Base de dados : MEDLINE
Pesquisa : D12.776.220.600.450 [Categoria DeCS]
Referências encontradas : 19555 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1956 ir para página                         

  1 / 19555 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29355525
[Au] Autor:Kim JL; Ha GH; Campo L; Breuer EK
[Ad] Endereço:Department of Radiation Oncology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, 60153, USA.
[Ti] Título:Negative regulation of BRCA1 by transforming acidic coiled-coil protein 3 (TACC3).
[So] Source:Biochem Biophys Res Commun;496(2):633-640, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In spite of the push to identify modifiers of BRCAness, it still remains unclear how tumor suppressor BRCA1 is lost in breast cancers in the absence of genetic or epigenetic aberrations. Mounting evidence indicates that the transforming acidic coiled-coil 3 (TACC3) plays an important role in the centrosome-microtubule network during mitosis and gene expression, and that deregulation of TACC3 is associated with breast cancer. However, the molecular mechanisms by which TACC3 contributes to breast cancer development have yet to be elucidated. Herein, we found that high levels of TACC3 in human mammary epithelial cells can cause genomic instability possibly in part through destabilizing BRCA1. We also found that high levels of TACC3 inhibited the interaction between BRCA1 and BARD1, thus subsequently allowing the BARD1-uncoupled BRCA1 to be destabilized by ubiquitin-mediated proteosomal pathway. Moreover, there is an inverse correlation between TACC3 and BRCA1 expression in breast cancer tissues. Overall, our findings provide a new insight into the role of TACC3 in genomic instability and breast tumorigenesis.
[Mh] Termos MeSH primário: Proteína BRCA1/metabolismo
Proteínas Associadas aos Microtúbulos/metabolismo
[Mh] Termos MeSH secundário: Neoplasias da Mama/genética
Neoplasias da Mama/metabolismo
Linhagem Celular
Feminino
Instabilidade Genômica
Seres Humanos
Mapas de Interação de Proteínas
Estabilidade Proteica
Proteólise
Proteínas Supressoras de Tumor/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BRCA1 Protein); 0 (Microtubule-Associated Proteins); 0 (TACC3 protein, human); 0 (Tumor Suppressor Proteins); EC 2.3.2.27 (BARD1 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[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:180123
[St] Status:MEDLINE


  2 / 19555 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29410090
[Au] Autor:Brewer RA; Collins HE; Berry RD; Brahma MK; Tirado BA; Peliciari-Garcia RA; Stanley HL; Wende AR; Taegtmeyer H; Rajasekaran NS; Darley-Usmar V; Zhang J; Frank SJ; Chatham JC; Young ME
[Ad] Endereço:Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
[Ti] Título:Temporal partitioning of adaptive responses of the murine heart to fasting.
[So] Source:Life Sci;197:30-39, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recent studies suggest that the time of day at which food is consumed dramatically influences clinically-relevant cardiometabolic parameters (e.g., adiposity, insulin sensitivity, and cardiac function). Meal feeding benefits may be the result of daily periods of feeding and/or fasting, highlighting the need for improved understanding of the temporal adaptation of cardiometabolic tissues (e.g., heart) to fasting. Such studies may provide mechanistic insight regarding how time-of-day-dependent feeding/fasting cycles influence cardiac function. We hypothesized that fasting during the sleep period elicits beneficial adaptation of the heart at transcriptional, translational, and metabolic levels. To test this hypothesis, temporal adaptation was investigated in wild-type mice fasted for 24-h, or for either the 12-h light/sleep phase or the 12-h dark/awake phase. Fasting maximally induced fatty acid responsive genes (e.g., Pdk4) during the dark/active phase; transcriptional changes were mirrored at translational (e.g., PDK4) and metabolic flux (e.g., glucose/oleate oxidation) levels. Similarly, maximal repression of myocardial p-mTOR and protein synthesis rates occurred during the dark phase; both parameters remained elevated in the heart of fasted mice during the light phase. In contrast, markers of autophagy (e.g., LC3II) exhibited peak responses to fasting during the light phase. Collectively, these data show that responsiveness of the heart to fasting is temporally partitioned. Autophagy peaks during the light/sleep phase, while repression of glucose utilization and protein synthesis is maximized during the dark/active phase. We speculate that sleep phase fasting may benefit cardiac function through augmentation of protein/cellular constituent turnover.
