, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The study aimed to seek potential biomarkers for acute myocardial infarction (AMI) detection and treatment.The dataset GSE48060 was used, consisting of 52 peripheral blood samples (31 AMI samples and 21 normal controls). By limma package, differentially expressed genes (DEGs) between 2 kinds of samples were identified, followed by enrichment analysis, subpathway analysis, protein-protein interaction (PPI) network analysis, and transcription factor network (TFN) analysis. Weighted gene co-expression network analysis was used to further extract key modules relating to AMI, followed by enrichment and TFN analyses. Expression validation was performed via meta-analysis of 2 datasets, GSE22229 and GSE29111.A set of 428 DEGs in AMI were screened out, and the upregulated toll-like receptor (TLR) family genes (TLR1, TLR2, and TLR10) were enriched in wound response, immune response and inflammatory response functions, and downregulated genes (GBP5, CXCL5, GZMA, CCL5, and CCL4) were correlated with immune response. CCL5, GZMA, GZMB, TLR2, and formyl peptide receptor 1 (FPR1) were predicted as crucial nodes in the PPI network. Signal transducer and activator of transcription 1 (STAT1) was the key transcription factor (TF) with multiple targets. The grey module was highly related to AMI. Genes in this module were closely related to regulation of macrophage activation, and spermatogenic leucine zipper 1 (SPZ1) was identified as a TF. Expressions of TLR2 and FPR1 were confirmed via the integrated matrix.Several potential biomarkers for AMI detection were identified, such as GZMB, GBP5, FPR1, TLR2, STAT1, and SPZ1. They might exert their functions via regulation of immune and inflammation responses. Genes in grey module play significant roles in AMI via regulation of macrophage activation.
[Mh] Termos MeSH primário: Perfilação da Expressão Gênica/métodos
Infarto do Miocárdio/genética
[Mh] Termos MeSH secundário: Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/genética
Biomarcadores
Regulação para Baixo
Diagnóstico Precoce
Proteínas de Ligação ao GTP/genética
Granzimas/genética
Seres Humanos
Mapas de Interação de Proteínas
Receptores de Formil Peptídeo/genética
Fator de Transcrição STAT1/genética
Receptor 2 Toll-Like/genética
Fatores de Transcrição
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Leucine Zipper Transcription Factors); 0 (Biomarkers); 0 (FPR1 protein, human); 0 (GBP5 protein, human); 0 (Receptors, Formyl Peptide); 0 (SPZ1 protein, human); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (TLR2 protein, human); 0 (Toll-Like Receptor 2); 0 (Transcription Factors); EC 3.4.21.- (GZMB protein, human); EC 3.4.21.- (Granzymes); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008375


  5 / 27595 MEDLINE  
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[PMID]:29325733
[Au] Autor:Zhang GM; Zheng L; He H; Song CC; Zhang ZJ; Cao XK; Lei CZ; Lan XY; Qi XL; Chen H; Huang YZ
[Ad] Endereço:College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, PR China.
[Ti] Título:Associations of GBP2 gene copy number variations with growth traits and transcriptional expression in Chinese cattle.
[So] Source:Gene;647:101-106, 2018 Mar 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Copy number variations (CNVs) recently have been recognized as another important genetic variability followed single nucleotide polymorphisms (SNPs). The guanylate binding protein 2 (GBP2) gene plays an important role in cell proliferation. This study was performed to determine the presence of GBP2 CNV (relative to Angus cattle) in 466 individuals representing six main cattle breeds from China, identify its relationship with growth, and explore the biological effects of gene expression. There were two CNV regions in the GBP2 gene, for three types, CNV1 loss type (relative to Angus cattle) was more frequent in XN than other breeds, and CNV2 loss type (relative to Angus cattle) was more frequent in XN and CDM than other breeds. Though the GBP2 gene copy number presented no correlation with the transcriptional expression of JX (P > .05), but the transcriptional expression in heart is higher than other tissues, and the copy number in muscles and fat of JX is higher than others breeds. Statistical analysis revealed that the GBP2 gene CNV1 and CNV2 were significantly associated with growth traits (P < .05). In conclusion, this research established the correlations between CNVs of GBP2 gene and growth traits in different cattle breeds, and our results suggested that the CNVs in GBP2 gene may be considered markers for the molecular breeding of Chinese beef cattle.
[Mh] Termos MeSH primário: Variações do Número de Cópias de DNA/genética
Proteínas de Ligação ao GTP/genética
Dosagem de Genes/genética
Locos de Características Quantitativas/genética
[Mh] Termos MeSH secundário: Animais
Cruzamento/métodos
Bovinos
China
Expressão Gênica/genética
Fenótipo
Polimorfismo de Nucleotídeo Único/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


