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Pesquisa : D12.776.306.366.100.300 [Categoria DeCS]
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[PMID]:29338044
[Au] Autor:Andley UP; Tycksen E; McGlasson-Naumann BN; Hamilton PD
[Ad] Endereço:Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri, United States of America.
[Ti] Título:Probing the changes in gene expression due to α-crystallin mutations in mouse models of hereditary human cataract.
[So] Source:PLoS One;13(1):e0190817, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mammalian eye lens expresses a high concentration of crystallins (α, ß and γ-crystallins) to maintain the refractive index essential for lens transparency. Crystallins are long-lived proteins that do not turnover throughout life. The structural destabilization of crystallins by UV exposure, glycation, oxidative stress and mutations in crystallin genes leads to protein aggregation and development of cataracts. Several destabilizing mutations in crystallin genes are linked with human autosomal dominant hereditary cataracts. To investigate the mechanism by which the α-crystallin mutations Cryaa-R49C and Cryab-R120G lead to cataract formation, we determined whether these mutations cause an altered expression of specific transcripts in the lens at an early postnatal age by RNA-seq analysis. Using knock-in mouse models previously generated in our laboratory, in the present work, we identified genes that exhibited altered abundance in the mutant lenses, including decreased transcripts for Clic5, an intracellular water channel in Cryaa-R49C heterozygous mutant lenses, and increased transcripts for Eno1b in Cryab-R120G heterozygous mutant lenses. In addition, RNA-seq analysis revealed increased histones H2B, H2A, and H4 gene expression in Cryaa-R49C mutant lenses, suggesting that the αA-crystallin mutation regulates histone expression via a transcriptional mechanism. Additionally, these studies confirmed the increased expression of histones H2B, H2A, and H4 by proteomic analysis of Cryaa-R49C knock-in and Cryaa;Cryab gene knockout lenses reported previously. Taken together, these findings offer additional insight into the early transcriptional changes caused by Cryaa and Cryab mutations associated with autosomal dominant human cataracts, and indicate that the transcript levels of certain genes are affected by the expression of mutant α-crystallin in vivo.
[Mh] Termos MeSH primário: Catarata/genética
Mutação
Cadeia A de alfa-Cristalina/genética
Cadeia B de alfa-Cristalina/genética
[Mh] Termos MeSH secundário: Animais
Carboxipeptidases/genética
Carboxipeptidases/metabolismo
Catarata/metabolismo
Canais de Cloreto/genética
Canais de Cloreto/metabolismo
Modelos Animais de Doenças
Expressão Gênica
Técnicas de Introdução de Genes
Histonas/genética
Histonas/metabolismo
Seres Humanos
Cristalino/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Camundongos Transgênicos
Proteínas/genética
Proteínas/metabolismo
Proteômica
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Cadeia A de alfa-Cristalina/metabolismo
Cadeia B de alfa-Cristalina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Aebp1 protein, mouse); 0 (CLIC5 protein, mouse); 0 (Chloride Channels); 0 (Cryab protein, mouse); 0 (Histones); 0 (Proteins); 0 (Repressor Proteins); 0 (alpha-Crystallin A Chain); 0 (alpha-Crystallin B Chain); 0 (vig1 protein, mouse); EC 3.4.- (Carboxypeptidases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190817


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[PMID]:28893927
[Au] Autor:Hong Y; Zhao T; Li XJ; Li S
[Ad] Endereço:Department of Human Genetics, Emory University School of Medicine, Atlanta, Georgia 30322.
[Ti] Título:Mutant Huntingtin Inhibits αB-Crystallin Expression and Impairs Exosome Secretion from Astrocytes.
