Base de dados : MEDLINE
Pesquisa : D08.811.277.040.330.300.400.462 [Categoria DeCS]
Referências encontradas : 1199 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 120 ir para página                         

  1 / 1199 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28982779
[Au] Autor:Parisis N; Krasinska L; Harker B; Urbach S; Rossignol M; Camasses A; Dewar J; Morin N; Fisher D
[Ad] Endereço:IGMM, CNRS Univ. Montpellier, Montpellier, France.
[Ti] Título:Initiation of DNA replication requires actin dynamics and formin activity.
[So] Source:EMBO J;36(21):3212-3231, 2017 Nov 02.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nuclear actin regulates transcriptional programmes in a manner dependent on its levels and polymerisation state. This dynamics is determined by the balance of nucleocytoplasmic shuttling, formin- and redox-dependent filament polymerisation. Here, using egg extracts and human somatic cells, we show that actin dynamics and formins are essential for DNA replication. In proliferating cells, formin inhibition abolishes nuclear transport and initiation of DNA replication, as well as general transcription. In replicating nuclei from transcriptionally silent egg extracts, we identified numerous actin regulators, and disruption of actin dynamics abrogates nuclear transport, preventing NLS (nuclear localisation signal)-cargo release from RanGTP-importin complexes. Nuclear formin activity is further required to promote loading of cyclin-dependent kinase (CDK) and proliferating cell nuclear antigen (PCNA) onto chromatin, as well as initiation and elongation of DNA replication. Therefore, actin dynamics and formins control DNA replication by multiple direct and indirect mechanisms.
[Mh] Termos MeSH primário: Actinas/genética
Cromatina/metabolismo
Replicação do DNA
Proteínas Fetais/genética
Proteínas dos Microfilamentos/genética
Proteínas Nucleares/genética
Transcrição Genética
[Mh] Termos MeSH secundário: Actinas/metabolismo
Transporte Ativo do Núcleo Celular/genética
Animais
Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Cromatina/química
Misturas Complexas/química
Citoplasma/metabolismo
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Proteínas Fetais/metabolismo
Regulação da Expressão Gênica
Células HeLa
Seres Humanos
Carioferinas/genética
Carioferinas/metabolismo
Proteínas dos Microfilamentos/metabolismo
Sinais de Localização Nuclear
Proteínas Nucleares/metabolismo
Antígeno Nuclear de Célula em Proliferação/genética
Antígeno Nuclear de Célula em Proliferação/metabolismo
Transdução de Sinais
Xenopus laevis
Zigoto/química
Proteína ran de Ligação ao GTP/genética
Proteína ran de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Chromatin); 0 (Complex Mixtures); 0 (Fetal Proteins); 0 (Karyopherins); 0 (Microfilament Proteins); 0 (Nuclear Localization Signals); 0 (Nuclear Proteins); 0 (Proliferating Cell Nuclear Antigen); 147336-47-8 (formin 1); EC 3.6.5.2 (ran GTP-Binding Protein)
[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:171007
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201796585


  2 / 1199 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28910618
[Au] Autor:Zu T; Cleary JD; Liu Y; Bañez-Coronel M; Bubenik JL; Ayhan F; Ashizawa T; Xia G; Clark HB; Yachnis AT; Swanson MS; Ranum LPW
[Ad] Endereço:Center for NeuroGenetics, University of Florida, Gainesville, FL 32610, USA; Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA.
[Ti] Título:RAN Translation Regulated by Muscleblind Proteins in Myotonic Dystrophy Type 2.
[So] Source:Neuron;95(6):1292-1305.e5, 2017 Sep 13.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several microsatellite-expansion diseases are characterized by the accumulation of RNA foci and RAN proteins, raising the possibility of a mechanistic connection. We explored this question using myotonic dystrophy type 2, a multisystemic disease thought to be primarily caused by RNA gain-of-function effects. We demonstrate that the DM2 CCTGâ‹…CAGG expansion expresses sense and antisense tetrapeptide poly-(LPAC) and poly-(QAGR) RAN proteins, respectively. In DM2 autopsy brains, LPAC is found in neurons, astrocytes, and glia in gray matter, and antisense QAGR proteins accumulate within white matter. LPAC and QAGR proteins are toxic to cells independent of RNA gain of function. RNA foci and nuclear sequestration of CCUG transcripts by MBNL1 is inversely correlated with LPAC expression. These data suggest a model that involves nuclear retention of expansion RNAs by RNA-binding proteins (RBPs) and an acute phase in which expansion RNAs exceed RBP sequestration capacity, are exported to the cytoplasm, and undergo RAN translation. VIDEO ABSTRACT.
