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Pesquisa : D12.776.260.755.199 [Categoria DeCS]
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  1 / 3255 MEDLINE  
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[PMID]:29262359
[Au] Autor:Hamsanathan S; Anthonymuthu TS; Bageshwar UK; Musser SM
[Ad] Endereço:Department of Molecular and Cellular Medicine, College of Medicine, The Texas A&M Health Science Center, Texas A&M University, College Station, Texas.
[Ti] Título:A Hinged Signal Peptide Hairpin Enables Tat-Dependent Protein Translocation.
[So] Source:Biophys J;113(12):2650-2668, 2017 Dec 19.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Tat machinery catalyzes the transport of folded proteins across the bacterial cytoplasmic membrane and the thylakoid membrane in plants. Using fluorescence quenching and cross-linking approaches, we demonstrate that the Escherichia coli TatBC complex catalyzes insertion of a pre-SufI signal peptide hairpin that penetrates about halfway across the membrane bilayer. Analysis of 512 bacterial Tat signal peptides using secondary structure prediction and docking algorithms suggest that this hairpin interaction mode is generally conserved. An internal cross-link in the signal peptide that blocks transport but does not affect binding indicates that a signal peptide conformational change is required during translocation. These results suggest, to our knowledge, a novel hairpin-hinge model in which the signal peptide hairpin unhinges during movement of the mature domain across the membrane. Thus, in addition to enabling the necessary recognition, the interaction of Tat signal peptides with the receptor complex plays a critical role in the transport process itself.
[Mh] Termos MeSH primário: Produtos do Gene tat/química
Produtos do Gene tat/metabolismo
Sinais Direcionadores de Proteínas
[Mh] Termos MeSH secundário: Bicamadas Lipídicas/metabolismo
Modelos Moleculares
Conformação Proteica
Transporte Proteico
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tat); 0 (Lipid Bilayers); 0 (Protein Sorting Signals); 059QF0KO0R (Water)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


  2 / 3255 MEDLINE  
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[PMID]:28968466
[Au] Autor:Sánchez-Del Cojo M; López-Huertas MR; Díez-Fuertes F; Rodríguez-Mora S; Bermejo M; López-Campos G; Mateos E; Jiménez-Tormo L; Gómez-Esquer F; Díaz-Gil G; Alcamí J; Coiras M
[Ad] Endereço:AIDS Immunopathology Unit, National Center of Microbiology, Instituto de Salud Carlos III, Madrid, Spain.
[Ti] Título:Changes in the cellular microRNA profile by the intracellular expression of HIV-1 Tat regulator: A potential mechanism for resistance to apoptosis and impaired proliferation in HIV-1 infected CD4+ T cells.
[So] Source:PLoS One;12(10):e0185677, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HIV-1 induces changes in the miRNA expression profile of infected CD4+ T cells that could improve viral replication. HIV-1 regulator Tat modifies the cellular gene expression and has been appointed as an RNA silencing suppressor. Tat is a 101-residue protein codified by two exons that regulates the elongation of viral transcripts. The first exon of Tat (amino acids 1-72) forms the transcriptionally active protein Tat72, but the presence of the second exon (amino acids 73-101) results in a more competent regulatory protein (Tat101) with additional functions. Intracellular, full-length Tat101 induces functional and morphological changes in CD4+ T cells that contribute to HIV-1 pathogenesis such as delay in T-cell proliferation and protection against FasL-mediated apoptosis. But the precise mechanism by which Tat produces these changes remains unknown. We analyzed how the stable expression of intracellular Tat101 and Tat72 modified the miRNA expression profile in Jurkat cells and if this correlated with changes in apoptotic pathways and cell cycle observed in Tat-expressing cells. Specifically, the enhanced expression of hsa-miR-21 and hsa-miR-222 in Jurkat-Tat101 cells was associated with the reduced expression of target mRNAs encoding proteins related to apoptosis and cell cycle such as PTEN, PDCD4 and CDKN1B. We developed Jurkat cells with stable expression of hsa-miR-21 or hsa-miR-222 and observed a similar pattern to Jurkat-Tat101 in resistance to FasL-mediated apoptosis, cell cycle arrest in G2/M and altered cell morphology. Consequently, upregulation of hsa-miR-21 and hsa-miR-222 by Tat may contribute to protect against apoptosis and to anergy observed in HIV-infected CD4+ T cells.