[Mh] Termos MeSH primário: Adaptação Fisiológica
Autofagia
Jejum/metabolismo
Miocárdio/metabolismo
Fases do Sono
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Proteínas Associadas aos Microtúbulos/metabolismo
Biossíntese de Proteínas/fisiologia
Proteínas Serina-Treonina Quinases/biossíntese
Serina-Treonina Quinases TOR/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MAP1LC3 protein, mouse); 0 (Microtubule-Associated Proteins); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.1 (mTOR protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.2 (pyruvate dehydrogenase (acetyl-transferring) kinase)
[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:180208
[St] Status:MEDLINE


  3 / 19555 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29288363
[Au] Autor:Hamurcu Z; Delibasi N; Geçene S; Sener EF; Dönmez-Altuntas H; Özkul Y; Canatan H; Ozpolat B
[Ad] Endereço:Department of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
[Ti] Título:Targeting LC3 and Beclin-1 autophagy genes suppresses proliferation, survival, migration and invasion by inhibition of Cyclin-D1 and uPAR/Integrin ß1/ Src signaling in triple negative breast cancer cells.
[So] Source:J Cancer Res Clin Oncol;144(3):415-430, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Autophagy is a catabolic process for degrading dysfunctional proteins and organelles, and closely associated with cancer cell survival under therapeutic, metabolic stress, hypoxia, starvation and lack of growth factors, contributing to resistance to therapies. However, the role of autophagy in breast cancer cells is not well understood. In the present study, we investigated the role of autophagy in highly aggressive and metastatic triple negative breast cancer (TNBC) and non-metastatic breast cancer cells and demonstrated that the knockdown of autophagy-related genes (LC3 and Beclin-1) inhibited autophagy and significantly suppressed cell proliferation, colony formation, migration/invasion and induced apoptosis in MDA-MB-231 and BT-549 TNBC cells. Knockdown of LC3 and Beclin-1 led to inhibition of multiple proto-oncogenic signaling pathways, including cyclin D1, uPAR/integrin-ß1/Src, and PARP1. In conclusion, our study suggests that LC3 and Beclin-1 are required for cell proliferation, survival, migration and invasion, and may contribute to tumor growth and progression of highly aggressive and metastatic TNBC cells and therapeutic targeting of autophagy genes may be a potential therapeutic strategy for TNBC in breast cancer.
[Mh] Termos MeSH primário: Beclina-1/antagonistas & inibidores
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Proteínas Associadas aos Microtúbulos/antagonistas & inibidores
Terapia de Alvo Molecular/métodos
RNA Interferente Pequeno/farmacologia
Neoplasias de Mama Triplo Negativas/patologia
[Mh] Termos MeSH secundário: Autofagia/genética
Beclina-1/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Ciclina D1/antagonistas & inibidores
Ciclina D1/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Integrina beta1/metabolismo
Células MCF-7
Proteínas Associadas aos Microtúbulos/genética
Receptores de Ativador de Plasminogênio Tipo Uroquinase/antagonistas & inibidores
Receptores de Ativador de Plasminogênio Tipo Uroquinase/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Neoplasias de Mama Triplo Negativas/genética
Quinases da Família src/antagonistas & inibidores
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Beclin-1); 0 (CCND1 protein, human); 0 (Integrin beta1); 0 (Microtubule-Associated Proteins); 0 (RNA, Small Interfering); 0 (Receptors, Urokinase Plasminogen Activator); 0 (light chain 3, human); 136601-57-5 (Cyclin D1); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2557-5


  4 / 19555 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29335463
[Au] Autor:Wang Q; Sun Q; Czajkowsky DM; Shao Z
[Ad] Endereço:Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, 200240, Shanghai, China.
[Ti] Título:Sub-kb Hi-C in D. melanogaster reveals conserved characteristics of TADs between insect and mammalian cells.
