Base de dados : MEDLINE
Pesquisa : A10.082.750 [Categoria DeCS]
Referências encontradas : 6723 [refinar]
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  1 / 6723 MEDLINE  
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[PMID]:28460472
[Au] Autor:Å Urga S; Nanut MP; Kos J; Sabotic J
[Ad] Endereço:Department of Biotechnology, Jožef Stefan Institute, Ljubljana, Slovenia.
[Ti] Título:Fungal lectin MpL enables entry of protein drugs into cancer cells and their subcellular targeting.
[So] Source:Oncotarget;8(16):26896-26910, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lectins have been recognized as promising carrier molecules for targeted drug delivery. They specifically bind carbohydrate moieties on cell membranes and trigger cell internalization. Fungal lectin MpL (Macrolepiota procera lectin) does not provoke cancer cell cytotoxicity but is able to bind aminopeptidase N (CD13) and integrin α3ß1, two glycoproteins that are overexpressed on the membrane of tumor cells. Upon binding, MpL is endocytosed in a clathrin-dependent manner and accumulates initially in the Golgi apparatus and, finally, in the lysosomes. For effective binding and internalization a functional binding site on the α-repeat is needed. To test the potential of MpL as a carrier for delivering protein drugs to cancer cells we constructed fusion proteins consisting of MpL and the cysteine peptidase inhibitors cystatin C and clitocypin. The fused proteins followed the same endocytic route as the unlinked MpL. Peptidase inhibitor-MpL fusions impaired both the intracellular degradation of extracellular matrix and the invasiveness of cancer cells. MpL is thus shown in vitro to be a lectin that can enable protein drugs to enter cancer cells, enhance their internalization and sort them to lysosomes and the Golgi apparatus.
[Mh] Termos MeSH primário: Portadores de Fármacos
Proteínas Fúngicas/metabolismo
Lectinas/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Membrana Celular/metabolismo
Colágeno Tipo IV/metabolismo
Endocitose
Glicoproteínas/metabolismo
Seres Humanos
Espaço Intracelular/metabolismo
Ligação Proteica
Transporte Proteico
Proteólise
Proteínas Recombinantes de Fusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type IV); 0 (Drug Carriers); 0 (Fungal Proteins); 0 (Glycoproteins); 0 (Lectins); 0 (Recombinant Fusion Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15849


  2 / 6723 MEDLINE  
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[PMID]:28460432
[Au] Autor:Huang W; Zhou W; Li C; Yang Y; Shang YK; Chen C; Zhang J; Yao R; Wang P; Wen W; Liu HQ; Wang L; Li X; Bian H; Chen ZN
[Ad] Endereço:National Translational Science Center for Molecular Medicine, Department of Cell Biology, Fourth Military Medical University, Xi'an, China.
[Ti] Título:Promoter mutations and cellular distribution of telomerase in non-clear cell and clear cell hepatocellular carcinoma.
[So] Source:Oncotarget;8(16):26288-26297, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reactivation of telomerase is a critical step in the development of hepatocellular carcinoma (HCC). Here we identified the frequency of mutations in telomerase reverse transcriptase (TERT) promoter was 34% in non-clear cell HCC (NCCHCC, n = 259) and 26.3% in clear cell HCC (CCHCC, n = 57). The mutations were independently associated with poor recurrence-free survival of HCCs. Interestingly immunohistochemical analysis demonstrated a higher positive rate of TERT cytoplasmic localization (95%) than nuclear localization (64%) in HCCs. In NCCHCCs, the mutations correlated with higher TERT nuclear expression and increased telomere-dependent telomerase activity. Higher cytoplasmic expression was found in adjacent tissues compared to tumor tissues, and was associated with tumor well-differentiation and lower level of α-fetoprotein. NCCHCCs with low nuclear as well as high cytoplasmic expression correlated with better prognosis. In CCHCCs, elevated TERT cytoplasmic expression was observed in CCHCCs harboring mutations. Higher TERT cytoplasmic expression was found in tumor tissues compared to adjacent tissues, and was associated with multiple numbers of tumors and poor prognosis of CCHCCs. In conclusion, mutations in TERT promoter disclose the significance of both nuclear and cytoplasmic TERT in HCC. Cytoplasmic TERT should also be considered when determining prognosis and treatment of HCCs.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/genética
Adenocarcinoma de Células Claras/metabolismo
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/metabolismo
Mutação
Regiões Promotoras Genéticas
Telômero/genética
Telômero/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/mortalidade
Adenocarcinoma de Células Claras/patologia
Adulto
Idoso
Carcinoma Hepatocelular/mortalidade
Carcinoma Hepatocelular/patologia
Feminino
Seguimentos
Seres Humanos
Espaço Intracelular/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/patologia
Masculino
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Transporte Proteico
Recidiva
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15458


  3 / 6723 MEDLINE  
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[PMID]:29211994
[Au] Autor:Wu XS; Elias S; Liu H; Heureaux J; Wen PJ; Liu AP; Kozlov MM; Wu LG
[Ad] Endereço:National Institute of Neurological Disorders and Stroke, Bethesda, Maryland.