[Mh] Termos MeSH primário: Apoptose
Linfócitos T CD4-Positivos/virologia
Proliferação Celular
Produtos do Gene tat/metabolismo
HIV-1/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Linfócitos T CD4-Positivos/citologia
Perfilação da Expressão Gênica
Vetores Genéticos
HIV-1/fisiologia
Seres Humanos
Células Jurkat
MicroRNAs/genética
Análise de Sequência com Séries de Oligonucleotídeos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tat); 0 (MIRN21 microRNA, human); 0 (MIRN222 microRNA, human); 0 (MicroRNAs)
[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:171003
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185677


  3 / 3255 MEDLINE  
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[PMID]:28842980
[Au] Autor:Browning DF; Richards KL; Peswani AR; Roobol J; Busby SJW; Robinson C
[Ad] Endereço:Institute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham, UK.
[Ti] Título:Escherichia coli "TatExpress" strains super-secrete human growth hormone into the bacterial periplasm by the Tat pathway.
[So] Source:Biotechnol Bioeng;114(12):2828-2836, 2017 Dec.
[Is] ISSN:1097-0290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Numerous high-value proteins are secreted into the Escherichia coli periplasm by the General Secretory (Sec) pathway, but Sec-based production chassis cannot handle many potential target proteins. The Tat pathway offers a promising alternative because it transports fully folded proteins; however, yields have been too low for commercial use. To facilitate Tat export, we have engineered the TatExpress series of super-secreting strains by introducing the strong inducible bacterial promoter, ptac, upstream of the chromosomal tatABCD operon, to drive its expression in E. coli strains commonly used by industry (e.g., W3110 and BL21). This modification significantly improves the Tat-dependent secretion of human growth hormone (hGH) into the bacterial periplasm, to the extent that secreted hGH is the dominant periplasmic protein after only 1 hr induction. TatExpress strains accumulate in excess of 30 mg L periplasmic recombinant hGH, even in shake flask cultures. A second target protein, an scFv, is also shown to be exported at much higher rates in TatExpress strains.
[Mh] Termos MeSH primário: Escherichia coli/genética
Escherichia coli/metabolismo
Produtos do Gene tat/genética
Melhoramento Genético/métodos
Hormônio do Crescimento/biossíntese
Periplasma/metabolismo
Via Secretória/genética
[Mh] Termos MeSH secundário: Hormônio do Crescimento/genética
Hormônio do Crescimento/isolamento & purificação
Seres Humanos
Redes e Vias Metabólicas/genética
Regiões Promotoras Genéticas/genética
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/genética
Proteínas Recombinantes/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tat); 0 (Recombinant Proteins); 9002-72-6 (Growth Hormone)
[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:170827
[St] Status:MEDLINE
[do] DOI:10.1002/bit.26434


  4 / 3255 MEDLINE  
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[PMID]:28796791
[Au] Autor:Wexler C; Cheng AL; Gautney B; Finocchario-Kessler S; Goggin K; Khamadi S; HITSystem Team
[Ad] Endereço:University of Kansas Medical Center, Department of Family Medicine, Kansas City, Kansas, United States of America.
[Ti] Título:Evaluating turnaround times for early infant diagnosis samples in Kenya from 2011-2014: A retrospective analysis of HITSystem program data.
[So] Source:PLoS One;12(8):e0181005, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long turnaround times (TAT) for the processing and posting of results of infant HIV DNA PCR samples can hinder the success of early infant diagnosis (EID) programs. The HITSystem is an eHealth intervention that alerts staff when services are overdue or results are delayed. We conducted a retrospective analysis of 3669 HIV-exposed infants enrolled in 15 Kenya hospital EID programs and three laboratories using the HITSystem from 2011-2014. We assessed mean and median TAT from when a sample was: 1) obtained to when it was shipped to the laboratory, 2) shipped to when it was received at the laboratory, 3) received to when a result was posted, and 4) the total time from obtaining the sample (step 1) to posting the result (step 3). TAT were compared by laboratory, clinic, year, and month of sample collection. 3625 infant samples had results posted by end of 2014. Mean TAT from sample collection to shipping was 5.2 days, from shipping to laboratory receipt was 2.0 days, and from laboratory receipt to result posting was 17.4 days. Altogether, it took an average of 24.7 days from sample collection until result posting. There was significant variation between laboratories, particularly in laboratory processing times (step 3). TAT showed a decreasing trend from 2011-2014, although TAT in December remained higher. Compared with other Kenyan studies, TAT in these HITSystem enrolled settings were shorter. Significant variation between laboratories, however, indicates the need to strengthen protocols and infrastructure to ensure that all laboratories can provide rapid, high-quality services.