[Mh] Termos MeSH primário: Distrofia Miotônica/metabolismo
Biossíntese de Proteínas
Proteínas de Ligação a RNA/metabolismo
Proteína ran de Ligação ao GTP/biossíntese
[Mh] Termos MeSH secundário: Encéfalo/metabolismo
Sobrevivência Celular
Células Cultivadas
Regulação da Expressão Gênica
Seres Humanos
Mutação
RNA/metabolismo
Proteínas de Ligação a RNA/genética
Proteína ran de Ligação ao GTP/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (CNBP protein, human); 0 (MBNL1 protein, human); 0 (RNA-Binding Proteins); 63231-63-0 (RNA); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE


  3 / 1199 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28796037
[Au] Autor:Ruan L; Yang Y; Huang Y; Ding L; Zhang C; Wu X
[Ad] Endereço:Department of Gerontology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
[Ti] Título:Functional prediction of miR-3144-5p in human cardiac myocytes based on transcriptome sequencing and bioinformatics.
[So] Source:Medicine (Baltimore);96(32):e7539, 2017 Aug.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: RAN guanine nucleotide release factor (RANGRF) encoding protein MOG1 plays an important role in cardiac arrhythmia, so we intended to investigate the regulatory miRNA of RANGRF and explore its potential regulatory mechanism in arrhythmogenesis. METHODS: Based on bioinformatic analysis, miR-3144-5p was predicted to be a regulatory miRNA of RANGRF, which were then validated through a dual-luciferase reporter plasmid assay. Subsequently, the expression level of miR-3144-5p in human cardiac myocytes (HCMs) was detected, followed by cell transfection with miR-3144-5p mimics. Transcriptome sequencing was then performed in HCMs with or without transfection. The sequencing results were subjected to bioinformatic analyses, including differentially expressed gene (DEG) analysis, functional enrichment analysis, protein-protein interaction (PPI) network analysis, miRNA-target gene analysis, and miRNA-transcription factor (TF)-target gene coregulatory network analysis. RESULTS: There really existed a regulatory relation between miR-3144-5p and RANGRF. The expression level of miR-3144-5p was low in HCMs. After cell transfection, miR-3144-5p expression level significantly increased in HCMs. Bioinformatic analyses of the transcriptome sequencing results identified 300 upregulated and 271 downregulated DEGs between miR-3144-5p mimic and control group. The upregulated genes ISL1 and neuregulin 1 (NRG1) were significantly enriched in cardiac muscle cell myoblast differentiation (GO:0060379). CCL21 was one of the hub genes in the PPI network and also a target gene of miR-3144-5p. Moreover, the TF of v-Myc avian myelocytomatosis viral oncogene neuroblastoma-derived homolog (MYCN) was involved in the miR-3144-5p-TF-target gene coregulatory network and interacted with the target genes of miR-3144-5p. CONCLUSION: ISL1, NRG1, CCL21, and MYCN were differentially expressed in the miR-3144-5p mimic group, suggesting that miR-3144-5p overexpression plays a role in HCMs by regulating these genes and TF. This study may provide new insight into the mechanisms behind the progression of cardiac arrhythmia.
[Mh] Termos MeSH primário: Biologia Computacional/métodos
MicroRNAs/biossíntese
Miócitos Cardíacos/metabolismo
Proteína ran de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Quimiocina CCL21/biossíntese
Perfilação da Expressão Gênica
Seres Humanos
Proteínas com Homeodomínio LIM/biossíntese
Proteína Proto-Oncogênica N-Myc/biossíntese
Neuregulina-1/biossíntese
Fatores de Transcrição/biossíntese
Transcriptoma
Regulação para Cima
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL21 protein, human); 0 (Chemokine CCL21); 0 (LIM-Homeodomain Proteins); 0 (MYCN protein, human); 0 (MicroRNAs); 0 (N-Myc Proto-Oncogene Protein); 0 (NRG1 protein, human); 0 (Neuregulin-1); 0 (Transcription Factors); 0 (insulin gene enhancer binding protein Isl-1); EC 3.6.1.- (RANGNRF protein, human); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170827
[Lr] Data última revisão:
170827
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007539


  4 / 1199 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28193732
[Au] Autor:Baumann C; Wang X; Yang L; Viveiros MM
[Ad] Endereço:Department of Physiology and Pharmacology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA.