[Ti] Título:Membrane Tension Inhibits Rapid and Slow Endocytosis in Secretory Cells.
[So] Source:Biophys J;113(11):2406-2414, 2017 Dec 05.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endocytosis generates spherical or ellipsoid-like vesicles from the plasma membrane, which recycles vesicles that fuse with the plasma member during exocytosis in neurons and endocrine secretory cells. Although tension in the plasma membrane is generally considered to be an important factor in regulating endocytosis, whether membrane tension inhibits or facilitates endocytosis remains debated in the endocytosis field, and has been rarely studied for vesicular endocytosis in secretory cells. Here we report that increasing membrane tension by adjusting osmolarity inhibited both the rapid (a few seconds) and slow (tens of seconds) endocytosis in calyx-type nerve terminals containing conventional active zones and in neuroendocrine chromaffin cells. We address the mechanism of this phenomenon by computational modeling of the energy barrier that the system must overcome at the stage of membrane budding by an assembling protein coat. We show that this barrier grows with increasing tension, which may slow down or prevent membrane budding. These results suggest that in live secretory cells, membrane tension exerts inhibitory action on endocytosis.
[Mh] Termos MeSH primário: Membrana Celular/metabolismo
Células Cromafins/citologia
Células Cromafins/metabolismo
Endocitose
[Mh] Termos MeSH secundário: Animais
Feminino
Espaço Intracelular/metabolismo
Cinética
Masculino
Camundongos
Concentração Osmolar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  4 / 6723 MEDLINE  
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[PMID]:28452248
[Au] Autor:Milisa M; Dikic D; Mandic T; Grozic D; Colic I; Ostojic A
[Ad] Endereço:a Department of Biology, Faculty of Science , University of Zagreb , Zagreb , Croatia.
[Ti] Título:Response of aquatic protists to electric field exposure.
[So] Source:Int J Radiat Biol;93(8):818-830, 2017 08.
[Is] ISSN:1362-3095
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To test the effects of short-term exposure of aquatic organisms to electric field (EF) with negligible magnetic component. MATERIALS AND METHODS: We built a plate capacitor that served as a source of EF of strengths that can be found in nature near transmission lines. We exposed two cultured protist species Euglena viridis and Paramecium caudatum to EFs for 24 hours and monitored their abundance, morphology, intracellular superoxide anion (by dihydroethidium [DHE]), hydrogen peroxide by (H DCF) and lipid peroxidation (MDA) contents, catalase (CAT) and superoxide dismutase (SOD) activity. RESULTS: We found that even short-term exposure to low strength EF causes changes in population abundance, morphology and oxidative stress response in both species. As the EF strength increased, abundance of both species decreased. However, at weaker EFs, fission rates were seemingly promoted. We noted a decrease in size in both organisms in directions perpendicular to their fission planes correlated with EF strength. DHE and H DCF fluorescence intensity and SOD activity were higher in organisms exposed to the stronger EFs. CONCLUSIONS: We suggest that the electric component of the field, rather than the magnetic, is the main cause of all the noted effects. As a result, aquatic organisms should be given greater importance in studies assessing the effects of EMFs in spite of the attenuating effects of water to EF strengths.
[Mh] Termos MeSH primário: Eletricidade
Euglena/metabolismo
Paramecium caudatum/metabolismo
[Mh] Termos MeSH secundário: Catalase/metabolismo
Membrana Celular/metabolismo
Peróxido de Hidrogênio/metabolismo
Espaço Intracelular/metabolismo
L-Lactato Desidrogenase/metabolismo
Peroxidação de Lipídeos
Malondialdeído/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
4Y8F71G49Q (Malondialdehyde); BBX060AN9V (Hydrogen Peroxide); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1080/09553002.2017.1321809


  5 / 6723 MEDLINE  
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[PMID]:27777042
[Au] Autor:Li YB; Li XR; Yang T; Wang JX; Zhao XF
[Ad] Endereço:Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Jinan, Shandong 250100, China.
