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Pesquisa : D08.811.277.352.355.350.715 [Categoria DeCS]
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[PMID]:29258713
[Au] Autor:Kayet A; Datta D; Das A; Dasgupta S; Pathak T
[Ad] Endereço:Department of Chemistry, IIT Kharagpur, Kharagpur 721302, India.
[Ti] Título:1,5-Disubstituted 1,2,3-triazole linked disaccharides: Metal-free syntheses and screening of a new class of ribonuclease A inhibitors.
[So] Source:Bioorg Med Chem;26(2):455-462, 2018 01 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1,5-Regioisomeric triazole linked disaccharides have been synthesized and screened for their inhibitory properties against ribonuclease A (RNase A). The angular constraint-driven 'crescent shaped' inhibitors accommodated themselves into the enzyme active site. An improved enzyme inhibition was observed with increased H-bonding ability of polar functional groups in the modified disaccharides. In this series, introduction of two carboxyl groups in the furanose rings elicited the best result with an inhibition constant of 50 ±â€¯3 µM. This is the first ever report on the use of disaccharides as RNase A inhibitors.
[Mh] Termos MeSH primário: Dissacarídeos/farmacologia
Inibidores Enzimáticos/farmacologia
Ribonuclease Pancreático/antagonistas & inibidores
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Dissacarídeos/química
Relação Dose-Resposta a Droga
Avaliação Pré-Clínica de Medicamentos
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Seres Humanos
Estrutura Molecular
Ribonuclease Pancreático/metabolismo
Relação Estrutura-Atividade
Triazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Disaccharides); 0 (Enzyme Inhibitors); 0 (Triazoles); EC 3.1.27.5 (Ribonuclease, Pancreatic)
[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


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[PMID]:28457141
[Au] Autor:Liu X; Zhang P; Rödl W; Maier K; Lächelt U; Wagner E
[Ad] Endereço:Pharmaceutical Biotechnology, Center for System-based Drug Research and Center for NanoScience (CeNS), Ludwig-Maximilians-Universität München , Butenandtstrasse 5-13, D-81377 Munich, Germany.
[Ti] Título:Toward Artificial Immunotoxins: Traceless Reversible Conjugation of RNase A with Receptor Targeting and Endosomal Escape Domains.
[So] Source:Mol Pharm;14(5):1439-1449, 2017 May 01.
[Is] ISSN:1543-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The specific transport of bioactive proteins into designated target cells is an interesting and challenging perspective for the generation of innovative biopharmaceuticals. Natural protein cytotoxins perform this task with outstanding efficacy. They enter cells with receptor-targeted specificity, respond to changing intracellular microenvironments, and by various mechanisms translocate their cytotoxic protein subunit into the cytosol. Here we imitate this toxin-based delivery strategy in an artificial setting, by bioreversible conjugation of a cytotoxic cargo protein (RNase A) with receptor-targeting PEG-folate and the pH-specific endosomolytic peptide INF7 as synthetic delivery domains. Covalent modification of the cargo protein was achieved using the pH-labile AzMMMan linker and copper-free click chemistry with DBCO-modified delivery modules. This linkage is supposed to enable traceless intracellular release of the RNase A after exposure to the endosomal weakly acidic environment. Delivery of RNase A via this polycation-free delivery strategy resulted in high cytotoxicity against receptor-positive KB tumor cells only when both PEG-folate and INF7 were attached.
[Mh] Termos MeSH primário: Química Click/métodos
Endossomos/metabolismo
Imunotoxinas/química
Ribonuclease Pancreático/química
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Eletroforese em Gel de Poliacrilamida
Ácido Fólico/análogos & derivados
Ácido Fólico/química
Seres Humanos
Concentração de Íons de Hidrogênio
Imunotoxinas/metabolismo
Modelos Biológicos
Peptídeos/química
Polietilenoglicóis/química
Ribonuclease Pancreático/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (INF7 peptide); 0 (Immunotoxins); 0 (Peptides); 0 (poly(ethylene glycol)-folate); 30IQX730WE (Polyethylene Glycols); 935E97BOY8 (Folic Acid); EC 3.1.27.5 (Ribonuclease, Pancreatic)
[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:170502
[St] Status:MEDLINE
[do] DOI:10.1021/acs.molpharmaceut.6b00701


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[PMID]:29190616
[Au] Autor:Jin Z; Cheng X; Feng H; Kuang J; Yang W; Peng C; Shen B; Qiu W
[Ad] Endereço:Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
[Ti] Título:Apatinib Inhibits Angiogenesis Via Suppressing Akt/GSK3ß/ANG Signaling Pathway in Anaplastic Thyroid Cancer.