[Ti] Título:Error-prone meiotic division and subfertility in mice with oocyte-conditional knockdown of pericentrin.
[So] Source:J Cell Sci;130(7):1251-1262, 2017 Apr 01.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mouse oocytes lack canonical centrosomes and instead contain unique acentriolar microtubule-organizing centers (aMTOCs). To test the function of these distinct aMTOCs in meiotic spindle formation, pericentrin (Pcnt), an essential centrosome/MTOC protein, was knocked down exclusively in oocytes by using a transgenic RNAi approach. Here, we provide evidence that disruption of aMTOC function in oocytes promotes spindle instability and severe meiotic errors that lead to pronounced female subfertility. Pcnt-depleted oocytes from transgenic (Tg) mice were ovulated at the metaphase-II stage, but show significant chromosome misalignment, aneuploidy and premature sister chromatid separation. These defects were associated with loss of key Pcnt-interacting proteins (γ-tubulin, Nedd1 and Cep215) from meiotic spindle poles, altered spindle structure and chromosome-microtubule attachment errors. Live-cell imaging revealed disruptions in the dynamics of spindle assembly and organization, together with chromosome attachment and congression defects. Notably, spindle formation was dependent on Ran GTPase activity in Pcnt-deficient oocytes. Our findings establish that meiotic division is highly error-prone in the absence of Pcnt and disrupted aMTOCs, similar to what reportedly occurs in human oocytes. Moreover, these data underscore crucial differences between MTOC-dependent and -independent meiotic spindle assembly.
[Mh] Termos MeSH primário: Antígenos/metabolismo
Técnicas de Silenciamento de Genes
Infertilidade/metabolismo
Infertilidade/patologia
Meiose
Oócitos/metabolismo
Oócitos/patologia
[Mh] Termos MeSH secundário: Aneuploidia
Animais
Sobrevivência Celular
Cromossomos de Mamíferos/metabolismo
Feminino
Imagem Tridimensional
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Centro Organizador dos Microtúbulos/metabolismo
Corpos Polares do Fuso/metabolismo
Proteína ran de Ligação ao GTP
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (pericentrin); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.196188


  5 / 1199 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28143772
[Au] Autor:Lai KKY; Kweon SM; Chi F; Hwang E; Kabe Y; Higashiyama R; Qin L; Yan R; Wu RP; Lai K; Fujii N; French S; Xu J; Wang JY; Murali R; Mishra L; Lee JS; Ntambi JM; Tsukamoto H
[Ad] Endereço:Southern California Research Center for ALPD and Cirrhosis, Department of Pathology, University of Southern California, Los Angeles, California.
[Ti] Título:Stearoyl-CoA Desaturase Promotes Liver Fibrosis and Tumor Development in Mice via a Wnt Positive-Signaling Loop by Stabilization of Low-Density Lipoprotein-Receptor-Related Proteins 5 and 6.