[Ti] Título:The steroid hormone 20-hydroxyecdysone promotes switching from autophagy to apoptosis by increasing intracellular calcium levels.
[So] Source:Insect Biochem Mol Biol;79:73-86, 2016 12.
[Is] ISSN:1879-0240
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Autophagy regulates cell survival (or cell death in several cases), whereas apoptosis regulates cell death. However, the relationship between autophagy and apoptosis and the regulative mechanism is unclear. We report that steroid hormone 20-hydroxyecdysone (20E) promotes switching from autophagy to apoptosis by increasing intracellular calcium levels in the midgut of the lepidopteran insect Helicoverpa armigera. Autophagy and apoptosis sequentially occurred during midgut programmed cell death under 20E regulation, in which lower concentrations of 20E induced microtubule-associated protein 1 light chain 3-phosphatidylethanolamine (LC3-II, also known as autophagy-related gene 8, ATG8) expression and autophagy. High concentrations of 20E induced cleavage of ATG5 to NtATG5 and pro-caspase-3 to active caspase-3, which led to a switch from autophagy to apoptosis. Blocking autophagy by knockdown of ATG5, ATG7, or ATG12, or with the autophagy inhibitor 3-methyladenine, inhibited 20E-induced autophagy and apoptosis. Blocking apoptosis by using the apoptosis inhibitor Ac-DEVD-CHO did not prevent 20E-induced autophagy, suggesting that apoptosis relies on autophagy. ATG5 knockdown resulted in abnormal pupation and delayed pupation time. High concentrations of 20E induced high levels of intracellular Ca , NtATG5, and active caspase-3, which mediated the switch from autophagy to apoptosis. Blocking 20E-mediated increase of cellular Ca caused a decrease of NtATG5 and active caspase-3 and repressed the transformation from autophagy to apoptosis, thereby promoting cell survival. 20E induces an increase in the concentration of intracellular Ca , thereby switching autophagic cell survival to apoptotic cell death.
[Mh] Termos MeSH primário: Apoptose
Autofagia
Cálcio/metabolismo
Ecdisterona/metabolismo
Mariposas/fisiologia
[Mh] Termos MeSH secundário: Animais
Trato Gastrointestinal/fisiologia
Espaço Intracelular/metabolismo
Larva/crescimento & desenvolvimento
Larva/fisiologia
Mariposas/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
5289-74-7 (Ecdysterone); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


  6 / 6723 MEDLINE  
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[PMID]:28457922
[Au] Autor:Yasuda J; Okada M; Yamawaki H
[Ad] Endereço:Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Higashi 23 Bancho 35-1, Towada, Aomori 034-8628, Japan.
[Ti] Título:T3 peptide, an active fragment of tumstatin, inhibits H O -induced apoptosis in H9c2 cardiomyoblasts.
[So] Source:Eur J Pharmacol;807:64-70, 2017 Jul 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Tumstatin, a cleaved fragment of α3 chain of type IV collagen, is an endogenous anti-angiogenetic peptide. Although the expression level of tumstatin changes in the heart tissues of certain experimental cardiac disease models, its effect on cardiomyocytes has not been clarified. In this study, we examined the effects of T3 peptide, an active subfragment of tumstatin, on hydrogen peroxide (H O )-induced cell death in H9c2 cardiomyoblasts. Cell viability was examined by a cell counting assay. Staining using 4', 6-diamidino-2-phenylindole was performed to observe nuclear morphology. Western blotting was performed to examine cleaved caspase-3 expression. Mitochondrial membrane potential and morphology were detected by a Mito Tracker Red staining. Intracellular reactive oxygen species production was examined by 2', 7'-dichlorodihydrofluorescein diacetate staining. T3 peptide (300, 1000ng/ml) suppressed H O (1mM)-induced cell death, apoptotic changes of nuclei and cleaved caspas-3 expression in a concentration-dependent manner. T3 peptide also inhibited H O -induced loss of mitochondrial membrane potential, mitochondrial fission and reactive oxygen species production. Cilengitide, an integrin α ß /α ß inhibitor, prevents the inhibitory effect of T3 peptide on H O -induced reactive oxygen species production. In conclusion, T3 peptide inhibits H O -induced apoptosis at least partly via the inhibition of intracellular reactive oxygen species production through the action on integrin.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autoantígenos/química
Colágeno Tipo IV/química
Peróxido de Hidrogênio/farmacologia
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Fragmentos de Peptídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Caspase 3/metabolismo
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Peróxido de Hidrogênio/antagonistas & inibidores
Espaço Intracelular/efeitos dos fármacos
Espaço Intracelular/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Dinâmica Mitocondrial/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Proteólise/efeitos dos fármacos
Ratos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantigens); 0 (Collagen Type IV); 0 (Peptide Fragments); 0 (Reactive Oxygen Species); 0 (type IV collagen alpha3 chain); BBX060AN9V (Hydrogen Peroxide); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  7 / 6723 MEDLINE  
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[PMID]:28465335
[Au] Autor:Li J; Miao L; Zhao C; Shaikh Qureshi WM; Shieh D; Guo H; Lu Y; Hu S; Huang A; Zhang L; Cai CL; Wan LQ; Xin H; Vincent P; Singer HA; Zheng Y; Cleaver O; Fan ZC; Wu M
[Ad] Endereço:Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA.