[So] Source:Nat Commun;9(1):188, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Topologically associating domains (TADs) are fundamental elements of the eukaryotic genomic structure. However, recent studies suggest that the insulating complexes, CTCF/cohesin, present at TAD borders in mammals are absent from those in Drosophila melanogaster, raising the possibility that border elements are not conserved among metazoans. Using in situ Hi-C with sub-kb resolution, here we show that the D. melanogaster genome is almost completely partitioned into >4000 TADs, nearly sevenfold more than previously identified. The overwhelming majority of these TADs are demarcated by the insulator complexes, BEAF-32/CP190, or BEAF-32/Chromator, indicating that these proteins may play an analogous role in flies as that of CTCF/cohesin in mammals. Moreover, extended regions previously thought to be unstructured are shown to consist of small contiguous TADs, a property also observed in mammals upon re-examination. Altogether, our work demonstrates that fundamental features associated with the higher-order folding of the genome are conserved from insects to mammals.
[Mh] Termos MeSH primário: Cromatina/ultraestrutura
Mapeamento Cromossômico/métodos
Cromossomos de Insetos/ultraestrutura
Drosophila melanogaster/genética
Genoma de Inseto
Mamíferos/genética
[Mh] Termos MeSH secundário: Animais
Evolução Biológica
Fator de Ligação a CCCTC/genética
Fator de Ligação a CCCTC/metabolismo
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Cromatina/química
Montagem e Desmontagem da Cromatina
Proteínas Cromossômicas não Histona/genética
Proteínas Cromossômicas não Histona/metabolismo
Mapeamento Cromossômico/instrumentação
Cromossomos de Insetos/química
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Proteínas de Drosophila/genética
Proteínas de Drosophila/metabolismo
Drosophila melanogaster/ultraestrutura
Proteínas do Olho/genética
Proteínas do Olho/metabolismo
Expressão Gênica
Seres Humanos
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
Conformação Molecular
Proteínas Associadas à Matriz Nuclear/genética
Proteínas Associadas à Matriz Nuclear/metabolismo
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BEAF-32 protein, Drosophila); 0 (CCCTC-Binding Factor); 0 (CP190 protein, Drosophila); 0 (CTCF protein, human); 0 (Cell Cycle Proteins); 0 (Chromatin); 0 (Chromosomal Proteins, Non-Histone); 0 (DNA-Binding Proteins); 0 (Drosophila Proteins); 0 (Eye Proteins); 0 (Microtubule-Associated Proteins); 0 (Nuclear Matrix-Associated Proteins); 0 (Nuclear Proteins); 0 (chromator protein, Drosophila); 0 (cohesins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02526-9


  5 / 19555 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29311554
[Au] Autor:Frudd K; Burgoyne T; Burgoyne JR
[Ad] Endereço:King's College London, Cardiovascular Division, The British Heart Foundation, Centre of Excellence, The Rayne Institute, St Thomas' Hospital, London, SE1 7EH, UK.
[Ti] Título:Oxidation of Atg3 and Atg7 mediates inhibition of autophagy.
[So] Source:Nat Commun;9(1):95, 2018 01 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Macroautophagy (autophagy) is a crucial cellular stress response for degrading defective macromolecules and organelles, as well as providing bioenergetic intermediates during hypoxia and nutrient deprivation. Here we report a thiol-dependent process that may account for impaired autophagy during aging. This is through direct oxidation of key autophagy-related (Atg) proteins Atg3 and Atg7. When inactive Atg3 and Atg7 are protected from oxidation due to stable covalent interaction with their substrate LC3. This interaction becomes transient upon activation of Atg3 and Atg7 due to transfer of LC3 to phosphatidylethanolamine (lipidation), a process crucial for functional autophagy. However, loss in covalent-bound LC3 also sensitizes the catalytic thiols of Atg3 and Atg7 to inhibitory oxidation that prevents LC3 lipidation, observed in vitro and in mouse aorta. Here findings provide a thiol-dependent process for negatively regulating autophagy that may contribute to the process of aging, as well as therapeutic targets to regulate autophagosome maturation.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Proteína 7 Relacionada à Autofagia/química