[So] Source:Gastroenterology;152(6):1477-1491, 2017 May.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Stearoyl-CoA desaturase (SCD) synthesizes monounsaturated fatty acids (MUFAs) and has been associated with the development of metabolic syndrome, tumorigenesis, and stem cell characteristics. We investigated whether and how SCD promotes liver fibrosis and tumor development in mice. METHODS: Rodent primary hepatic stellate cells (HSCs), mouse liver tumor-initiating stem cell-like cells (TICs), and human hepatocellular carcinoma (HCC) cell lines were exposed to Wnt signaling inhibitors and changes in gene expression patterns were analyzed. We assessed the functions of SCD by pharmacologic and conditional genetic manipulation in mice with hepatotoxic or cholestatic induction of liver fibrosis, orthotopic transplants of TICs, or liver tumors induced by administration of diethyl nitrosamine. We performed bioinformatic analyses of SCD expression in HCC vs nontumor liver samples collected from patients, and correlated levels with HCC stage and patient mortality. We performed nano-bead pull-down assays, liquid chromatography-mass spectrometry, computational modeling, and ribonucleoprotein immunoprecipitation analyses to identify MUFA-interacting proteins. We examined the effects of SCD inhibition on Wnt signaling, including the expression and stability of low-density lipoprotein-receptor-related proteins 5 and 6 (LRP5 and LRP6), by immunoblot and quantitative polymerase chain reaction analyses. RESULTS: SCD was overexpressed in activated HSC and HCC cells from patients; levels of SCD messenger RNA (mRNA) correlated with HCC stage and patient survival time. In rodent HSCs and TICs, the Wnt effector ß-catenin increased sterol regulatory element binding protein 1-dependent transcription of Scd, and ß-catenin in return was stabilized by MUFAs generated by SCD. This loop required MUFA inhibition of binding of Ras-related nuclear protein 1 (Ran1) to transportin 1 and reduced nuclear import of elav-like protein 1 (HuR), increasing cytosolic levels of HuR and HuR-mediated stabilization of mRNAs encoding LRP5 and LRP6. Genetic disruption of Scd and pharmacologic inhibitors of SCD reduced HSC activation and TIC self-renewal and attenuated liver fibrosis and tumorigenesis in mice. Conditional disruption of Scd2 in activated HSCs prevented growth of tumors from TICs and reduced the formation of diethyl nitrosamine-induced liver tumors in mice. CONCLUSIONS: In rodent HSCs and TICs, we found SCD expression to be regulated by Wnt-ß-catenin signaling, and MUFAs produced by SCD provided a forward loop to amplify Wnt signaling via stabilization of Lrp5 and Lrp6 mRNAs, contributing to liver fibrosis and tumor growth. SCD expressed by HSCs promoted liver tumor development in mice. Components of the identified loop linking HSCs and TICs might be therapeutic targets for liver fibrosis and tumors.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Ácidos Graxos Monoinsaturados/metabolismo
Cirrose Hepática/metabolismo
Neoplasias Hepáticas/metabolismo
Estearoil-CoA Dessaturase/genética
Estearoil-CoA Dessaturase/metabolismo
Via de Sinalização Wnt/genética
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/induzido quimicamente
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Estudos de Casos e Controles
Linhagem Celular Tumoral
Colestase/complicações
Dietilnitrosamina
Proteína Semelhante a ELAV 1/metabolismo
Células Estreladas do Fígado
Seres Humanos
Cirrose Hepática/etiologia
Cirrose Hepática/patologia
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Proteína-5 Relacionada a Receptor de Lipoproteína de Baixa Densidade/genética
Proteína-5 Relacionada a Receptor de Lipoproteína de Baixa Densidade/metabolismo
Proteína-6 Relacionada a Receptor de Lipoproteína de Baixa Densidade/genética
Proteína-6 Relacionada a Receptor de Lipoproteína de Baixa Densidade/metabolismo
Masculino
Camundongos
Estadiamento de Neoplasias
Transplante de Neoplasias
Células-Tronco Neoplásicas
RNA Mensageiro/metabolismo
Ratos
Ratos Wistar
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Taxa de Sobrevida
Transcrição Genética
beta Catenina/metabolismo
beta Carioferinas/metabolismo
Proteína ran de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ELAV-Like Protein 1); 0 (Elavl1 protein, mouse); 0 (Fatty Acids, Monounsaturated); 0 (Low Density Lipoprotein Receptor-Related Protein-5); 0 (Low Density Lipoprotein Receptor-Related Protein-6); 0 (RNA, Messenger); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Tnpo1 protein, mouse); 0 (beta Catenin); 0 (beta Karyopherins); 3IQ78TTX1A (Diethylnitrosamine); EC 1.14.19.1 (Scd2 protein, mouse); EC 1.14.19.1 (Stearoyl-CoA Desaturase); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170202
[St] Status:MEDLINE


  6 / 1199 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27761921
[Au] Autor:Krans A; Kearse MG; Todd PK
[Ad] Endereço:Department of Neurology, University of Michigan, Ann Arbor, MI.