[Ti] Título:CDC42 is required for epicardial and pro-epicardial development by mediating FGF receptor trafficking to the plasma membrane.
[So] Source:Development;144(9):1635-1647, 2017 05 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The epicardium contributes to multiple cardiac lineages and is essential for cardiac development and regeneration. However, the mechanism of epicardium formation is unclear. This study aimed to establish the cellular and molecular mechanisms underlying the dissociation of pro-epicardial cells (PECs) from the pro-epicardium (PE) and their subsequent translocation to the heart to form the epicardium. We used lineage tracing, conditional deletion, mosaic analysis and ligand stimulation in mice to determine that both villous protrusions and floating cysts contribute to PEC translocation to myocardium in a CDC42-dependent manner. We resolved a controversy by demonstrating that physical contact of the PE with the myocardium constitutes a third mechanism for PEC translocation to myocardium, and observed a fourth mechanism in which PECs migrate along the surface of the inflow tract to reach the ventricles. Epicardial-specific deletion disrupted epicardium formation, and null PECs proliferated less, lost polarity and failed to form villous protrusions and floating cysts. FGF signaling promotes epicardium formation , and biochemical studies demonstrated that CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardium formation.
[Mh] Termos MeSH primário: Membrana Celular/metabolismo
Pericárdio/citologia
Pericárdio/metabolismo
Receptores de Fatores de Crescimento de Fibroblastos/metabolismo
Proteína cdc42 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Polaridade Celular
Proliferação Celular
Embrião de Mamíferos/citologia
Embrião de Mamíferos/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Fator 2 de Crescimento de Fibroblastos/metabolismo
Espaço Intracelular/metabolismo
Camundongos Knockout
Modelos Biológicos
Miocárdio/citologia
Miocárdio/metabolismo
Fosforilação
Transporte Proteico
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Fibroblast Growth Factor); 103107-01-3 (Fibroblast Growth Factor 2); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.6.5.2 (cdc42 GTP-Binding Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1242/dev.147173


  8 / 6723 MEDLINE  
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[PMID]:29096074
[Au] Autor:Rost BR; Schneider-Warme F; Schmitz D; Hegemann P
[Ad] Endereço:German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany; Neuroscience Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany.
[Ti] Título:Optogenetic Tools for Subcellular Applications in Neuroscience.
[So] Source:Neuron;96(3):572-603, 2017 Nov 01.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability to study cellular physiology using photosensitive, genetically encoded molecules has profoundly transformed neuroscience. The modern optogenetic toolbox includes fluorescent sensors to visualize signaling events in living cells and optogenetic actuators enabling manipulation of numerous cellular activities. Most optogenetic tools are not targeted to specific subcellular compartments but are localized with limited discrimination throughout the cell. Therefore, optogenetic activation often does not reflect context-dependent effects of highly localized intracellular signaling events. Subcellular targeting is required to achieve more specific optogenetic readouts and photomanipulation. Here we first provide a detailed overview of the available optogenetic tools with a focus on optogenetic actuators. Second, we review established strategies for targeting these tools to specific subcellular compartments. Finally, we discuss useful tools and targeting strategies that are currently missing from the optogenetics repertoire and provide suggestions for novel subcellular optogenetic applications.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos Celulares/fisiologia
Espaço Intracelular/genética
Neurônios/fisiologia
Neurociências/métodos
Optogenética/métodos
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Espaço Intracelular/química
Espaço Intracelular/metabolismo
Neurônios/química
Neurociências/tendências
Optogenética/tendências
Rodopsina/análise
Rodopsina/genética
Sistemas do Segundo Mensageiro/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
9009-81-8 (Rhodopsin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171103
[St] Status:MEDLINE


  9 / 6723 MEDLINE  
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[PMID]:29020068
[Au] Autor:Cai C; Zhou J; Sun X; Sun T; Xie W; Cui J
[Ad] Endereço:Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, P. R. China.
