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Pesquisa : B04.820.455.600.650.700.800 [Categoria DeCS]
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  1 / 919 MEDLINE  
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[PMID]:28456782
[Au] Autor:Lee CH; Nishikawa T; Kaneda Y
[Ad] Endereço:Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.
[Ti] Título:Salmonella mediated the hemagglutinating virus of Japan-envelope transfer suppresses tumor growth.
[So] Source:Oncotarget;8(21):35048-35060, 2017 May 23.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Salmonella can target to tumor microenvironments after systemic treatment. The hemagglutinating virus of Japan-envelope (HVJ-E) induced apoptosis in tumor cells without toxicity in normal cells. Current HVJ-E therapeutic strategies, aimed at using HVJ-E for intratumor treatment, have shown great promise in animal models but have achieved only limited systemic treatment. The purpose of this study was to investigate the modulation of the anti-tumor efficiency of HVJ-E by coating the particles with poly (allylamine hydrochloride) (PAH), designated as P-HVJ-E. Treatment with P-HVJ-E resulted in decreased hemagglutinating activity and maintained tumor cell-selective apoptosis and anti-tumor immunity. The use of Salmonella as a coating for P-HVJ-E (PHS) enhanced the antitumor activity and maintained the tumor-targeting activity. Treatment with PHS resulted in delayed tumor growth in tumor-bearing mice. Furthermore, a Western blot assay of the tumors revealed that HVJ-E targeted to the tumor after systemic treatment with PHS. These results indicate that Salmonella coating viral particles may provide a new approach for tumor therapy.
[Mh] Termos MeSH primário: Neoplasias Experimentais/tratamento farmacológico
Poliaminas/química
Salmonella/fisiologia
Vírus Sendai/metabolismo
Proteínas do Envelope Viral/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Seres Humanos
Camundongos
Microambiente Tumoral
Proteínas do Envelope Viral/química
Proteínas do Envelope Viral/farmacologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Polyamines); 0 (Viral Envelope Proteins); 30551-89-4 (polyallylamine)
[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:170501
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.17037


  2 / 919 MEDLINE  
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[PMID]:29293661
[Au] Autor:Monson EA; Crosse KM; Das M; Helbig KJ
[Ad] Endereço:Department of Physiology, Anatomy and Microbiology, La Trobe University, Melbourne, Victoria.
[Ti] Título:Lipid droplet density alters the early innate immune response to viral infection.
[So] Source:PLoS One;13(1):e0190597, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cellular localisation of many innate signalling events following viral infection has yet to be elucidated, however there has been a few cases in which membranes of certain cellular organelles have acted as platforms to these events. Of these, lipid droplets (LDs) have recently been identified as signalling platforms for innate TLR7 and 9 signalling. Despite their wide range of similar roles in various metabolic pathways, LDs have been overlooked as potential platforms for antiviral innate signalling events. This study established an in vitro model to evaluate the efficiency of the early innate immune response in cells with reduced LD content to the viral mimics, dsDNA and dsRNA, and Sendai viral infection. Using RT-qPCR, the expression of IFN-ß and IFN-λ was quantified following stimulation along with the expression of specific ISGs. Luciferase based assays evaluated the combined expression of ISRE-promoter driven ISGs under IFN-ß stimulation. Cellular LD content did not alter the entry of fluorescently labelled viral mimics into cells, but significantly decreased the ability of both Huh-7 and HeLa cells to produce type I and III IFN, as well as downstream ISG expression, indicative of an impeded innate immune response. This observation was also seen during Sendai virus infection of HeLa cells, where both control and LD reduced cells replicated the virus to the same level, but a significantly impaired type I and III IFN response was observed in the LD reduced cells. In addition to altered IFN production, cells with reduced LD content exhibited decreased expression of specific antiviral ISGs: Viperin, IFIT-1 and OAS-1 under IFN-ß stimulation; However the overall induction of the ISRE-promoter was not effected. This study implicates a role for LDs in an efficient early innate host response to viral infection and future work will endeavour to determine the precise role these important organelles play in induction of an antiviral response.
[Mh] Termos MeSH primário: Imunidade Inata
Gotículas Lipídicas/metabolismo
Viroses/imunologia
[Mh] Termos MeSH secundário: Western Blotting
Linhagem Celular
Meios de Cultura
Seres Humanos
Interferon Tipo I/imunologia
Ácidos Nucleicos/metabolismo
RNA de Cadeia Dupla/imunologia
Reação em Cadeia da Polimerase em Tempo Real
Vírus Sendai/patogenicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media); 0 (Interferon Type I); 0 (Nucleic Acids); 0 (RNA, Double-Stranded)
[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:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190597