[So] Source:J Neurosci;37(39):9550-9563, 2017 Sep 27.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the brain, astrocytes secrete diverse substances that regulate neuronal function and viability. Exosomes, which are vesicles produced through the formation of multivesicular bodies and their subsequent fusion with the plasma membrane, are also released from astrocytes via exocytotic secretion. Astrocytic exosomes carry heat shock proteins that can reduce the cellular toxicity of misfolded proteins and prevent neurodegeneration. Although mutant huntingtin (mHtt) affects multiple functions of astrocytes, it remains unknown whether mHtt impairs the production of exosomes from astrocytes. We found that mHtt is not present in astrocytic exosomes, but can decrease exosome secretion from astrocytes in HD140Q knock-in (KI) mice. N-terminal mHtt accumulates in the nuclei and forms aggregates, causing decreased secretion of exosomes from cultured astrocytes. Consistently, there is a significant decrease in secreted exosomes in both female and male HD KI mouse striatum in which abundant nuclear mHtt aggregates are present. Conversely, injection of astrocytic exosomes into the striatum of HD140Q KI mice reduces the density of mHtt aggregates. Further, mHtt in astrocytes decreased the expression of αB-crystallin, a small heat shock protein that is enriched in astrocytes and mediates exosome secretion, by reducing the association of Sp1 with the enhancer of the α gene. Importantly, overexpression of αB-crystallin rescues defective exosome release from HD astrocytes as well as mHtt aggregates in the striatum of HD140Q KI mice. Our results demonstrate that mHtt reduces the expression of αB-crystallin in astrocytes to decrease exosome secretion in the HD brains, contributing to non-cell-autonomous neurotoxicity in HD. Huntington's disease (HD) is characterized by selective neurodegeneration that preferentially occurs in the striatal medium spiny neurons. Recent studies in different HD mouse models demonstrated that dysfunction of astrocytes, a major type of glial cell, leads to neuronal vulnerability. Emerging evidence shows that exosomes secreted from astrocytes contain neuroprotective cargoes that could support the survival of neighboring neurons. We found that mHtt in astrocytes impairs exosome secretion by decreasing αB-crystallin, a protein that is expressed mainly in glial cells and mediates exosome secretion. Overexpression of αB-crystallin could alleviate the deficient exosome release and neuropathology in HD mice. Our results revealed a new pathological pathway that affects the critical support of glial cells to neurons in the HD brain.
[Mh] Termos MeSH primário: Astrócitos/secreção
Exossomos/secreção
Proteína Huntingtina/genética
Doença de Huntington/metabolismo
Cadeia B de alfa-Cristalina/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Células Cultivadas
Corpo Estriado/metabolismo
Exocitose
Feminino
Proteína Huntingtina/metabolismo
Masculino
Camundongos
Mutação
Cadeia B de alfa-Cristalina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Htt protein, mouse); 0 (Huntingtin Protein); 0 (alpha-Crystallin B Chain)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171015
[Lr] Data última revisão:
171015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1418-17.2017


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[PMID]:28796798
[Au] Autor:Li Q; Wang Y; Lai Y; Xu P; Yang Z
[Ad] Endereço:Songjiang Hospital Affiliated Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai, China.
[Ti] Título:HspB5 correlates with poor prognosis in colorectal cancer and prompts epithelial-mesenchymal transition through ERK signaling.
[So] Source:PLoS One;12(8):e0182588, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alpha B-crystallin (HspB5) is abnormally expressed in tumor tissues and portends a poor prognosis in cancer patients. However, the role of HspB5 in colorectal cancer (CRC) is still unclear. Seventy CRC patients and 40 healthy volunteers were sampled from August 2012 to March 2015 in order to determine the clinical significance of HspB5. In vitro cellular studies were used to validate its molecular mechanisms in CRC. Our clinical data indicated that HspB5 was up-regulated, and had a positive association with TNM stage CRC patients. The expression level of HspB5 in CRC patients was closely correlated with MMP7 and E-cadherin, two core epithelial-mesenchymal transition (EMT) gene products. The in vitro studies revealed that high HspB5 expression could prompt tumor cell proliferation and invasion, as well as EMT. Gene-microarray analysis suggested three significant signaling pathways (PI3K, p38 and ERK) were involved in HspB5-induced EMT. Signal transduction pathway inhibitors and HspB5 gene knockdown models suggested that HspB5 promotes CRC tumorigenesis and EMT progression through ERK signaling pathways. In summary, HspB5 maybe trigger the EMT in CRC by activating the ERK signaling pathway. It is a potential tumor biomarker for CRC diagnosis and prognosis.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Neoplasias Colorretais/metabolismo
Transição Epitelial-Mesenquimal
Sistema de Sinalização das MAP Quinases
Cadeia B de alfa-Cristalina/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Estudos de Casos e Controles
Proliferação Celular
Neoplasias Colorretais/mortalidade
Neoplasias Colorretais/patologia
Feminino
Expressão Gênica
Células HCT116
Seres Humanos
Masculino
Invasividade Neoplásica
Prognóstico
Análise de Sobrevida
Cadeia B de alfa-Cristalina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CRYAB protein, human); 0 (alpha-Crystallin B Chain)
[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:170811
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182588


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[PMID]:28720498
[Au] Autor:Mallik PK; Shi H; Pande J
[Ad] Endereço:Department of Chemistry, University at Albany, State University of New York, 1400 Washington Avenue, Albany 12222, N.Y, United States.