[Ti] Título:Repeat-associated non-AUG translation from antisense CCG repeats in fragile X tremor/ataxia syndrome.
[So] Source:Ann Neurol;80(6):871-881, 2016 Dec.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Repeat-associated non-AUG (RAN) translation drives production of toxic proteins from pathogenic repeat sequences in multiple untreatable neurodegenerative disorders. Fragile X-associated tremor/ataxia syndrome (FXTAS) is one such condition, resulting from a CGG trinucleotide repeat expansion in the 5' leader sequence of the FMR1 gene. RAN proteins from the CGG repeat accumulate in ubiquitinated inclusions in FXTAS patient brains and elicit toxicity. In addition to the CGG repeat, an antisense mRNA containing a CCG repeat is also transcribed from the FMR1 locus. We evaluated whether this antisense CCG repeat supports RAN translation and contributes to pathology in FXTAS patients. METHODS: We generated a series of CCG RAN translation-specific reporters and utilized them to measure RAN translation from CCG repeats in multiple reading frames in transfected cells. We also developed antibodies against predicted CCG RAN proteins and used immunohistochemistry and immunofluorescence on FXTAS patient tissues to measure their accumulation and distribution. RESULTS: RAN translation from CCG repeats is supported in all 3 potential reading frames, generating polyproline, polyarginine, and polyalanine proteins, respectively. Their production occurs whether or not the natural AUG start upstream of the repeat in the proline reading frame is present. All 3 frames show greater translation at larger repeat sizes. Antibodies targeted to the antisense FMR polyproline and polyalanine proteins selectively stain nuclear and cytoplasmic aggregates in FXTAS patients and colocalize with ubiquitinated neuronal inclusions. INTERPRETATION: RAN translation from antisense CCG repeats generates novel proteins that accumulate in ubiquitinated inclusions in FXTAS patients. Ann Neurol 2016;80:871-881.
[Mh] Termos MeSH primário: Ataxia/genética
Ataxia/metabolismo
Síndrome do Cromossomo X Frágil/genética
Síndrome do Cromossomo X Frágil/metabolismo
Biossíntese de Proteínas/genética
RNA Antissenso/genética
Tremor/genética
Tremor/metabolismo
Expansão das Repetições de Trinucleotídeos/genética
[Mh] Termos MeSH secundário: Proteína do X Frágil de Retardo Mental/genética
Seres Humanos
Proteína ran de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FMR1 protein, human); 0 (RNA, Antisense); 139135-51-6 (Fragile X Mental Retardation Protein); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24800


  7 / 1199 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27633000
[Au] Autor:Madugula V; Lu L
[Ad] Endereço:School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, 637551 Singapore.
[Ti] Título:A ternary complex comprising transportin1, Rab8 and the ciliary targeting signal directs proteins to ciliary membranes.
[So] Source:J Cell Sci;129(20):3922-3934, 2016 Oct 15.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The sensory functions of cilia are dependent on the enrichment of cilium-resident proteins. Although it is known that ciliary targeting signals (CTSs) specifically target ciliary proteins to cilia, it is still unclear how CTSs facilitate the entry and retention of cilium-resident proteins at the molecular level. We found that non-ciliary membrane reporters can passively diffuse into cilia through the lateral transport pathway, and the translocation of membrane reporters through the ciliary diffusion barrier is facilitated by importin binding motifs and domains. Screening known CTSs of ciliary membrane residents uncovered that fibrocystin, photoreceptor retinol dehydrogenase, rhodopsin and retinitis pigmentosa 2 interact with transportin1 (TNPO1) through previously identified CTSs. We further discovered that a new ternary complex, comprising TNPO1, Rab8 and a CTS, can assemble or disassemble under the guanine nucleotide exchange activity of Rab8. Our study suggests a new mechanism in which the TNPO1-Rab8-CTS complex mediates selective entry into and retention of cargos within cilia.