[Mh] Termos MeSH primário: Infecções por HIV/diagnóstico
HIV/isolamento & purificação
Doenças do Recém-Nascido/diagnóstico
[Mh] Termos MeSH secundário: Diagnóstico Precoce
Produtos do Gene tat/análise
Infecções por HIV/epidemiologia
Infecções por HIV/virologia
Seres Humanos
Lactente
Recém-Nascido
Doenças do Recém-Nascido/epidemiologia
Doenças do Recém-Nascido/virologia
Quênia/epidemiologia
Laboratórios/economia
Estudos Retrospectivos
Manejo de Espécimes/economia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tat)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181005


  5 / 3255 MEDLINE  
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[PMID]:28699375
[Au] Autor:Wu G; Su P; Wang B; Zhang Y; Qian G; Liu F
[Ad] Endereço:All authors: Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, Nanjing 210095, China/Key Laboratory of Integrated Management of Crop Diseases and Pests (Nanjing Agricultural University), Ministry of Education, P.R. China; and sixth author: Institute of Plan
[Ti] Título:Novel Insights into Tat Pathway in Xanthomonas oryzae pv. oryzae Stress Adaption and Virulence: Identification and Characterization of Tat-Dependent Translocation Proteins.
[So] Source:Phytopathology;107(9):1011-1021, 2017 09.
[Is] ISSN:0031-949X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Xanthomonas oryzae pv. oryzae, an economically important bacterium, causes a serious disease in rice production worldwide called bacterial leaf blight. How X. oryzae pv. oryzae infects rice and causes symptoms remains incompletely understood. Our earlier works demonstrated that the twin-arginine translocation (Tat) pathway plays an vital role in X. oryzae pv. oryzae fitness and virulence but the underlying mechanism is unknown. In this study, we used strain PXO99 as a working model, and identified 15 potential Tat-dependent translocation proteins (TDTP) by using comparative proteomics and bioinformatics analyses. Combining systematic mutagenesis, phenotypic characterization, and gene expression, we found that multiple TDTP play key roles in X. oryzae pv. oryzae adaption or virulence. In particular, four TDTP (PXO_02203, PXO_03477, PXO_02523, and PXO_02951) were involved in virulence, three TDTP (PXO_02203, PXO_03477, and PXO_02523) contributed to colonization in planta, one TDTP (PXO_02671) had a key role in attachment to leaf surface, four TDTP (PXO_02523, PXO_02951, PXO_03132, and PXO_03841) were involved in tolerance to multiple stresses, and two TDTP (PXO_02523 and PXO_02671) were required for full swarming motility. These findings suggest that multiple TDTP may have differential contributions to involvement of the Tat pathway in X. oryzae pv. oryzae adaption, physiology, and pathogenicity.
[Mh] Termos MeSH primário: Adaptação Fisiológica/fisiologia
Proteínas de Bactérias/metabolismo
Estresse Fisiológico/fisiologia
Xanthomonas/metabolismo
Xanthomonas/patogenicidade
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Regulação Bacteriana da Expressão Gênica
Produtos do Gene tat/genética
Produtos do Gene tat/metabolismo
Movimento
Oryza/microbiologia
Doenças das Plantas
Transporte Proteico
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Gene Products, tat)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1094/PHYTO-02-17-0053-R


  6 / 3255 MEDLINE  
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[PMID]:28279738
[Au] Autor:Mesken J; Iltzsche A; Mulac D; Langer K
[Ad] Endereço:Institute of Pharmaceutical Technology and Biopharmacy, University of Münster, Corrensstraße 48, 48149 Münster, Germany.