[So] Source:Cell Physiol Biochem;44(4):1471-1484, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Anaplastic thyroid carcinoma (ATC) is one of the most lethal human malignancies, and there is no efficient method to slow its process. Apatinib, a novel tyrosine kinase inhibitor (TKI), has been confirmed for its efficacy and safety in the treatment of advanced gastric carcinoma patients. However, the effects of Apatinib in ATC are still unknown. METHODS: In this study, we explored the effects and mechanisms of Apatinib on tumor growth and angiogenesis in vitro and in vitro in ATC cells. Angiogenesis antibodies array was utilized to detect the expression of angiogenesis-related genes after Apatinib treatment in ATC cells. In addition, we used Akt activator, Akt inhibitor and GSK3ß inhibitor to further study the mechanism for how Apatinib suppressed angiogenesis. RESULTS: Apatinib treatment could suppress the growth of ATC cells in a dose- and time-dependent manner via inducing apoptosis and blocking cell cycle progression at G0/G1 phase. Moreover, Apatinib treatment decreased the expression of angiogenin (ANG) and inhibited angiogenesis of ATC cells in vitro and in vitro. We further confirmed that recombinant human ANG (rhANG) significantly abrogated Apatinib-mediated anti-angiogenic ability in ATC cells. Additionally, Apatinib treatment decreased the level of p-Akt and p-GSK3ß. Moreover, the Apatinib-mediated decrease of ANG and anti-angiogenic ability were partly reversed when an Akt activator, SC79, was administered. Furthermore, the anti-angiogenic ability of Apatinib can be enhanced in the presence of Akt inhibitor, and the inhibition of GSK3ß attenuated the anti-angiogenic ability of Apatinib. CONCLUSION: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3ß/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.
[Mh] Termos MeSH primário: Antineoplásicos/toxicidade
Neovascularização Fisiológica/efeitos dos fármacos
Piridinas/toxicidade
Transdução de Sinais/efeitos dos fármacos
Carcinoma Anaplásico da Tireoide/patologia
Neoplasias da Glândula Tireoide/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Glicogênio Sintase Quinase 3 beta/antagonistas & inibidores
Glicogênio Sintase Quinase 3 beta/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/genética
Proteínas Recombinantes/farmacologia
Ribonuclease Pancreático/genética
Ribonuclease Pancreático/metabolismo
Carcinoma Anaplásico da Tireoide/metabolismo
Neoplasias da Glândula Tireoide/metabolismo
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Pyridines); 0 (Recombinant Proteins); 5S371K6132 (apatinib); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.27.- (angiogenin); EC 3.1.27.5 (Ribonuclease, Pancreatic)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1159/000485583


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[PMID]:29223155
[Au] Autor:Grunina TM; Demidenko AV; Lyaschuk AM; Poponova MS; Galushkina ZM; Soboleva LA; Cherepushkin SA; Polyakov NB; Grumov DA; Solovyev AI; Zhukhovitsky VG; Boksha IS; Subbotina ME; Gromov AV; Lunin VG; Karyagina AS
[Ad] Endereço:Gamaleya National Research Center of Epidemiology and Microbiology, Ministry of Health of the Russian Federation, Moscow, 123098, Russia. alexander.v.gromov@gmail.com.
[Ti] Título:Recombinant Human Erythropoietin with Additional Processable Protein Domains: Purification of Protein Synthesized in Escherichia coli Heterologous Expression System.