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[PMID]:29287086
[Au] Autor:Liao KL; Melvin CE; Sozzani R; Jones RD; Elston TC; Jones AM
[Ad] Endereço:Departments of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America.
[Ti] Título:Dose-Duration Reciprocity for G protein activation: Modulation of kinase to substrate ratio alters cell signaling.
[So] Source:PLoS One;12(12):e0190000, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In animal cells, activation of heterotrimeric G protein signaling generally occurs when the system's cognate signal exceeds a threshold, whereas in plant cells, both the amount and the exposure time of at least one signal, D-glucose, are used toward activation. This unusual signaling property called Dose-Duration Reciprocity, first elucidated in the genetic model Arabidopsis thaliana, is achieved by a complex that is comprised of a 7-transmembrane REGULATOR OF G SIGNALING (RGS) protein (AtRGS1), a Gα subunit that binds and hydrolyzes nucleotide, a Gßγ dimer, and three WITH NO LYSINE (WNK) kinases. D-glucose is one of several signals such as salt and pathogen-derived molecular patterns that operates through this protein complex to activate G protein signaling by WNK kinase transphosphorylation of AtRGS1. Because WNK kinases compete for the same substrate, AtRGS1, we hypothesize that activation is sensitive to the AtRGS1 amount and that modulation of the AtRGS1 pool affects the response to the stimulant. Mathematical simulation revealed that the ratio of AtRGS1 to the kinase affects system sensitivity to D-glucose, and therefore illustrates how modulation of the cellular AtRGS1 level is a means to change signal-induced activation. AtRGS1 levels change under tested conditions that mimic physiological conditions therefore, we propose a previously-unknown mechanism by which plants react to changes in their environment.
[Mh] Termos MeSH primário: Proteínas de Arabidopsis/metabolismo
Arabidopsis/metabolismo
Proteínas de Ligação ao GTP/metabolismo
Fosfotransferases/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Arabidopsis/enzimologia
Arabidopsis/genética
Arabidopsis/crescimento & desenvolvimento
Genótipo
Fosforilação
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arabidopsis Proteins); EC 2.7.- (Phosphotransferases); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190000


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[PMID]:29206860
[Au] Autor:Sundström L; Myhre S; Sundqvist M; Ahnmark A; McCoull W; Raubo P; Groombridge SD; Polla M; Nyström AC; Kristensson L; Någård M; Winzell MS
[Ad] Endereço:Discovery Sciences, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.
[Ti] Título:The acute glucose lowering effect of specific GPR120 activation in mice is mainly driven by glucagon-like peptide 1.
[So] Source:PLoS One;12(12):e0189060, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mechanism behind the glucose lowering effect occurring after specific activation of GPR120 is not completely understood. In this study, a potent and selective GPR120 agonist was developed and its pharmacological properties were compared with the previously described GPR120 agonist Metabolex-36. Effects of both compounds on signaling pathways and GLP-1 secretion were investigated in vitro. The acute glucose lowering effect was studied in lean wild-type and GPR120 null mice following oral or intravenous glucose tolerance tests. In vitro, in GPR120 overexpressing cells, both agonists signaled through Gαq, Gαs and the ß-arrestin pathway. However, in mouse islets the signaling pathway was different since the agonists reduced cAMP production. The GPR120 agonists stimulated GLP-1 secretion both in vitro in STC-1 cells and in vivo following oral administration. In vivo GPR120 activation induced significant glucose lowering and increased insulin secretion after intravenous glucose administration in lean mice, while the agonists had no effect in GPR120 null mice. Exendin 9-39, a GLP-1 receptor antagonist, abolished the GPR120 induced effects on glucose and insulin following an intravenous glucose challenge. In conclusion, GLP-1 secretion is an important mechanism behind the acute glucose lowering effect following specific GPR120 activation.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Peptídeo 1 Semelhante ao Glucagon/farmacologia
Receptores Acoplados a Proteínas-G/agonistas
[Mh] Termos MeSH secundário: Animais
Células CHO
Linhagem Celular
Cricetulus
AMP Cíclico/biossíntese
Feminino
Proteínas de Ligação ao GTP/metabolismo
Teste de Tolerância a Glucose
Seres Humanos
Insulina/secreção
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Transdução de Sinais
beta-Arrestinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (GPR20 protein, human); 0 (Insulin); 0 (Receptors, G-Protein-Coupled); 0 (beta-Arrestins); 89750-14-1 (Glucagon-Like Peptide 1); E0399OZS9N (Cyclic AMP); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189060