Proteínas Relacionadas à Autofagia/química
Autofagia/efeitos dos fármacos
Peróxido de Hidrogênio/farmacologia
Proteínas Associadas aos Microtúbulos/química
Enzimas de Conjugação de Ubiquitina/química
[Mh] Termos MeSH secundário: Animais
Aorta/citologia
Aorta/efeitos dos fármacos
Aorta/metabolismo
Autofagossomos/efeitos dos fármacos
Autofagossomos/metabolismo
Proteína 7 Relacionada à Autofagia/metabolismo
Proteínas Relacionadas à Autofagia/metabolismo
Células HEK293
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Proteínas Associadas aos Microtúbulos/metabolismo
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Oxirredução
Fosfatidiletanolaminas/química
Fosfatidiletanolaminas/metabolismo
Cultura Primária de Células
Ratos
Compostos de Sulfidrila/química
Enzimas de Conjugação de Ubiquitina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Atg7 protein, mouse); 0 (Autophagy-Related Proteins); 0 (MAP1LC3 protein, mouse); 0 (Microtubule-Associated Proteins); 0 (Phosphatidylethanolamines); 0 (Sulfhydryl Compounds); 39382-08-6 (phosphatidylethanolamine); BBX060AN9V (Hydrogen Peroxide); EC 2.3.2.23 (Ubiquitin-Conjugating Enzymes); EC 6.2.1.45 (Autophagy-Related Protein 7); EC 6.3.2.- (Atg3 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02352-z


  6 / 19555 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29374705
[Au] Autor:Nakamura A; Matsunaga W; Gotoh A
[Ad] Endereço:Laboratory of Cell and Gene Therapy, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Japan.
[Ti] Título:Autophagy Induced by Naftopidil Inhibits Apoptosis of Human Gastric Cancer Cells.
[So] Source:Anticancer Res;38(2):803-809, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:AIM: Naftopidil is used to treat benign prostate hyperplasia. Moreover, previous studies have shown that naftopidil reduced viability of many types of cancer cells. Therefore, we investigated the antitumor mechanism of naftopidil in this study. MATERIALS AND METHODS: We used the HGC27 human gastric cancer cell line. It was treated with naftopidil, pan-caspase inhibitor, and chloroquine diphosphate (CQ). Cell viability and cell death were investigated by the assay and annexin V/ propidium iodide assay. Phosphorylation of protein kinase B (AKT) (Ser473) was measured by western blotting. Alteration of light chain 3B (LC3B) was investigated by western blotting and immunofluorescence. RESULTS: Naftopidil reduced phospho-AKT (Ser473) and altered LC3B. Combination of naftopidil and CQ reduced cell viability and phospho-AKT (Ser 473). CONCLUSION: Naftopidil induces apoptosis and autophagy of HGC27 cells, however, autophagy is considered to inhibit apoptosis. We concluded naftopidil and CQ have a synergistic antitumor effect.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Naftalenos/farmacologia
Piperazinas/farmacologia
Neoplasias Gástricas/tratamento farmacológico
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Cloroquina/administração & dosagem
Cloroquina/análogos & derivados
Cloroquina/farmacologia
Sinergismo Farmacológico
Seres Humanos
Proteínas Associadas aos Microtúbulos/metabolismo
Naftalenos/administração & dosagem
Fosforilação
Piperazinas/administração & dosagem
Proteínas Proto-Oncogênicas c-akt/metabolismo
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MAP1LC3B protein, human); 0 (Microtubule-Associated Proteins); 0 (Naphthalenes); 0 (Piperazines); 6E17K3343P (chloroquine diphosphate); 886U3H6UFF (Chloroquine); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); R9PHW59SFN (naftopidil)
[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


  7 / 19555 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29241732
[Au] Autor:Park YS; Choi SE; Koh HC
[Ad] Endereço:Department of Pharmacology, College of Medicine, Hanyang University, Seoul, Republic of Korea; Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Republic of Korea.
[Ti] Título:PGAM5 regulates PINK1/Parkin-mediated mitophagy via DRP1 in CCCP-induced mitochondrial dysfunction.