  3 / 919 MEDLINE  
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[PMID]:28988534
[Au] Autor:Zhirnov OP
[Ad] Endereço:Ivanovsky Institute of Virology, Gamaleya Microbiology and Epidemiology Research Center, Moscow, 123098, Russia. zhirnov@inbox.ru.
[Ti] Título:Biochemical Variations in Cytolytic Activity of Ortho- and Paramyxoviruses in Human Lung Tumor Cell Culture.
[So] Source:Biochemistry (Mosc);82(9):1048-1054, 2017 Sep.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human lung cancer cells (Calu-3 line) were studied for the development of apoptosis, necrosis, and autophagy in response to infection with ortho- and paramyxoviruses. Biochemical pathways underlying various mechanisms of cell death differed for different viruses. When infected with murine Sendai paramyxovirus, Calu-3 cells demonstrated typical necrotic features such as cell swelling (but not shrinkage), lack of chromatin DNA laddering, of caspase 3 and 8 activation, and of apoptotic cleavage of poly(ADP-ribose) polymerase (PARP) protein; an activation of antiapoptotic protein kinase Akt was also revealed. In contrast, infection with avian influenza virus A/FPV/Rostock/34 (H7N1 subtype) or Newcastle disease virus (NDV, avian paramyxovirus) caused the development of typical apoptotic markers such as cell shrinkage, ladder-type chromosomal DNA fragmentation, caspase 3 and 8 activation, and proteolytic cleavage of PARP in the absence of Akt activation. Notably, no upregulation of p53 protein phosphorylation was observed in all infected cells, which indicates that p53 is not involved in the virus-induced death of Calu-3 cells. Cell death caused by the influenza virus was accompanied by overstimulation of autophagy, whereas no stimulation of autophagy was observed in the NDV-infected cells. Infection with Sendai virus caused moderate stimulation of autophagy, which suggests that the mechanism of the virus-induced cell death and the balance between autophagy and cell death in infected cancer cells depend on the virus type and might significantly differ even for closely related viruses. Therefore, an optimal strategy for oncolytic virus-mediated destruction of tumor cells in cancer patients requires selection of the most appropriate oncolytic virus based on the mechanism of its cytolytic action in a particular type of tumor.
[Mh] Termos MeSH primário: Apoptose
Vírus da Influenza A Subtipo H7N1
Neoplasias Pulmonares/virologia
Vírus da Doença de Newcastle
Vírus Oncolíticos
Vírus Sendai
[Mh] Termos MeSH secundário: Autofagia
Seres Humanos
Neoplasias Pulmonares/patologia
Necrose
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:171010
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917090085


  4 / 919 MEDLINE  
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[PMID]:28934360
[Au] Autor:Yan BR; Zhou L; Hu MM; Li M; Lin H; Yang Y; Wang YY; Shu HB
[Ad] Endereço:College of Life Sciences, Wuhan University, Wuhan, China.
[Ti] Título:PKACs attenuate innate antiviral response by phosphorylating VISA and priming it for MARCH5-mediated degradation.
[So] Source:PLoS Pathog;13(9):e1006648, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sensing of viral RNA by RIG-I-like receptors initiates innate antiviral response, which is mediated by the central adaptor VISA. How the RIG-I-VISA-mediated antiviral response is terminated at the late phase of infection is enigmatic. Here we identified the protein kinase A catalytic (PKAC) subunits α and ß as negative regulators of RNA virus-triggered signaling in a redundant manner. Viral infection up-regulated cellular cAMP levels and activated PKACs, which then phosphorylated VISA at T54. This phosphorylation abrogated virus-induced aggregation of VISA and primed it for K48-linked polyubiquitination and degradation by the E3 ligase MARCH5, leading to attenuation of virus-triggered induction of downstream antiviral genes. PKACs-deficiency or inactivation by the inhibitor H89 potentiated innate immunity to RNA viruses in cells and mice. Our findings reveal a critical mechanism of attenuating innate immune response to avoid host damage at the late phase of viral infection by the house-keeping PKA kinase.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/imunologia
Subunidades Catalíticas da Proteína Quinase Dependente de AMP Cíclico/imunologia
Imunidade Inata/imunologia
Proteínas de Membrana/imunologia
Infecções por Respirovirus/imunologia
Ubiquitina-Proteína Ligases/imunologia
[Mh] Termos MeSH secundário: Animais
Células HEK293
Seres Humanos
Immunoblotting
Imunoprecipitação
Camundongos
Fosforilação
Vírus Sendai
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Membrane Proteins); 0 (VISA protein, human); EC 2.3.2.27 (MARCH5 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinase Catalytic Subunits)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006648