[So] Source:Biochemistry (Mosc);82(11):1285-1294, 2017 Nov.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Three variants of human recombinant erythropoietin (rhEPO) with additional N-terminal protein domains were obtained by synthesis in an Escherichia coli heterologous expression system. These domains included (i) maltose-binding protein (MBP), (ii) MBP with six histidine residues (6His) in N-terminal position, (iii) s-tag (15-a.a. oligopeptide derived from bovine pancreatic ribonuclease A) with N-terminal 6His. Both variants of the chimeric protein containing MBP domain were prone to aggregation under nondenaturing conditions, and further purification of EPO after the domain cleavage by enterokinase proved to be impossible. In the case of 6His-s-tag-EPO chimeric protein, the products obtained after cleavage with enterokinase were successfully separated by column chromatography, and rhEPO without additional domains was obtained. Results of MALDI-TOF mass spectrometry showed that after refolding 6His-s-tag-EPO formed a structure similar to that of one of native EPO with two disulfide bonds. Both 6His-s-tag-EPO and rhEPO without additional protein domains purified after proteolysis possessed the same biological activity in vitro in the cell culture.
[Mh] Termos MeSH primário: Eritropoetina/biossíntese
Eritropoetina/isolamento & purificação
Escherichia coli/metabolismo
Proteínas Recombinantes de Fusão/biossíntese
[Mh] Termos MeSH secundário: Cromatografia
Enteropeptidase/metabolismo
Eritropoetina/genética
Escherichia coli/genética
Expressão Gênica
Histidina
Seres Humanos
Proteínas Ligantes de Maltose/química
Proteínas Ligantes de Maltose/genética
Oligopeptídeos
Fragmentos de Peptídeos
Conformação Proteica
Domínios Proteicos
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/isolamento & purificação
Ribonuclease Pancreático/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EPO protein, human); 0 (His-His-His-His-His-His); 0 (Maltose-Binding Proteins); 0 (Oligopeptides); 0 (Peptide Fragments); 0 (Recombinant Fusion Proteins); 11096-26-7 (Erythropoietin); 4QD397987E (Histidine); EC 3.1.27.5 (Ribonuclease, Pancreatic); EC 3.4.21.9 (Enteropeptidase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917110062


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[PMID]:29042175
[Au] Autor:Trujillo V; Marín-Luevano P; González-Curiel I; Rodríguez-Carlos A; Ramírez-Reyes M; Layseca-Espinosa E; Enciso-Moreno JA; Díaz L; Rivas-Santiago B
[Ad] Endereço:Unidad de Investigación Biomédica-Zacatecas, IMSS, Mexico; Centro de Investigacion en Ciencias de la Salud y Biomedicina, Facultad de Medicina, Universidad Autónoma de San Luis Potosi, Mexico.
[Ti] Título:Calcitriol promotes proangiogenic molecules in keratinocytes in a diabetic foot ulcer model.
[So] Source:J Steroid Biochem Mol Biol;174:303-311, 2017 Nov.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Foot ulceration is one of the most common and complex sequelae of diabetes mellitus, generally posing a therapeutic challenge due to poor healing responses and high rates of complications, including peripheral vascular disease, ischemia and infections. Calcitriol, the most active vitamin D metabolite, induces antimicrobial peptides production in keratinocytes from diabetic foot ulcers (DFU); however, little is known about its effects on angiogenic factors in this pathology. Herein we aimed at studying whether calcitriol induces angiogenic molecules in keratinocytes under normoxic and hypoxic conditions, and if these molecules are able to improve cell migration in vitro. Evaluation of DFU samples by immunohistochemistry showed increased VEGF and decreased angiogenin and HIF-1α expression compared to controls, suggesting an altered pattern of angiogenic factors in DFU. Interestingly, incubation of keratinocytes with calcitriol significantly upregulated VEGFA, HIF-1α and angiogenin gene expression, while the resulting cell culture media stimulated both endothelial cells and keratinocytes migration in an in vitro wound closure assay under a normoxic environment (p<0.05). Moreover, the culture media of calcitriol-treated keratinocytes stimulated cell migration in a similar extent as exogenous VEGF or EGF in endothelial and keratinocytes cells. These results suggest that the altered profile of angiogenic molecules in DFU might be improved by local or systemic treatment with calcitriol under normoxic conditions, which could probably be achieved with hyperbaric oxygen therapy. Given that calcitriol not only augments proangiogenic factors but also induces antimicrobial peptides expression, this hormone should be further investigated in clinical trials of DFU.