[Ti] Título:Modifying plasmid-loaded HSA-nanoparticles with cell penetrating peptides - Cellular uptake and enhanced gene delivery.
[So] Source:Int J Pharm;522(1-2):198-209, 2017 Apr 30.
[Is] ISSN:1873-3476
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Gene therapy bears great potential for the cure of a multitude of human diseases. Research efforts focussed on the use of viral delivery vectors in the past decades, neglecting non-viral gene therapies of physical or chemical origin due to low transfection efficiency. However, side effects such as activation of oncogenes and inflammatory reactions upon immune cell activation are major obstacles impeding the clinical applicability of viral gene therapy vectors. The aim of this study was the development of a non-viral gene delivery system based on plasmid-loaded human serum albumin nanoparticles, which are biocompatible, biodegradable, and non-toxic in relevant concentrations. The surface of said nanoparticles was modified with different cell penetrating peptides, namely Tat, nona-arginine R9, and the penetratin analogue EB1. We hypothesise that the surface modified nanoparticles can effectively enter HEK 293T cells based on the cell penetrating properties of the different peptides attached. A variety of inhibitors were used targeting distinct uptake pathways in an effort to understand the mechanisms utilized by the various cell penetrating peptides on the surface of the nanoparticles. A significant increase in transfection efficiency compared to free DNA or polyplexes was seen for these novel delivery vectors.
[Mh] Termos MeSH primário: Peptídeos Penetradores de Células/administração & dosagem
Peptídeos Penetradores de Células/química
Técnicas de Transferência de Genes
Terapia Genética/métodos
Nanopartículas/química
Plasmídeos/química
Albumina Sérica/química
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
DNA/administração & dosagem
DNA/química
Excipientes
Produtos do Gene tat/química
Células HEK293
Seres Humanos
Albumina Sérica/antagonistas & inibidores
Albumina Sérica/toxicidade
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell-Penetrating Peptides); 0 (Excipients); 0 (Gene Products, tat); 0 (Serum Albumin); 9007-49-2 (DNA)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE


  7 / 3255 MEDLINE  
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[PMID]:28198575
[Au] Autor:Lee SJ; Kang HK; Eum WS; Park J; Choi SY; Kwon HY
[Ad] Endereço:Department of Physiology, College of Medicine, Hallym University, Chuncheon , 24252, Republic of Korea.
[Ti] Título:Tat-biliverdin reductase A protects INS-1 cells from human islet amyloid polypeptide-induced cytotoxicity by alleviating oxidative stress and ER stress.
[So] Source:Cell Biol Int;41(5):514-524, 2017 May.
[Is] ISSN:1095-8355
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human islet amyloid polypeptide (hIAPP), a major constituent of islet amyloid deposits, induces pancreatic ß-cell apoptosis and eventually contributes to ß-cell deficit in patients with type 2 diabetes mellitus (T2DM). In this study, Tat-mediated transduction of biliverdin reductase A (BLVRA) was investigated in INS-1 cells to examine whether exogenous supplementation of BLVRA prevented hIAPP-induced apoptosis and dysfunction in insulin secretion in ß-cells. Tat-BLVRA fusion protein was efficiently delivered into INS-1 cells in a time- and dose-dependent manner. Exposure of cells to hIAPP induced apoptotic cell death, which was dose-dependently inhibited by pre-treatment with Tat-BLVRA for 1 h. Transduced Tat-BLVRA reduced hIAPP-evoked generation of reactive oxygen species, a crucial mediator of ß-cell destruction. Immunoblot analysis showed that Tat-BLVRA suppressed hIAPP-induced increase in the levels of proteins involved in endoplasmic reticulum (ER) stress and apoptosis signaling. Transduced Tat-BLVRA also recovered hIAPP-induced dysfunction in basal and glucose-stimulated insulin secretions. These results suggested that transduced Tat-BLVRA enhanced the tolerance of ß-cells against IAPP-induced cytotoxicity by alleviating oxidative stress and ER stress. Therefore, Tat-mediated transduction of BLVRA may provide a potential tool to ameliorate ß-cell deficit in pancreas with T2DM.