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[PMID]:29216247
[Au] Autor:Brinkmann C; Hoffmann M; Lübke A; Nehlmeier I; Krämer-Kühl A; Winkler M; Pöhlmann S
[Ad] Endereço:Infection Biology Unit, German Primate Center, Kellnerweg 4, Göttingen, Germany.
[Ti] Título:The glycoprotein of vesicular stomatitis virus promotes release of virus-like particles from tetherin-positive cells.
[So] Source:PLoS One;12(12):e0189073, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vesicular stomatitis virus (VSV) release from infected cells is inhibited by the interferon (IFN)-inducible antiviral host cell factor tetherin (BST-2, CD317). However, several viruses encode tetherin antagonists and it is at present unknown whether residual VSV spread in tetherin-positive cells is also promoted by a virus-encoded tetherin antagonist. Here, we show that the viral glycoprotein (VSV-G) antagonizes tetherin in transfected cells, although with reduced efficiency as compared to the HIV-1 Vpu protein. Tetherin antagonism did not involve alteration of tetherin expression and was partially dependent on a GXXXG motif in the transmembrane domain of VSV-G. However, mutation of the GXXXG motif did not modulate tetherin sensitivity of infectious VSV. These results identify VSV-G as a tetherin antagonist in transfected cells but fail to provide evidence for a contribution of tetherin antagonism to viral spread.
[Mh] Termos MeSH primário: Antígeno 2 do Estroma da Médula Óssea/metabolismo
Vesiculovirus/metabolismo
Proteínas Virais/fisiologia
Vírion/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígeno 2 do Estroma da Médula Óssea/imunologia
Linhagem Celular
Proteínas de Ligação ao GTP/imunologia
Seres Humanos
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Marrow Stromal Antigen 2); 0 (Viral Proteins); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189073


  9 / 27595 MEDLINE  
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[PMID]:28449065
[Au] Autor:Chatzispyrou IA; Alders M; Guerrero-Castillo S; Zapata Perez R; Haagmans MA; Mouchiroud L; Koster J; Ofman R; Baas F; Waterham HR; Spelbrink JN; Auwerx J; Mannens MM; Houtkooper RH; Plomp AS
[Ad] Endereço:Laboratory Genetic Metabolic Diseases, Academic Medical Center, 1105 AZ Amsterdam, The Netherlands.
[Ti] Título:A homozygous missense mutation in ERAL1, encoding a mitochondrial rRNA chaperone, causes Perrault syndrome.
[So] Source:Hum Mol Genet;26(13):2541-2550, 2017 07 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Perrault syndrome (PS) is a rare recessive disorder characterized by ovarian dysgenesis and sensorineural deafness. It is clinically and genetically heterogeneous, and previously mutations have been described in different genes, mostly related to mitochondrial proteostasis. We diagnosed three unrelated females with PS and set out to identify the underlying genetic cause using exome sequencing. We excluded mutations in the known PS genes, but identified a single homozygous mutation in the ERAL1 gene (c.707A > T; p.Asn236Ile). Since ERAL1 protein binds to the mitochondrial 12S rRNA and is involved in the assembly of the small mitochondrial ribosomal subunit, the identified variant represented a likely candidate. In silico analysis of a 3D model for ERAL1 suggested that the mutated residue hinders protein-substrate interactions, potentially affecting its function. On a molecular basis, PS skin fibroblasts had reduced ERAL1 protein levels. Complexome profiling of the cells showed an overall decrease in the levels of assembled small ribosomal subunit, indicating that the ERAL1 variant affects mitochondrial ribosome assembly. Moreover, levels of the 12S rRNA were reduced in the patients, and were rescued by lentiviral expression of wild type ERAL1. At the physiological level, mitochondrial respiration was markedly decreased in PS fibroblasts, confirming disturbed mitochondrial function. Finally, knockdown of the C. elegans ERAL1 homologue E02H1.2 almost completely blocked egg production in worms, mimicking the compromised fertility in PS-affected women. Our cross-species data in patient cells and worms support the hypothesis that mutations in ERAL1 can cause PS and are associated with changes in mitochondrial metabolism.
[Mh] Termos MeSH primário: Proteínas de Ligação ao GTP/genética
Disgenesia Gonadal 46 XX/genética
Perda Auditiva Neurossensorial/genética
Proteínas de Ligação a RNA/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos/genética
Animais
Caenorhabditis elegans/genética
Exoma
Feminino
Proteínas de Ligação ao GTP/metabolismo
Disgenesia Gonadal 46 XX/metabolismo
Perda Auditiva Neurossensorial/metabolismo
Homozigoto
Seres Humanos
Mitocôndrias/genética
Proteínas Mitocondriais/metabolismo
Chaperonas Moleculares/metabolismo
Mutação
Mutação de Sentido Incorreto/genética
RNA Ribossômico/genética
RNA Ribossômico/metabolismo
Proteínas de Ligação a RNA/metabolismo
Sequenciamento Completo do Exoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitochondrial Proteins); 0 (Molecular Chaperones); 0 (RNA, Ribosomal); 0 (RNA, ribosomal, 12S); 0 (RNA-Binding Proteins); EC 3.6.1.- (ERAL1 protein, human); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171218
[Lr] Data última revisão:
171218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx152