[So] Source:Toxicol Lett;284:120-128, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dynamics and mitophagy are critical processes for regulating mitochondrial homeostasis. Phosphoglycerate mutase family member 5 (PGAM5) is a mitochondrial protein that plays crucial roles in apoptosis and necroptosis, but the roles of PGAM5 in mitochondrial dynamics and mitophagy remain unclear. In this study, we investigated the role of PGAM5 in carbonyl cyanide m-chlorophenylhydrazone (CCCP)-induced mitochondrial damage and the correlation between mitochondrial dynamics and mitophagy using SH-SY5Y cells. We found that CCCP decreased mitochondrial membrane potential, resulting in mitochondrial dysfunction. CCCP increased PGAM5, dynamin-related protein 1 (DRP1), and optic atrophy 1 (OPA1) expression of the mitochondrial fraction in a time-dependent manner. Knockdown of PGAM5 inhibited DRP1 translocation without a change in OPA1 expression in CCCP-treated cells. Furthermore, knockdown of PGAM5 and DRP1 significantly blocked the increase of PTEN-induced putative protein kinase 1 (PINK1) and Parkin expression in the mitochondrial fraction of CCCP-treated cells. Interestingly, CCCP did not alter PINK1/Parkin expression in the mitochondrial fraction of OPA1 knockdown cells. Inhibiting mitophagy by PGAM5 knockdown accelerated CCCP-induced apoptosis. CCCP treatment also results in PINK1 stabilization on the mitochondrial membrane, which subsequently increases Parkin recruitment from the cytosol to abnormal mitochondria. In addition, we found that CCCP increased the level of mitochondrial LC3II, indicating that Parkin recruitment of PINK1 is a result of mitophagy. We propose that activation of PGAM5 is associated with DRP1 recruitment and PINK1 stabilization, which contribute to the modulation of mitophagy in CCCP-treated cells with mitochondrial dysfunction. In conclusion, we demonstrated that PGAM5 regulates PINK1-Parkin-mediated mitophagy, which can exert a neuroprotective effect against CCCP-induced apoptosis.
[Mh] Termos MeSH primário: Carbonil Cianeto m-Clorofenil Hidrazona/toxicidade
GTP Fosfo-Hidrolases/metabolismo
Proteínas Associadas aos Microtúbulos/metabolismo
Degradação Mitocondrial/efeitos dos fármacos
Proteínas Mitocondriais/metabolismo
Fosfoproteínas Fosfatases/metabolismo
Proteínas Quinases/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
GTP Fosfo-Hidrolases/genética
Técnicas de Silenciamento de Genes
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Proteínas Associadas aos Microtúbulos/genética
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Proteínas Mitocondriais/genética
Fosfoproteínas Fosfatases/genética
Proteínas Quinases/genética
Ubiquitina-Proteína Ligases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Microtubule-Associated Proteins); 0 (Mitochondrial Proteins); 555-60-2 (Carbonyl Cyanide m-Chlorophenyl Hydrazone); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.3.2.27 (parkin protein); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (PTEN-induced putative kinase); EC 3.1.3.16 (PGAM5 protein, human); EC 3.1.3.16 (Phosphoprotein Phosphatases); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.5.5 (DNM1L protein, human)
[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:171216
[St] Status:MEDLINE


  8 / 19555 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28493473
[Au] Autor:Tahrir FG; Shanmughapriya S; Ahooyi TM; Knezevic T; Gupta MK; Kontos CD; McClung JM; Madesh M; Gordon J; Feldman AM; Cheung JY; Khalili K
[Ad] Endereço:Department of Neuroscience, Center for Neurovirology, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania.
[Ti] Título:Dysregulation of mitochondrial bioenergetics and quality control by HIV-1 Tat in cardiomyocytes.