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Pé Diabético/metabolismo
Queratinócitos/efeitos dos fármacos
Vitaminas/farmacologia
[Mh] Termos MeSH secundário: Adulto
Linhagem Celular
Pé Diabético/genética
Feminino
Expressão Gênica
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Queratinócitos/metabolismo
Masculino
Meia-Idade
Neovascularização Fisiológica
Ribonuclease Pancreático/genética
Ribonuclease Pancreático/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
Cicatrização/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (Vitamins); EC 3.1.27.- (angiogenin); EC 3.1.27.5 (Ribonuclease, Pancreatic); FXC9231JVH (Calcitriol)
[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:171019
[St] Status:MEDLINE


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[PMID]:29022711
[Au] Autor:Shimodaira S; Asano Y; Arai K; Iwaoka M
[Ad] Endereço:Department of Chemistry, School of Science, Tokai University , Kitakaname, Hiratsuka-shi, Kanagawa 259-1292, Japan.
[Ti] Título:Selenoglutathione Diselenide: Unique Redox Reactions in the GPx-Like Catalytic Cycle and Repairing of Disulfide Bonds in Scrambled Protein.
[So] Source:Biochemistry;56(42):5644-5653, 2017 Oct 24.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Selenoglutathione (GSeH) is a selenium analogue of naturally abundant glutathione (GSH). In this study, this water-soluble small tripeptide was synthesized in a high yield (up to 98%) as an oxidized diselenide form, i.e., GSeSeG (1), by liquid-phase peptide synthesis (LPPS). Obtained 1 was applied to the investigation of the glutathione peroxidase (GPx)-like catalytic cycle. The important intermediates, i.e., GSe and GSeSG, besides GSeO H were characterized by Se NMR spectroscopy. Thiol exchange of GSeSG with various thiols, such as cysteine and dithiothreitol, was found to promote the conversion to GSe significantly. In addition, disproportionation of GSeSR to 1 and RSSR, which would be initiated by heterolytic cleavage of the Se-S bond and catalyzed by the generated selenolate, was observed. On the basis of these redox behaviors, it was proposed that the heterolytic cleavage of the Se-S bond can be facilitated by the interaction between the Se atom and an amino or aromatic group, which is present at the GPx active site. On the other hand, when a catalytic amount of 1 was reacted with scrambled 4S species of RNase A in the presence of NADPH and glutathione reductase, native protein was efficiently regenerated, suggesting a potential use of 1 to repair misfolded proteins through reduction of the non-native SS bonds.
[Mh] Termos MeSH primário: Dissulfetos/química
Glutationa Peroxidase/química
Glutationa/análogos & derivados
Glutationa/química
Ribonuclease Pancreático/química
Selênio/química
[Mh] Termos MeSH secundário: Glutationa/síntese química
Oxirredução
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Disulfides); EC 1.11.1.9 (Glutathione Peroxidase); EC 3.1.27.5 (Ribonuclease, Pancreatic); GAN16C9B8O (Glutathione); H6241UJ22B (Selenium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00751


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[PMID]:28602978
[Au] Autor:Sui H; Zhao J; Zhou L; Wen H; Deng W; Li C; Ji Q; Liu X; Feng Y; Chai N; Zhang Q; Cai J; Li Q
[Ad] Endereço:Department of Medical Oncology & Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
[Ti] Título:Tanshinone IIA inhibits ß-catenin/VEGF-mediated angiogenesis by targeting TGF-ß1 in normoxic and HIF-1α in hypoxic microenvironments in human colorectal cancer.