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[PMID]:29222550
[Au] Autor:Raychaudhuri U; Millar JC; Clark AF
[Ad] Endereço:North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas, United States.
[Ti] Título:Tissue Transglutaminase Elevates Intraocular Pressure in Mice.
[So] Source:Invest Ophthalmol Vis Sci;58(14):6197-6211, 2017 Dec 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Tissue transglutaminase (TGM2) is elevated in glaucomatous trabecular meshwork (TM) tissues. We investigated whether increased expression of TGM2 increases extracellular matrix crosslinking in the TM, thereby increasing aqueous humor outflow resistance and elevating intraocular pressure (IOP) in mouse eyes. Methods: GTM3, primary human GTM 125-05, and cultured mouse TM cells were transduced with adenovirus serotype 5 expressing human transglutaminase 2 (Ad5.TGM2; multiplicity of infection [MOI]-75) and fixed for immunocytochemistry. To test the effect on IOP in living eyes, Ad5.TGM2 was injected intravitreally into one eye of BALB/cJ (n = 18) or C57BL/6J mice (n = 9). The uninjected contralateral eye and Ad5.GFP served as controls. Daytime conscious IOPs were measured twice per week. Aqueous outflow facility (C) was measured by constant flow infusion on completion of IOP measurements. Immunohistochemistry was performed on BALB/cJ mouse eyes to study TGM2 expression and activity. Results: The treatment of cultured TM cells with Ad5.TGM2 increased immunostaining of N-ε(γ-glutamyl) lysine crosslinks. Ad5.TGM2 injection significantly increased IOP in BALB/cJ (15.86 mm Hg [injected] vs. 10.70 mm Hg [control]) and in C57BL/6J mice (17.09 mm Hg [injected] vs. 12.01 mm Hg [control]). Mean aqueous outflow facility in the injected eyes of BALB/cJ (0.013 µL/min/mm Hg) and C57BL/6J mice (0.012 µL/min/mm Hg) was significantly lower than in the uninjected control eyes (BALB/cJ, 0.021 µL/min/mm Hg; C57BL/6J, 0.019 µL/min/mm Hg). The Ad5.TGM2 transduction of mouse eyes increased TGM2 expression in the TM region and increased N-ε(γ-glutamyl) lysine crosslinks. Conclusions: The increased expression of TGM2 in the TM increases N-ε(γ-glutamyl) lysine crosslinking in the TM, increases aqueous outflow resistance, and elevates IOP in mice. TGM2 may be at least partially responsible for ocular hypertension in POAG.
[Mh] Termos MeSH primário: Humor Aquoso/enzimologia
Proteínas de Ligação ao GTP/genética
Regulação da Expressão Gênica
Glaucoma de Ângulo Aberto/genética
Pressão Intraocular
RNA/genética
Malha Trabecular/enzimologia
Transglutaminases/genética
[Mh] Termos MeSH secundário: Animais
Western Blotting
Células Cultivadas
Proteínas de Ligação ao GTP/biossíntese
Glaucoma de Ângulo Aberto/enzimologia
Glaucoma de Ângulo Aberto/patologia
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos C57BL
Malha Trabecular/patologia
Transglutaminases/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
63231-63-0 (RNA); EC 2.3.2.- (transglutaminase 2); EC 2.3.2.13 (Transglutaminases); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22236



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