[Mh] Termos MeSH primário: Estresse do Retículo Endoplasmático/efeitos dos fármacos
Produtos do Gene tat/metabolismo
Polipeptídeo Amiloide das Ilhotas Pancreáticas/toxicidade
Estresse Oxidativo/efeitos dos fármacos
Oxirredutases atuantes sobre Doadores de Grupo CH-CH/metabolismo
Substâncias Protetoras/farmacologia
Proteínas Recombinantes de Fusão/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Seres Humanos
Insulina/secreção
Ratos
Espécies Reativas de Oxigênio/metabolismo
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tat); 0 (Insulin); 0 (Islet Amyloid Polypeptide); 0 (Protective Agents); 0 (Reactive Oxygen Species); 0 (Recombinant Fusion Proteins); EC 1.3.- (Oxidoreductases Acting on CH-CH Group Donors); EC 1.3.1.24 (biliverdin reductase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE
[do] DOI:10.1002/cbin.10750


  8 / 3255 MEDLINE  
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[PMID]:28153495
[Au] Autor:Chen X; Liu S; Deme B; Cristiglio V; Marquardt D; Weller R; Rao P; Wang Y; Bradshaw J
[Ad] Endereço:College of Biological Science and Biotechnology, Fuzhou University, 2 Xue Yuan Road, University Town, 350116 Fuzhou, Fujian, PR China.; The University of Edinburgh, Medical Research Council Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh EH16
[Ti] Título:Efficient internalization of TAT peptide in zwitterionic DOPC phospholipid membrane revealed by neutron diffraction.
[So] Source:Biochim Biophys Acta;1859(5):910-916, 2017 05.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The aim of this study is to investigate the interactions between TAT peptides and a neutral DOPC bilayer by using neutron lamellar diffraction. The distribution of TAT peptides and the perturbation of water distribution across the DOPC bilayer were revealed. When compared to our previous study on an anionic DOPC/DOPS bilayer (X. Chen et al., Biochim Biophys Acta. 2013. 1828 (8), 1982-1988), a much deeper insertion of TAT peptides was found in the hydrophobic core of DOPC bilayer at a depth of 6.0Å from the center of the bilayer, a position close to the double bond of fatty acyl chain. We conclude that the electrostatic attractions between the positively charged TAT peptides and the negatively charged headgroups of phospholipid are not essential for the direct translocation. Furthermore, the interactions of TAT peptides with the DOPC bilayer were found to vary in a concentration-dependent manner. A limited number of peptides first associate with the phosphate moieties on the lipid headgroups by using the guanidinium ions pairing. Then the energetically favorable water defect structures are adopted to maintain the arginine residues hydrated by drawing water molecules and lipid headgroups into the bilayer core. Such bilayer deformations consequently lead to the deep intercalation of TAT peptides into the bilayer core. Once a threshold concentration of TAT peptide in the bilayer is reached, a significant rearrangement of bilayer will happen and steady-state water pores will form.
[Mh] Termos MeSH primário: Produtos do Gene tat/química
Bicamadas Lipídicas/química
Difração de Nêutrons/métodos
Fosfatidilcolinas/química
[Mh] Termos MeSH secundário: Interações Hidrofóbicas e Hidrofílicas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gene Products, tat); 0 (Lipid Bilayers); 0 (Phosphatidylcholines); EDS2L3ODLV (1,2-oleoylphosphatidylcholine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE


  9 / 3255 MEDLINE  
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[PMID]:28052764
[Au] Autor:Jo HS; Kim DW; Shin MJ; Cho SB; Park JH; Lee CH; Yeo EJ; Choi YJ; Yeo HJ; Sohn EJ; Son O; Cho SW; Kim DS; Yu YH; Lee KW; Park J; Eum WS; Choi SY
[Ad] Endereço:Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, 24252, Korea.
[Ti] Título:Tat-HSP22 inhibits oxidative stress-induced hippocampal neuronal cell death by regulation of the mitochondrial pathway.
[So] Source:Mol Brain;10(1):1, 2017 01 04.