[Ti] Título:Integrated modeling and analysis of intracellular and intercellular mechanisms in shaping the interferon response to viral infection.
[So] Source:PLoS One;12(10):e0186105, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interferons (IFNs) responses to viral infection are heterogeneous, while the underlying mechanisms for variability among cells are still not clear. In this study, we developed a hybrid model to systematically identify the sources of IFN induction heterogeneity. The experiment-integrated simulation demonstrated that the viral dose/type, the diversity in transcriptional factors activation and the intercellular paracrine signaling could strikingly shape the heterogeneity of IFN expression. We further determined that the IFNß and IFNλ1 induced diverse dynamics of IFN-stimulated genes (ISGs) production. Collectively, our findings revealed the intracellular and intercellular mechanisms contributing to cell-to-cell variation in IFN induction, and further demonstrated the significant effects of IFN heterogeneity on antagonizing viruses.
[Mh] Termos MeSH primário: Espaço Extracelular/metabolismo
Interferons/farmacologia
Espaço Intracelular/metabolismo
Modelos Biológicos
Estomatite Vesicular/metabolismo
[Mh] Termos MeSH secundário: Células A549
Forma Celular/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Células HEK293
Seres Humanos
Comunicação Parácrina/efeitos dos fármacos
Fatores de Tempo
Fatores de Transcrição/metabolismo
Ativação Transcricional/efeitos dos fármacos
Ativação Transcricional/genética
Estomatite Vesicular/genética
Estomatite Vesicular/patologia
Vesiculovirus/efeitos dos fármacos
Vesiculovirus/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transcription Factors); 9008-11-1 (Interferons)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186105


  10 / 6723 MEDLINE  
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[PMID]:28952698
[Au] Autor:Popov SV; Guseinov RG; Martov AG; Muratov TM; Tabynbaev NB
[Ad] Endereço:St. Lukes Clinical Hospital, St. Petersburg, Russia.
[Ti] Título:[Molecular and cellular mechanisms of damage to renal parenchyma in renal warm ischemia].
[So] Source:Urologiia;(4):79-84, 2017 Sep.
[Is] ISSN:1728-2985
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Warm ischemia of the renal parenchyma is a forced feature of laparoscopic partial nephrectomy. It is accompanied by oxygen deprivation of the organ and followed by re-oxygenation, which can cause additional damage to the renal tissue. This damage can result in acute functional and structural disorders of individual parts of the nephron, increasing the risk for a renal dysfunction. Timely diagnosis of the dysfunction is vital for the success of the treatment. The article provides an overview of current scientific data on the mechanisms of ischemic and reperfusion injuries at the molecular-cellular level and describes the current methods of their detection. Experimental and clinical study of the molecular-cellular mechanisms of ischemic-reperfusion injury of the renal tissue made it possible, first, to determine the main targets of alteration (cytolemma, mitochondria, lysosomes), and second, to establish its consequences, among which the most important are hypoergosis, DNA damage, simultaneous activation of intracellular systems of the suicidal program and induction of electrical breakdown of membranes of target nephrocytes; thirdly, to reveal the range of possibilities for limiting the consequences of hypoxia and/or re-oxygenation, among which interference in the metabolism of purines, measures ensuring the preservation of colloid osmotic pressure inside and outside the cell and membrane stabilization, antioxidant defense and inhibition of cysteine proteinases, etc. However, despite the advances in understanding the pathogenesis of cell damage, including ischemic-hypoxic injury, the problem of intraoperative ischemia-reperfusion safety remains relevant.
[Mh] Termos MeSH primário: Rim/patologia
Tecido Parenquimatoso/patologia
Traumatismo por Reperfusão/patologia
Isquemia Quente/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Apoptose
Cálcio/metabolismo
Calpaína/metabolismo
Hipóxia Celular
Radicais Livres/metabolismo
Seres Humanos
Espaço Intracelular/metabolismo
Rim/irrigação sanguínea
Rim/metabolismo
Tecido Parenquimatoso/metabolismo
Proteólise
Traumatismo por Reperfusão/etiologia
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Free Radicals); EC 3.4.22.- (Calpain); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE



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