[Ti] Título:RNA aptamers targeted for human αA-crystallin do not bind αB-crystallin, and spare the α-crystallin domain.
[So] Source:Biochem Biophys Res Commun;491(2):423-428, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular chaperones, α-crystallins, belong to the small heat shock protein (sHSP) family and prevent the aggregation and insolubilization of client proteins. Studies in vivo have shown that the chaperone activity of the α-crystallins is raised or lowered in various disease states. Therefore, the development of tools to control chaperone activity may provide avenues for therapeutic intervention, as well as enable a molecular understanding of chaperone function. The major human lens α-crystallins, αA- (HAA) and αB- (HAB), share 57% sequence identity and show similar activity towards some clients, but differing activities towards others. Notably, both crystallins contain the "α-crystallin domain" (ACD, the primary client binding site), like all other members of the sHSP family. Here we show that RNA aptamers selected for HAA, in vitro, exhibit specific affinity to HAA but do not bind HAB. Significantly, these aptamers also exclude the ACD. This study thus demonstrates that RNA aptamers against sHSPs can be designed that show high affinity and specificity - yet exclude the primary client binding region - thereby facilitating the development of RNA aptamer-based therapeutic intervention strategies.
[Mh] Termos MeSH primário: Aptâmeros de Nucleotídeos/química
Cadeia A de alfa-Cristalina/química
Cadeia B de alfa-Cristalina/química
[Mh] Termos MeSH secundário: Aptâmeros de Nucleotídeos/síntese química
Sequência de Bases
Sítios de Ligação
Expressão Gênica
Seres Humanos
Meliteno/química
Octoxinol/química
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes/química
Técnica de Seleção de Aptâmeros
Tensoativos/química
Cadeia A de alfa-Cristalina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aptamers, Nucleotide); 0 (Recombinant Proteins); 0 (Surface-Active Agents); 0 (alpha-Crystallin A Chain); 0 (alpha-Crystallin B Chain); 20449-79-0 (Melitten); 9002-93-1 (Octoxynol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE


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[PMID]:28679593
[Au] Autor:Pleasant L; Ma Q; Devarajan M; Parameswaran P; Drake K; Siroky B; Shay-Winkler K; Robbins J; Devarajan P
[Ad] Endereço:Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; and.
[Ti] Título:Increased susceptibility to structural acute kidney injury in a mouse model of presymptomatic cardiomyopathy.
[So] Source:Am J Physiol Renal Physiol;313(3):F699-F705, 2017 Sep 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The early events that signal renal dysfunction in presymptomatic heart failure are unclear. We tested the hypothesis that functional and mechanistic changes occur in the kidney that precede the development of symptomatic heart failure. We employed a transgenic mouse model with cardiomyocyte-specific overexpression of mutant α-B-crystallin that develops slowly progressive cardiomyopathy. Presymptomatic transgenic mice displayed an increase in serum creatinine (1.17 ± 0.34 vs. wild type 0.65 ± 0.16 mg/dl, < 0.05) and in urinary neutrophil gelatinase-associated lipocalin (NGAL; 278.92 ± 176.24 vs. wild type 49.11 ± 22.79 ng/ml, < 0.05) but no renal fibrosis. Presymptomatic transgenic mouse kidneys exhibited a twofold upregulation of the gene, marked overexpression of renin protein in the tubules, and a worsened response to ischemia-reperfusion injury based on serum creatinine (2.77 ± 0.66 in transgenic mice vs. 2.01 ± 0.58 mg/dl in wild type, < 0.05), urine NGAL (9,198.79 ± 3,799.52 in transgenic mice vs. 3,252.94 ± 2,420.36 ng/ml in wild type, < 0.05), tubule dilation score (3.4 ± 0.5 in transgenic mice vs. 2.6 ± 0.5 in wild type, < 0.05), tubule cast score (3.2 ± 0.4 in transgenic mice vs. 2.5 ± 0.5 in wild type, < 0.05), and TdT-mediated dUTP nick-end labeling (TUNEL)-positive nuclei (10.1 ± 2.1 in the transgenic group vs. 5.7 ± 1.6 per 100 cells counted in wild type, < 0.01). Our findings indicate functional renal impairment, urinary biomarker elevations, and induction of renin gene and protein expression in the kidney that occur in early presymptomatic heart failure, which increase the susceptibility to subsequent acute kidney injury.