[Is] ISSN:1756-6606
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Oxidative stress plays an important role in the progression of various neuronal diseases including ischemia. Heat shock protein 22 (HSP22) is known to protect cells against oxidative stress. However, the protective effects and mechanisms of HSP22 in hippocampal neuronal cells under oxidative stress remain unknown. In this study, we determined whether HSP22 protects against hydrogen peroxide (H O )-induced oxidative stress in HT-22 using Tat-HSP22 fusion protein. We found that Tat-HSP22 transduced into HT-22 cells and that H O -induced cell death, oxidative stress, and DNA damage were significantly reduced by Tat-HSP22. In addition, Tat-HSP22 markedly inhibited H O -induced mitochondrial membrane potential, cytochrome c release, cleaved caspase-3, and Bax expression levels, while Bcl-2 expression levels were increased in HT-22 cells. Further, we showed that Tat-HSP22 transduced into animal brain and inhibited cleaved-caspase-3 expression levels as well as significantly inhibited hippocampal neuronal cell death in the CA1 region of animals in the ischemic animal model. In the present study, we demonstrated that transduced Tat-HSP22 attenuates oxidative stress-induced hippocampal neuronal cell death through the mitochondrial signaling pathway and plays a crucial role in inhibiting neuronal cell death, suggesting that Tat-HSP22 protein may be used to prevent oxidative stress-related brain diseases including ischemia.
[Mh] Termos MeSH primário: Produtos do Gene tat/farmacologia
Proteínas de Choque Térmico/farmacologia
Hipocampo/patologia
Mitocôndrias/metabolismo
Neurônios/patologia
Estresse Oxidativo/efeitos dos fármacos
Proteínas Serina-Treonina Quinases/farmacologia
Proteínas Recombinantes de Fusão/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Morte Celular/efeitos dos fármacos
Permeabilidade da Membrana Celular/efeitos dos fármacos
Gerbillinae
Peróxido de Hidrogênio/farmacologia
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Fármacos Neuroprotetores/farmacologia
Proteínas Recombinantes de Fusão/isolamento & purificação
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gene Products, tat); 0 (Heat-Shock Proteins); 0 (Neuroprotective Agents); 0 (Recombinant Fusion Proteins); BBX060AN9V (Hydrogen Peroxide); EC 2.7.1.- (HSPB8 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE
[do] DOI:10.1186/s13041-016-0281-8


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[PMID]:27797603
[Au] Autor:Rice AP
[Ad] Endereço:a Department of Molecular Virology and Microbiology , Baylor College of Medicine , Houston , TX USA.
[Ti] Título:Cyclin-dependent kinases as therapeutic targets for HIV-1 infection.
[So] Source:Expert Opin Ther Targets;20(12):1453-1461, 2016 Dec.
[Is] ISSN:1744-7631
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: A number of cyclin-dependent kinases (CDKs) mediate key steps in the HIV-1 replication cycle and therefore have potential to serve as therapeutic targets for HIV-1 infection, especially in HIV-1 cure strategies. Current HIV-1 cure strategies involve the development of small molecules that are able to activate HIV-1 from latent infection, thereby allowing the immune system to recognize and clear infected cells. Areas covered: The role of seven CDK family members in the HIV-1 replication cycle is reviewed, with a focus on CDK9, as the mechanism whereby the viral Tat protein utilizes CDK9 to enhance viral replication is known in considerable detail. Expert opinion: Given the essential roles of CDKs in cellular proliferation and gene expression, small molecules that inhibit CDKs are unlikely to be feasible therapeutics for HIV-1 infection. However, small molecules that activate CDK9 and other select CDKs such as CDK11 have potential to reactivate latent HIV-1 and contribute to a functional cure of infection.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/farmacologia
Quinases Ciclina-Dependentes/metabolismo
Infecções por HIV/tratamento farmacológico
[Mh] Termos MeSH secundário: Quinase 9 Dependente de Ciclina/metabolismo
Produtos do Gene tat/metabolismo
Infecções por HIV/enzimologia
Infecções por HIV/virologia
HIV-1/enzimologia
Seres Humanos
Terapia de Alvo Molecular
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Gene Products, tat); EC 2.7.11.22 (Cyclin-Dependent Kinase 9); EC 2.7.11.22 (Cyclin-Dependent Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170529
[Lr] Data última revisão:
170529
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE



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