[Mh] Termos MeSH primário: Cílios/metabolismo
Membranas Intracelulares/metabolismo
Complexos Multiproteicos/metabolismo
Transdução de Sinais
beta Carioferinas/metabolismo
Proteínas rab de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Oxirredutases do Álcool/metabolismo
Motivos de Aminoácidos
Membrana Celular/metabolismo
Difusão
Técnicas de Silenciamento de Genes
Genes Reporter
Nucleotídeos de Guanina/metabolismo
Células HEK293
Células HeLa
Seres Humanos
Ligação Proteica
Domínios Proteicos
Transporte Proteico
Receptores de Superfície Celular/metabolismo
Rodopsina/metabolismo
Proteína ran de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Guanine Nucleotides); 0 (Multiprotein Complexes); 0 (PKHD1 protein, human); 0 (Receptors, Cell Surface); 0 (TNPO1 protein, human); 0 (beta Karyopherins); 9009-81-8 (Rhodopsin); EC 1.1.- (Alcohol Oxidoreductases); EC 3.6.1.-. (RAB8A protein, human); EC 3.6.5.2 (rab GTP-Binding Proteins); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160917
[St] Status:MEDLINE


  8 / 1199 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27626406
[Au] Autor:Yan JJ; Xie B; Zhang L; Li SJ; van Peer AF; Wu TJ; Chen BZ; Xie BG
[Ad] Endereço:Mycological Research Center, College of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China. junjie017@163.com.
[Ti] Título:Small GTPases and Stress Responses of vvran1 in the Straw Mushroom Volvariella volvacea.
[So] Source:Int J Mol Sci;17(9), 2016 Sep 10.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Small GTPases play important roles in the growth, development and environmental responses of eukaryotes. Based on the genomic sequence of the straw mushroom Volvariella volvacea, 44 small GTPases were identified. A clustering analysis using human small GTPases as the references revealed that V. volvacea small GTPases can be grouped into five families: nine are in the Ras family, 10 are in the Rho family, 15 are in the Rab family, one is in the Ran family and nine are in the Arf family. The transcription of vvran1 was up-regulated upon hydrogen peroxide (H2O2) stress, and could be repressed by diphenyleneiodonium chloride (DPI), a NADPH oxidase-specific inhibitor. The number of vvran1 transcripts also increased upon cold stress. Diphenyleneiodonium chloride, but not the superoxide dismutase (SOD) inhibitor diethy dithiocarbamate (DDC), could suppress the up-regulation of vvran1 gene expression to cold stress. These results combined with the high correlations between gene expression and superoxide anion (O2(-)) generation indicated that vvran1 could be one of the candidate genes in the downstream of O2(-) mediated pathways that are generated by NADPH oxidase under low temperature and oxidative stresses.
[Mh] Termos MeSH primário: Peróxido de Hidrogênio/farmacologia
Proteínas Monoméricas de Ligação ao GTP/genética
Estresse Fisiológico
Volvariella/enzimologia
[Mh] Termos MeSH secundário: Temperatura Baixa
Proteínas Fúngicas/genética
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Regulação Fúngica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Família Multigênica
Oniocompostos/farmacologia
Filogenia
Análise de Sequência de DNA
Homologia de Sequência de Aminoácidos
Volvariella/genética
Proteína ran de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungal Proteins); 0 (Onium Compounds); 6HJ411TU98 (diphenyleneiodonium); BBX060AN9V (Hydrogen Peroxide); EC 3.6.5.2 (Monomeric GTP-Binding Proteins); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160915
[St] Status:MEDLINE


  9 / 1199 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27611467
[Au] Autor:Kim MN; Kim JO; Lee SM; Park H; Lee JH; Rim KS; Hwang SG; Kim NK
[Ad] Endereço:Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, South Korea.
[Ti] Título:Variation in the Dicer and RAN Genes Are Associated with Survival in Patients with Hepatocellular Carcinoma.