[Mh] Termos MeSH primário: Lesão Renal Aguda/etiologia
Síndrome Cardiorrenal/etiologia
Cardiomiopatias/etiologia
Insuficiência Cardíaca/etiologia
Rim/patologia
Traumatismo por Reperfusão/etiologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/genética
Lesão Renal Aguda/patologia
Lesão Renal Aguda/fisiopatologia
Animais
Doenças Assintomáticas
Biomarcadores/urina
Síndrome Cardiorrenal/genética
Síndrome Cardiorrenal/patologia
Síndrome Cardiorrenal/fisiopatologia
Cardiomiopatias/genética
Creatinina/urina
Modelos Animais de Doenças
Progressão da Doença
Predisposição Genética para Doença
Insuficiência Cardíaca/genética
Rim/metabolismo
Rim/fisiopatologia
Lipocalina-2/urina
Camundongos Transgênicos
Mutação
Fenótipo
Renina/genética
Renina/metabolismo
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/patologia
Traumatismo por Reperfusão/fisiopatologia
Fatores de Tempo
Regulação para Cima
Cadeia B de alfa-Cristalina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Lipocalin-2); 0 (alpha-Crystallin B Chain); 126469-30-5 (Lcn2 protein, mouse); AYI8EX34EU (Creatinine); EC 3.4.23.15 (Renin)
[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:170707
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00505.2016


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[PMID]:28640093
[Au] Autor:Cui XJ; Lv FY; Li FH; Zeng K
[Ad] Endereço:aDepartment of Ophthalmology, Linyi People's Hospital bDepartment of Infectious Diseases, Affiliated Hospital of Shandong Medical College, Linyi cShenzhen Key Laboratory of Ophthalmology, Shenzhen Eye Hospital, Shenzhen, P.R. China.
[Ti] Título:Correlations of single nucleotide polymorphisms of CRYAA and CRYAB genes with the risk and clinicopathological features of children suffering from congenital cataract.
[So] Source:Medicine (Baltimore);96(25):e7158, 2017 Jun.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The study aims to explore the correlations of the single nucleotide polymorphisms (SNPs) of CRYAA and CRYAB with the risk and clinicopathological features of children with congenital cataract. METHODS: The study enrolled 168 children diagnosed as congenital cataract (case group) and 172 normal children (control group) from May 2015 to May 2016. Genomic DNA extraction was performed using a QIAamp DNA blood mini kit. Polymerase chain reaction (PCR) products were genotyped using an ABI direct sequencer. Haplotype, allele, and genotype frequencies of CRYAA and CRYAB gene polymorphisms analyses were carried out using the SHEsis software. Logistic regression analysis was performed in order to analyze the risk factors for children suffering from congenital cataract. RESULTS: Presence of significant differences between the case and control groups' genotype and allele frequencies of CRYAA rs7278468 and CRYAB rs370803064/rs387907338. TA of CRYAB gene might increase congenital cataract risk in children, while GCG of CRYAA gene and GC of CRYAB gene might decrease congenital cataract risk in children. CRYAA rs7278468, CRYAB rs370803064/rs387907338 polymorphisms were significantly correlated to uncorrected visual acuity, best-corrected visual acuity, nystagmus, visual axis opacification, microcornea, lens opacity, posterior capsular thickening, and degrees of posterior capsule opacification after operation in children with congenital cataract. Logistic regression analysis revealed that the T allele of CRYAA rs7278468, A allele of CRYAB rs370803064, T allele of CRYAB rs387907338, family history, and TA haplotype of CRYAB gene were risk factors for children with congenital cataract. CONCLUSION: Our findings demonstrated that CRYAA rs7278468 and CRYAB rs370803064/rs387907338 are correlated with the risk and clinicopathological features of children suffering from congenital cataract.