  5 / 919 MEDLINE  
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[PMID]:28636653
[Au] Autor:Dilley KA; Voorhies AA; Luthra P; Puri V; Stockwell TB; Lorenzi H; Basler CF; Shabman RS
[Ad] Endereço:Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States of America.
[Ti] Título:The Ebola virus VP35 protein binds viral immunostimulatory and host RNAs identified through deep sequencing.
[So] Source:PLoS One;12(6):e0178717, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ebola virus and Marburg virus are members of the Filovirdae family and causative agents of hemorrhagic fever with high fatality rates in humans. Filovirus virulence is partially attributed to the VP35 protein, a well-characterized inhibitor of the RIG-I-like receptor pathway that triggers the antiviral interferon (IFN) response. Prior work demonstrates the ability of VP35 to block potent RIG-I activators, such as Sendai virus (SeV), and this IFN-antagonist activity is directly correlated with its ability to bind RNA. Several structural studies demonstrate that VP35 binds short synthetic dsRNAs; yet, there are no data that identify viral immunostimulatory RNAs (isRNA) or host RNAs bound to VP35 in cells. Utilizing a SeV infection model, we demonstrate that both viral isRNA and host RNAs are bound to Ebola and Marburg VP35s in cells. By deep sequencing the purified VP35-bound RNA, we identified the SeV copy-back defective interfering (DI) RNA, previously identified as a robust RIG-I activator, as the isRNA bound by multiple filovirus VP35 proteins, including the VP35 protein from the West African outbreak strain (Makona EBOV). Moreover, RNAs isolated from a VP35 RNA-binding mutant were not immunostimulatory and did not include the SeV DI RNA. Strikingly, an analysis of host RNAs bound by wild-type, but not mutant, VP35 revealed that select host RNAs are preferentially bound by VP35 in cell culture. Taken together, these data support a model in which VP35 sequesters isRNA in virus-infected cells to avert RIG-I like receptor (RLR) activation.
[Mh] Termos MeSH primário: Ebolavirus/fisiologia
Doença pelo Vírus Ebola/imunologia
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Interações Hospedeiro-Patógeno/imunologia
RNA de Cadeia Dupla/metabolismo
Proteínas Virais Reguladoras e Acessórias/metabolismo
[Mh] Termos MeSH secundário: Doença pelo Vírus Ebola/genética
Doença pelo Vírus Ebola/virologia
Seres Humanos
Interferons/antagonistas & inibidores
Vírus Sendai/genética
Vírus Sendai/imunologia
Transdução de Sinais
Proteínas Virais Reguladoras e Acessórias/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Double-Stranded); 0 (VP35 protein, filovirus); 0 (Viral Regulatory and Accessory Proteins); 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:170622
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178717