[So] Source:J Cell Physiol;233(2):748-758, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiovascular disease remains a leading cause of morbidity and mortality in HIV-positive patients, even in those whose viral loads are well controlled with antiretroviral therapy. However, the underlying molecular events responsible for the development of cardiac disease in the setting of HIV remain unknown. The HIV-encoded Tat protein plays a critical role in the activation of HIV gene expression and profoundly impacts homeostasis in both HIV-infected cells and uninfected cells that have taken up released Tat via a bystander effect. Since cardiomyocyte function, including excitation-contraction coupling, greatly depends on energy provided by the mitochondria, in this study, we performed a series of experiments to assess the impact of Tat on mitochondrial function and bioenergetics pathways in a primary cell culture model derived from neonatal rat ventricular cardiomyocytes (NRVCs). Our results show that the presence of Tat in cardiomyocytes is accompanied by a decrease in oxidative phosphorylation, a decline in the levels of ATP, and an accumulation of reactive oxygen species (ROS). Tat impairs the uptake of mitochondrial Ca ([Ca ] ) and the electrophysiological activity of cardiomyocytes. Tat also affects the protein clearance pathway and autophagy in cardiomyocytes under stress due to hypoxia-reoxygenation conditions. A reduction in the level of ubiquitin along with dysregulated degradation of autophagy proteins including SQSTM1/p62 and a reduction of LC3 II were detected in cardiomyocytes harboring Tat. These results suggest that, by targeting mitochondria and protein quality control, Tat significantly impacts bioenergetics and autophagy resulting in dysregulation of cardiomyocyte health and homeostasis.
[Mh] Termos MeSH primário: Metabolismo Energético
HIV-1/metabolismo
Mitocôndrias Cardíacas/metabolismo
Miócitos Cardíacos/metabolismo
Produtos do Gene tat do Vírus da Imunodeficiência Humana/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Apoptose
Autofagia
Cálcio/metabolismo
Canais de Cálcio/metabolismo
Hipóxia Celular
Células Cultivadas
Interações Hospedeiro-Patógeno
Potenciais da Membrana
Proteínas Associadas aos Microtúbulos/metabolismo
Mitocôndrias Cardíacas/virologia
Degradação Mitocondrial
Miócitos Cardíacos/virologia
Fosforilação Oxidativa
Cultura Primária de Células
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Proteína Sequestossoma-1/metabolismo
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (LC3 protein, rat); 0 (Microtubule-Associated Proteins); 0 (Reactive Oxygen Species); 0 (Sequestosome-1 Protein); 0 (Sqstm1 protein, rat); 0 (mitochondrial calcium uniporter); 0 (tat Gene Products, Human Immunodeficiency Virus); 8L70Q75FXE (Adenosine Triphosphate); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26002


  9 / 19555 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29259037
[Au] Autor:Falch CM; Sundaram AYM; Øystese KA; Normann KR; Lekva T; Silamikelis I; Eieland AK; Andersen M; Bollerslev J; Olarescu NC
[Ad] Endereço:Section of Specialized EndocrinologyDepartment of Endocrinology cafal14@student.sdu.dk.
[Ti] Título:Gene expression profiling of fast- and slow-growing non-functioning gonadotroph pituitary adenomas.
[So] Source:Eur J Endocrinol;178(3):295-307, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Reliable biomarkers associated with aggressiveness of non-functioning gonadotroph adenomas (GAs) are lacking. As the growth of tumor remnants is highly variable, molecular markers for growth potential prediction are necessary. We hypothesized that fast- and slow-growing GAs present different gene expression profiles and reliable biomarkers for tumor growth potential could be identified, focusing on the specific role of epithelial-mesenchymal transition (EMT). DESIGN AND METHODS: Eight GAs selected for RNA sequencing were equally divided into fast- and slow-growing group by the tumor volume doubling time (TVDT) median (27.75 months). Data were analyzed by tophat2, cufflinks and cummeRbund pipeline. 40 genes were selected for RT-qPCR validation in 20 GAs based on significance, fold-change and pathway analyses. The effect of silencing (metadherin) and (endomucin) on migration of human adenoma cells was evaluated. RESULTS: 350 genes were significantly differentially expressed (282 genes upregulated and 68 downregulated in the fast group, -adjusted <0.05). Among 40 selected genes, 11 showed associations with TVDT (-0.669< <-0.46, < 0.05). These were and six EMT-related genes ( and ). , but not , demonstrated involvement in cell migration and association with EMT markers. CONCLUSIONS: Fast- and slow-growing GAs present different gene expression profiles, and genes related to EMT have higher expression in fast-growing tumors. In addition to , identified as an important contributor to aggressiveness, the other genes might represent markers for tumor growth potential and possible targets for drug therapy.