[Mh] Termos MeSH primário: Catarata/genética
Cristalinas/genética
Predisposição Genética para Doença
Polimorfismo de Nucleotídeo Único
Cadeia B de alfa-Cristalina/genética
[Mh] Termos MeSH secundário: Catarata/patologia
Catarata/fisiopatologia
Extração de Catarata
Pré-Escolar
Feminino
Frequência do Gene
Técnicas de Genotipagem
Haplótipos
Seres Humanos
Modelos Logísticos
Masculino
Reação em Cadeia da Polimerase
Software
Resultado do Tratamento
Acuidade Visual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRYAA protein, human); 0 (CRYAB protein, human); 0 (Crystallins); 0 (alpha-Crystallin B Chain)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007158


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[PMID]:28551403
[Au] Autor:Semenyuk PI; Kurochkina LP; Gusev NB; Izumrudov VA; Muronetz VI
[Ad] Endereço:Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia. Electronic address: psemenyuk@belozersky.msu.ru.
[Ti] Título:Chaperone-like activity of synthetic polyanions can be higher than the activity of natural chaperones at elevated temperature.
[So] Source:Biochem Biophys Res Commun;489(2):200-205, 2017 Jul 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Polyelectrolytes are a prospective tool for protection of proteins against aggregation. We compared synthetic polyanion, poly(styrene sulfonate), and natural chaperones of different types, namely, GroEL-like chaperonin from Pseudomonas aeruginosa phage EL and human small heat shock protein HspB5 (αB-crystallin), in their ability to prevent aggregation of client proteins. At 45 °C, all three agents efficiently suppressed thermal aggregation of phage endolysin. At higher temperatures, HspB5 and poly(styrene sulfonate) also inhibited endolysin aggregation, though polyanion became less efficient than HspB5 at 55 °C and 60 °C. However, the polyanion completely protected another protein, glyceraldehyde-3-phosphate dehydrogenase, even at 60 °C, in contrast to both natural chaperones whose effect disappeared at 50-55 °C. These results provide a platform for the development of artificial chaperones based on synthetic polyelectrolytes.
[Mh] Termos MeSH primário: Temperatura Alta
Chaperonas Moleculares/metabolismo
Poliestirenos/metabolismo
Pseudomonas aeruginosa/química
Cadeia B de alfa-Cristalina/metabolismo
[Mh] Termos MeSH secundário: Endopeptidases/metabolismo
Seres Humanos
Chaperonas Moleculares/química
Poliestirenos/química
Pseudomonas aeruginosa/metabolismo
Cadeia B de alfa-Cristalina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRYAB protein, human); 0 (Molecular Chaperones); 0 (Polystyrenes); 0 (alpha-Crystallin B Chain); 70KO0R01RY (polystyrene sulfonic acid); EC 3.4.- (Endopeptidases); EC 3.4.99.- (endolysin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE


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[PMID]:28506831
[Au] Autor:Shi C; Yang X; Bu X; Hou N; Chen P
[Ad] Endereço:Department of Pathology and Pathophysiology, Medical School of Southeast University, Nanjing 210009, PR China. Electronic address: chuanbingshi78@126.com.
[Ti] Título:Alpha B-crystallin promotes the invasion and metastasis of colorectal cancer via epithelial-mesenchymal transition.