[So] Source:PLoS One;11(9):e0162279, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Single-nucleotide polymorphisms (SNPs) in microRNA machinery genes might affect microRNA processing and subsequently impact tumorigenesis. The aim of this study was to investigate the associations between SNPs in microRNA machinery genes and hepatocellular carcinoma (HCC) in a Korean population. Genotyping of six SNPs in microRNA machinery genes was performed using blood samples from 147 patients with HCC and 209 healthy control subjects. None of the six SNPs in microRNA machinery genes were significantly associated with HCC development. However, among the models for six polymorphic loci-DICER (rs3742330 and rs13078), DROSHA (rs10719 and rs6877842), RAN (rs14035) and XPO5 (rs11077)-one allele combination (A-A-T-C-C-C) showed synergistic effects in terms of an increased risk of HCC development (odds ratio = 8.881, 95% confidence interval [CI] = 1.889-41.750; P = 0.002). Multivariate Cox proportional hazard regression analysis showed a significant survival benefit for the DICER rs3742330 GG compared with the AA type (hazard ratio [HR], 0.314; 95% CI, 0.135-0.730; P = 0.007) and for the RAN rs14035 CT compared with the CC genotype (HR, 0.587; 95% CI, 0.349-0.987; P = 0.044). Although we found no direct association between DICER (rs3742330 and rs13078), DROSHA (rs10719 and rs6877842), RAN (rs14035) or XPO5 (rs11077) polymorphisms and HCC risk, we demonstrated that DICER (rs3742330) and RAN (rs14035) were associated with the survival of HCC patients. Future studies with larger samples are needed to determine associations of SNPs in microRNA machinery genes with HCC risk and prognosis.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
RNA Helicases DEAD-box/genética
Neoplasias Hepáticas/genética
Ribonuclease III/genética
Sobreviventes
Proteína ran de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Feminino
Haplótipos
Seres Humanos
Carioferinas/genética
Masculino
MicroRNAs/genética
Meia-Idade
Polimorfismo de Nucleotídeo Único
Prognóstico
Análise de Regressão
República da Coreia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Karyopherins); 0 (MicroRNAs); 0 (RAN protein, human); 0 (XPO5 protein, human); EC 3.1.26.3 (DICER1 protein, human); EC 3.1.26.3 (DROSHA protein, human); EC 3.1.26.3 (Ribonuclease III); EC 3.6.4.13 (DEAD-box RNA Helicases); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160910
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0162279


  10 / 1199 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27541860
[Au] Autor:Vijayaraghavan B; Jafferali MH; Figueroa RA; Hallberg E
[Ti] Título:Samp1, a RanGTP binding transmembrane protein in the inner nuclear membrane.
[So] Source:Nucleus;7(4):415-23, 2016 Jul 03.
[Is] ISSN:1949-1042
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Samp1 is a transmembrane protein of the inner nuclear membrane (INM), which interacts with the nuclear lamina and the Linker of Nucleoskeleton and Cytoskeleton (LINC) complex in interphase and during mitosis, it localizes to the mitotic spindle. Samp1 was recently found to coprecipitate a protein complex containing Ran, a GTPase with fundamental regulatory functions both in interphase and in mitosis. To investigate the interaction between Samp1 and Ran in further detail, we have designed and expressed recombinant fusion proteins of the Chaetomium thermophilum homolog of Samp1 (Ct.Samp1) and human Ran. Pulldown experiments show that Samp1 binds directly to Ran and that Samp1 binds better to RanGTP compared to RanGDP. Samp1 also preferred RanGTP over RanGDP in living tsBN2 cells. We also show that the Ran binding domain is located between amino acids 75-135 in the nucleoplasmically exposed N-terminal tail of Samp1. This domain is unique for Samp1, without homology in any other proteins in fungi or metazoa. Samp1 is the first known transmembrane protein that binds to Ran and could provide a unique local binding site for RanGTP in the INM. Samp1 overexpression resulted in increased Ran concentrations in the nuclear periphery supporting this idea.
[Mh] Termos MeSH primário: Proteínas Fúngicas/metabolismo
Proteínas de Membrana/metabolismo
Membrana Nuclear/metabolismo
Proteína ran de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Chaetomium
Proteínas Fúngicas/química
Seres Humanos
Proteínas de Membrana/química
Ligação Proteica
Domínios Proteicos
Transporte Proteico
Especificidade por Substrato
Proteína ran de Ligação ao GTP/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungal Proteins); 0 (Membrane Proteins); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160820
[St] Status:MEDLINE
[do] DOI:10.1080/19491034.2016.1220465



página 1 de 120 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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