[Mh] Termos MeSH primário: Adenoma/genética
Transição Epitelial-Mesenquimal/genética
Neoplasias Hipofisárias/genética
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Adenoma/metabolismo
Adulto
Idoso
Caderinas/genética
Moléculas de Adesão Celular/genética
Movimento Celular/genética
Subunidades Catalíticas da Proteína Quinase Dependente de AMP Cíclico/genética
Feminino
Hormônio Foliculoestimulante/metabolismo
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Inativação Gênica
Seres Humanos
Técnicas In Vitro
Peptídeos e Proteínas de Sinalização Intracelular/genética
Hormônio Luteinizante/metabolismo
Masculino
Glicoproteínas de Membrana/genética
Proteínas Associadas aos Microtúbulos/genética
Meia-Idade
Miosina Tipo I/genética
Proteínas do Tecido Nervoso/genética
Neoplasias Hipofisárias/metabolismo
Proteínas Proto-Oncogênicas/genética
Receptores de Superfície Celular/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Ribonucleases/genética
Sialoglicoproteínas/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Cadherins); 0 (Cell Adhesion Molecules); 0 (EMCN protein, human); 0 (GPM6A protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (MTDH protein, human); 0 (MYO1B protein, human); 0 (Membrane Glycoproteins); 0 (Microtubule-Associated Proteins); 0 (Nerve Tissue Proteins); 0 (PCDH18 protein, human); 0 (Proto-Oncogene Proteins); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (SKIL protein, human); 0 (SPAG9 protein, human); 0 (Sialoglycoproteins); 0 (UNC5H4 protein, human); 0 (hook1 protein, human); 9002-67-9 (Luteinizing Hormone); 9002-68-0 (Follicle Stimulating Hormone); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinase Catalytic Subunits); EC 2.7.11.11 (PRKACB protein, human); EC 3.1.- (CNOT6L protein, human); EC 3.1.- (Ribonucleases); EC 3.6.1.- (Myosin Type I)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0702


  10 / 19555 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29177545
[Au] Autor:Gu Y; Zhou Y; Shi X; Xin Y; Shan Y; Chen C; Cao T; Fang W; Li X
[Ad] Endereço:Institute of Preventive Veterinary Medicine, Zhejiang University, Hangzhou, 310058, China.
[Ti] Título:Porcine teschovirus 2 induces an incomplete autophagic response in PK-15 cells.
[So] Source:Arch Virol;163(3):623-632, 2018 Mar.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Autophagy is a homeostatic process that has been shown to be vital in the innate immune defense against pathogens. However, little is known about the regulatory role of autophagy in porcine teschovirus 2 (PTV-2) replication. In this study, we found that PTV-2 infection induces a strong increase in GFP-LC3 punctae and endogenous LC3 lipidation. However, PTV-2 infection did not enhance autophagic protein degradation. When cellular autophagy was pharmacologically inhibited by wortmannin or 3-methyladenine, PTV-2 replication increased. The increase in virus yield via autophagy inhibition was further confirmed by silencing atg5, which is required for autophagy. Furthermore, PTV-2 replication was suppressed when autophagy was activated by rapamycin. Together, the results suggest that PTV-2 infection activates incomplete autophagy and that autophagy then inhibits further PTV-2 replication.
[Mh] Termos MeSH primário: Proteína 5 Relacionada à Autofagia/antagonistas & inibidores
Autofagia/efeitos dos fármacos
Células Epiteliais/virologia
Interações Hospedeiro-Patógeno
Teschovirus/efeitos dos fármacos
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenina/análogos & derivados
Adenina/farmacologia
Androstadienos/farmacologia
Animais
Autofagia/genética
Proteína 5 Relacionada à Autofagia/genética
Proteína 5 Relacionada à Autofagia/metabolismo
Linhagem Celular
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Regulação da Expressão Gênica
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Rim
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Sirolimo/farmacologia
Suínos
Teschovirus/genética
Teschovirus/crescimento & desenvolvimento
Teschovirus/metabolismo
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androstadienes); 0 (Autophagy-Related Protein 5); 0 (Microtubule-Associated Proteins); 0 (RNA, Small Interfering); 147336-22-9 (Green Fluorescent Proteins); 5142-23-4 (3-methyladenine); JAC85A2161 (Adenine); W36ZG6FT64 (Sirolimus); XVA4O219QW (wortmannin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3652-2



página 1 de 1956 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