[So] Source:Biochem Biophys Res Commun;489(4):369-374, 2017 Aug 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alpha B-crystallin (CRYAB, HSPB5) is a protein that was first discovered in the lens of the eye. It is a member of the small heat-shock protein family (sHsps). CRYAB functions primarily as a molecular chaperone to prevent the aggregation and degradation of damaged unfolded proteins due to cellular damage resulting from heat shock, radiation, oxidative stress, and other insults, thereby promoting cell survival and preventing apoptosis. In recent years, the role of CRYAB in tumorigenesis, tumor invasion, and metastasis has received increasing attention. CRYAB is highly expressed in a variety of cancers, including breast cancer, head and neck cancer, and kidney cancer, and is likely associated with the prognosis of cancer. However, few studies have examined CRYAB in colorectal cancer (CRC). To study the effect of CRYAB on CRC, we transfected the CRC cell line SW480, which expresses high levels of CRYAB, with a lentiviral vector that inhibits CRYAB expression. The messenger RNA (mRNA) and protein expression of CRYAB was examined in the transfected SW480 cells (Si-CRYAB) using quantitative real-time polymerase chain reaction (qPCR) and Western blotting (WB) assays. Moreover, a growth curve was plotted to examine the proliferation of Si-CRYAB cells, and transwell assays were used to examine the migration of Si-CRYAB cells. Apoptosis and the cell cycle were examined in Si-CRYAB cells using flow cytometry (FCM), and the tumorigenic capability of Si-CRYAB cells was assessed in a nude mouse tumor model. Immunohistochemistry (IHC) was employed to examine CRYAB protein expression and the markers of epithelial-mesenchymal transition (EMT), such as E-cadherin, fibronectin, vimentin, and slug, in tumor tissues from nude mice and clinical invasive CRC and hepatic metastasis specimens. The qPCR and WB results showed that CRYAB was downregulated at the protein and mRNA level in Si-CRYAB cells, and the growth curve indicated that the proliferation of Si-CRYAB cells was reduced. Moreover, Si-CRYAB cells exhibited reduced migration capability in the transwell assay as well as increased apoptosis and G1 arrest in the FCM assay. The tumorigenesis study in nude mice showed that Si-CRYAB cells formed smaller tumors, indicating decreased tumorigenic capability. IHC results showed reduced CRYAB expression and lower levels of EMT in Si-CRYAB cells, whereas clinical specimens of invasive CRC and hepatic metastases exhibited elevated CRYAB expression and enhanced levels of EMT. These results demonstrated that CRYAB promoted the invasion and metastasis of CRC tumor cells via EMT.
[Mh] Termos MeSH primário: Movimento Celular
Neoplasias Colorretais/patologia
Transição Epitelial-Mesenquimal
Cadeia B de alfa-Cristalina/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Ciclo Celular
Proliferação Celular
Neoplasias Colorretais/metabolismo
Seres Humanos
Camundongos
Camundongos Nus
Metástase Neoplásica
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (alpha-Crystallin B Chain)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE


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[PMID]:28482007
[Au] Autor:Bolton J; Montastier E; Carayol J; Bonnel S; Mir L; Marques MA; Astrup A; Saris W; Iacovoni J; Villa-Vialaneix N; Valsesia A; Langin D; Viguerie N
[Ad] Endereço:Institut National de la Santé et de la Recherche Médicale, Obesity Research Laboratory, Institute of Metabolic and Cardiovascular Diseases, 31432 Toulouse, France.
[Ti] Título:Molecular Biomarkers for Weight Control in Obese Individuals Subjected to a Multiphase Dietary Intervention.
[So] Source:J Clin Endocrinol Metab;102(8):2751-2761, 2017 Aug 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Although calorie restriction has proven beneficial for weight loss, long-term weight control is variable between individuals. Objective: To identify biomarkers of successful weight control during a dietary intervention (DI). Design, Setting, and Participants: Adipose tissue (AT) transcriptomes were compared between 21 obese individuals who either maintained weight loss or regained weight during the DI. Results were validated on 310 individuals from the same study using quantitative reverse transcription polymerase chain reaction and protein levels of potential circulating biomarkers measured by enzyme-linked immunosorbent assay. Intervention: Individuals underwent 8 weeks of low-calorie diet, then 6 months of ad libitum diet. Outcome Measure: Weight changes at the end of the DI. Results: We evaluated six genes that had altered expression during DI, encode secreted proteins, and have not previously been implicated in weight control (EGFL6, FSTL3, CRYAB, TNMD, SPARC, IGFBP3), as well as genes for which baseline expression differed between those with good and poor weight control (ASPN, USP53). Changes in plasma concentrations of EGFL6, FSTL3, and CRYAB mirrored AT messenger RNA expression; all decreased during DI in individuals with good weight control. ASPN and USP53 had higher baseline expression in individuals who went on to have good weight control. Expression quantitative trait loci analysis found polymorphisms associated with expression levels of USP53 in AT. A regulatory network was identified in which transforming growth factor ß1 (TGF-ß1) was responsible for downregulation of certain genes during DI in good controllers. Interestingly, ASPN is a TGF-ß1 inhibitor. Conclusions: We found circulating biomarkers associated with weight control that could influence weight management strategies and genes that may be prognostic for successful weight control.