  6 / 919 MEDLINE  
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[PMID]:28631605
[Au] Autor:Sánchez-Aparicio MT; Garcin D; Rice CM; Kolakofsky D; García-Sastre A; Baum A
[Ad] Endereço:1​Department of Microbiology, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, New York, NY 10029, USA 2​Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, New York, NY 10029, USA.
[Ti] Título:Loss of Sendai virus C protein leads to accumulation of RIG-I immunostimulatory defective interfering RNA.
[So] Source:J Gen Virol;98(6):1282-1293, 2017 Jun.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Retinoic acid inducible gene (RIG-I)-mediated innate immunity plays a pivotal role in defence against virus infections. Previously we have shown that Sendai virus (SeV) defective interfering (DI) RNA functions as an exclusive and potent RIG-I ligand in DI-RNA-rich SeV-Cantell infected cells. To further understand how RIG-I is activated during SeV infection, we used a different interferon (IFN)-inducing SeV strain, recombinant SeVΔC, which, in contrast to SeV-Cantell is believed to stimulate IFN production due to the lack of the SeV IFN antagonist protein C. Surprisingly, we found that in SevΔC-infected cells, DI RNAs also functioned as an exclusive RIG-I ligand. Infections with wild-type SeV failed to generate any RIG-I-associated immunostimulatory RNA and this correlated with the lack of DI genomes in infected cells, as well as with the absence of cellular innate immune responses. Supplementation of the C protein in the context of SeVΔC infection led to a reduction in the number of DI RNAs, further supporting the potential role of the C protein as a negative regulator of DI generation and/or accumulation. Our findings indicate that limiting DI genome production is an important function of viral IFN antagonist proteins.
[Mh] Termos MeSH primário: Proteína DEAD-box 58/metabolismo
Deleção de Genes
Regulação Viral da Expressão Gênica
RNA Interferente Pequeno/metabolismo
Vírus Sendai/imunologia
Proteínas Virais/genética
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/metabolismo
Teste de Complementação Genética
Células HeLa
Seres Humanos
RNA Viral/metabolismo
Vírus Sendai/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (RNA, Small Interfering); 0 (RNA, Viral); 0 (Viral Proteins); 0 (nonstructural C protein, Sendai virus); EC 3.6.1.- (DDX58 protein, human); EC 3.6.4.13 (DEAD Box Protein 58)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000815


  7 / 919 MEDLINE  
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[PMID]:28605636
[Au] Autor:Russell CJ; Jones BG; Sealy RE; Surman SL; Mason JN; Hayden RT; Tripp RA; Takimoto T; Hurwitz JL
[Ad] Endereço:Department of Infectious Diseases, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA; Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA.
[Ti] Título:A Sendai virus recombinant vaccine expressing a gene for truncated human metapneumovirus (hMPV) fusion protein protects cotton rats from hMPV challenge.
[So] Source:Virology;509:60-66, 2017 Sep.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human metapneumovirus (hMPV) infections pose a serious health risk to young children, particularly in cases of premature birth. No licensed vaccine exists and there is no standard treatment for hMPV infections apart from supportive hospital care. We describe the production of a Sendai virus (SeV) recombinant that carries a gene for a truncated hMPV fusion (F) protein (SeV-MPV-Ft). The vaccine induces binding and neutralizing antibody responses toward hMPV and protection against challenge with hMPV in a cotton rat system. Results encourage advanced development of SeV-MPV-Ft to prevent the morbidity and mortality caused by hMPV infections in young children.
[Mh] Termos MeSH primário: Antígenos Virais/imunologia
Portadores de Fármacos
Metapneumovirus/imunologia
Infecções por Paramyxoviridae/prevenção & controle
Vírus Sendai/genética
Proteínas Virais de Fusão/imunologia
Vacinas Virais/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/sangue
Anticorpos Antivirais/sangue
Antígenos Virais/genética
Modelos Animais de Doenças
Metapneumovirus/genética
Infecções por Paramyxoviridae/imunologia
Sigmodontinae
Resultado do Tratamento
Vacinas Sintéticas/administração & dosagem
Vacinas Sintéticas/genética
Vacinas Sintéticas/imunologia
Proteínas Virais de Fusão/genética
Vacinas Virais/administração & dosagem
Vacinas Virais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Antibodies, Viral); 0 (Antigens, Viral); 0 (Drug Carriers); 0 (Vaccines, Synthetic); 0 (Viral Fusion Proteins); 0 (Viral Vaccines)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170812
[Lr] Data última revisão:
170812
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE


  8 / 919 MEDLINE  
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[PMID]:28413006
[Au] Autor:Zhang S; Lv Z; Hu Y; Liu L; Gong W; Li Q; Wu H
[Ad] Endereço:Department of Spine Surgery, The 1st Hospital of Jilin University, Changchun 130021, China.
[Ti] Título:Generation of a human induced pluripotent stem cell (iPSC) line from a 64year old male patient with multiple schwannoma.
[So] Source:Stem Cell Res;19:49-51, 2017 Mar.
[Is] ISSN:1876-7753
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Peripheral blood was collected from a clinically diagnosed 64-year old male multiple schwannoma patient. Peripheral blood mononuclear cells (PBMCs) were reprogrammed with the Yamanaka KMOS reprogramming factors using the Sendai-virus reprogramming system. The transgene-free iPSC line showed pluripotency verified by immunofluorescent staining for pluripotency markers, and the iPSC line was able to differentiate into the 3 germ layers in vivo. The iPSC line also showed normal karyotype. This in vitro cellular model will be useful for further pathological studies of multiple schwannoma.
[Mh] Termos MeSH primário: Células-Tronco Pluripotentes Induzidas/citologia
Neurilemoma/patologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Reprogramação Celular
Vetores Genéticos/genética
Vetores Genéticos/metabolismo
Camadas Germinativas/citologia
Camadas Germinativas/metabolismo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Cariótipo
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/metabolismo
Masculino
Meia-Idade
Neurilemoma/metabolismo
Vírus Sendai/genética
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transcription Factors)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE


  9 / 919 MEDLINE  
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[PMID]:28413002
[Au] Autor:Zhang S; Lv Z; Zhang S; Liu L; Li Q; Gong W; Sha H; Wu H
[Ad] Endereço:Department of Spine Surgery, The 1st Hospital of Jilin University, Changchun 130021, China.
[Ti] Título:Characterization of human induced pluripotent stem cell (iPSC) line from a 72year old male patient with later onset Alzheimer's disease.
[So] Source:Stem Cell Res;19:34-36, 2017 Mar.
[Is] ISSN:1876-7753
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Peripheral blood was collected from a clinically diagnosed 72-year old male patient with later onset Alzheimer's disease. Peripheral blood mononuclear cells (PBMCs) were reprogrammed with the Yamanaka KMOS reprogramming factors using the Sendai-virus reprogramming system. The transgene-free iPSC line showed pluripotency verified by immunofluorescent staining for pluripotency markers, and the iPSC line was able to differentiate into the 3 germ layers in vivo. The iPSC line also showed normal karyotype. This in vitro cellular model will be useful for studying the pathological mechanism of Alzheimer's disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/patologia
Células-Tronco Pluripotentes Induzidas/citologia
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/metabolismo
Diferenciação Celular
Linhagem Celular
Reprogramação Celular
Vetores Genéticos/genética
Vetores Genéticos/metabolismo
Camadas Germinativas/citologia
Camadas Germinativas/metabolismo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Cariótipo
Masculino
Microscopia de Fluorescência
Vírus Sendai/genética
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transcription Factors)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE


  10 / 919 MEDLINE  
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[PMID]:28413001
[Au] Autor:Zhang S; Lv Z; Liu Y; Li Q; Gong W; Liu L; Wu H
[Ad] Endereço:Department of Spine Surgery, The 1st Hospital of Jilin University, Changchun 130021, China.
[Ti] Título:Development of human induced pluripotent stem cell (iPSC) line from a 60year old female patient with multiple schwannoma.
[So] Source:Stem Cell Res;19:31-33, 2017 Mar.
[Is] ISSN:1876-7753
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Peripheral blood was collected from a clinically diagnosed 60-year old female patient with multiple schwannoma. Peripheral blood mononuclear cells (PBMCs) were reprogrammed with the Yamanaka KMOS reprogramming factors using the Sendai-virus reprogramming system. The transgene-free iPSC line showed pluripotency verified by immunofluorescent staining for pluripotency markers, and the iPSC line was able to differentiate into the 3 germ layers in vivo. The iPSC line also showed normal karyotype. This in vitro cellular model will be useful for further pathological studies of multiple schwannoma.
[Mh] Termos MeSH primário: Células-Tronco Pluripotentes Induzidas/citologia
Neurilemoma/patologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Linhagem Celular
Reprogramação Celular
Feminino
Vetores Genéticos/genética
Vetores Genéticos/metabolismo
Camadas Germinativas/citologia
Camadas Germinativas/metabolismo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Cariótipo
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/metabolismo
Microscopia de Fluorescência
Meia-Idade
Neurilemoma/metabolismo
Vírus Sendai/genética
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transcription Factors)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE



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