[Mh] Termos MeSH primário: Restrição Calórica
Obesidade/dietoterapia
RNA Mensageiro/metabolismo
Gordura Subcutânea/metabolismo
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/metabolismo
Regulação para Baixo
Ensaio de Imunoadsorção Enzimática
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Feminino
Proteínas Relacionadas à Folistatina/genética
Proteínas Relacionadas à Folistatina/metabolismo
Perfilação da Expressão Gênica
Redes Reguladoras de Genes
Seres Humanos
Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Masculino
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Análise em Microsséries
Meia-Idade
Obesidade/genética
Obesidade/metabolismo
Osteonectina/genética
Osteonectina/metabolismo
Polimorfismo Genético
Locos de Características Quantitativas
Reação em Cadeia da Polimerase em Tempo Real
Fator de Crescimento Transformador beta1/metabolismo
Proteases Específicas de Ubiquitina/genética
Proteases Específicas de Ubiquitina/metabolismo
Cadeia B de alfa-Cristalina/genética
Cadeia B de alfa-Cristalina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ASPN protein, human); 0 (Biomarkers); 0 (CRYAB protein, human); 0 (EGFL6 protein, human); 0 (Extracellular Matrix Proteins); 0 (Follistatin-Related Proteins); 0 (Fstl3 protein, human); 0 (IGFBP3 protein, human); 0 (Insulin-Like Growth Factor Binding Protein 3); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (Osteonectin); 0 (RNA, Messenger); 0 (SPARC protein, human); 0 (TGFB1 protein, human); 0 (TNMD protein, human); 0 (Transforming Growth Factor beta1); 0 (alpha-Crystallin B Chain); EC 3.4.19.12 (USP53 protein, human); EC 3.4.19.12 (Ubiquitin-Specific Proteases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-3997


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[PMID]:28476624
[Au] Autor:Yamashita A; Hiraki Y; Yamazaki T
[Ad] Endereço:Department of Molecular Cell Biology and Medicine, Graduate School of Biomedical Sciences, Tokushima University, 1-78-1, Sho-machi, Tokushima 770-8505, Japan.
[Ti] Título:Identification of CLN6 as a molecular entity of endoplasmic reticulum-driven anti-aggregate activity.
[So] Source:Biochem Biophys Res Commun;487(4):917-922, 2017 Jun 10.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:αB-crystallin (αBC) is a small heat shock protein. Mutations in the αBC gene are linked to α-crystallinopathy, a hereditary myopathy histologically characterized by intracellular accumulation of protein aggregates. The disease-causing R120G αBC mutant, harboring an arginine-to-glycine replacement at position 120, is an aggregate-prone protein. We previously showed that the R120G mutant's aggregation in HeLa cells was prevented by enforced expression of αBC on the endoplasmic reticulum (ER). To elucidate the molecular nature of the preventive effect on the R120G mutant, we isolated proteins binding to ER-anchored αBC (TMαBC). The ER transmembrane CLN6 protein was identified as a TMαBC's binder. CLN6 knockdown in HeLa cells attenuated TMαBC's anti-aggregate activity against the R120G mutant. Conversely, CLN6 overexpression enhanced the activity, indicating that CLN6 operates as a downstream effector of TMαBC. CLN6 physically interacted with the R120G mutant, and repressed its aggregation in HeLa cells even when TMαBC was not co-expressed. Furthermore, CLN6's antagonizing effect on the R120G mutant was compromised upon treatment with a lysosomal inhibitor, suggesting CLN6 requires the intact autophagy-lysosome system to prevent the R120G mutant from aggregating. We hence conclude that CLN6 is not only a molecular entity of the anti-aggregate activity conferred by the ER manipulation using TMαBC, but also serves as a potential target of therapeutic interventions.
[Mh] Termos MeSH primário: Retículo Endoplasmático/metabolismo
Proteínas de Membrana/metabolismo
Agregados Proteicos
Cadeia B de alfa-Cristalina/metabolismo
[Mh] Termos MeSH secundário: Células HeLa
Seres Humanos
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CLN6 protein, human); 0 (Membrane Proteins); 0 (Protein Aggregates); 0 (alpha-Crystallin B Chain)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE



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