[So] Source:Cancer Lett;403:86-97, 2017 Sep 10.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In a previous study, we demonstrated that Tanshinone IIA effectively inhibits CRC angiogenesis in vivo, but the underlying mechanisms were not elucidated. In this report, we describe experiments in which HIF-1α levels were manipulated to probe the effect of hypoxia on CRC cell angiogenesis. We studied the effects of Tan IIA on CRC pro-angiogenic factor and on human umbilical vein endothelial cell angiogenesis in normoxia and hypoxia. Our results show that Tan IIA not only lowers HIF-1α levels and inhibits secretion of VEGF and bFGF, but also efficiently suppresses the proliferation, tube formation and metastasis of HUVECs. Interruption of the HIF-1α/ß-catenin/TCF3/LEF1 signaling pathway occurs in the hypoxic microenvironment. The mechanism involves HIF-1α inhibition of TGF-ß1 secretion, which drives angiogenesis by promoting ß-catenin nuclear localization and TCF/LEF activation. To test an improved delivery system for Tan IIA, we loaded the drug into mesoporous silica nanoparticles (MSN-NH ) and found that it effectively targets HIF-1α overexpression in a mouse colon tumor model. Finally, Tan IIA sodium sulfonate exhibits anti-angiogenesis activity in CRC patients by reducing levels of angiogenin, VEGF and bFGF expression. Our research provides a new anti-angiogenesis strategy and strengthens support for the use of Tan IIA as an angiogenesis inhibitor.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Neoplasias Colorretais/tratamento farmacológico
Diterpenos Abietanos/farmacologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Neovascularização Patológica
Fator de Crescimento Transformador beta1/metabolismo
Hipóxia Tumoral
Microambiente Tumoral
Fator A de Crescimento do Endotélio Vascular/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Embrião de Galinha
Neoplasias Colorretais/irrigação sanguínea
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Relação Dose-Resposta a Droga
Feminino
Fator 2 de Crescimento de Fibroblastos/metabolismo
Células HCT116
Células HT29
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Fator 1 de Ligação ao Facilitador Linfoide/genética
Fator 1 de Ligação ao Facilitador Linfoide/metabolismo
Masculino
Camundongos Nus
Meia-Idade
Neovascularização Fisiológica/efeitos dos fármacos
Ribonuclease Pancreático/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transfecção
Carga Tumoral/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (CTNNB1 protein, human); 0 (Diterpenes, Abietane); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (LEF1 protein, human); 0 (Lymphoid Enhancer-Binding Factor 1); 0 (TCF3 protein, human); 0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (beta Catenin); 03UUH3J385 (tanshinone); 103107-01-3 (Fibroblast Growth Factor 2); EC 3.1.27.- (angiogenin); EC 3.1.27.5 (Ribonuclease, Pancreatic)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE


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[PMID]:28591277
[Au] Autor:Esposito E; Aldrees S; Mastromonaco C; Zoroquiain P; Vila N; Logan PT; Hari S; Burnier MN
[Ad] Endereço:Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, Quebec, Canada.
[Ti] Título:Evaluation of nicotinamide as an anti-inflammatory and anti-angiogenic agent in uveal melanoma cell lines.
[So] Source:Arq Bras Oftalmol;80(2):74-77, 2017 Mar-Apr.
[Is] ISSN:1678-2925
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Purpose:: To investigate the effect of nicotinamide on the secretion of pro-an giogenic and pro-inflammatory cytokines in uveal melanoma cell lines. Methods:: Two human uveal melanoma cell lines (92.1 and OCM-1) were treated with nicotinamide (10 mmol/L) or control media for 48 hours in culture. The su perna tant from each culture was used in sandwich enzyme-linked immuno sorbent assay-based angiogenesis and inflammation arrays to evaluate the effects of exogenously administered nicotinamide on the secretion of a total of 20 pro-an gio genic and pro-inflammatory proteins. Results:: Seven pro-angiogenic cytokines were detected under control conditions for both uveal melanoma cell lines. Treatment with nicotinamide resulted in a significant decrease in secretion of the following pro-angiogenic cytokines: angiogenin, angiopoietin-2, epidermal growth factor, and vascular epithelial growth factor-A in the 92.1 cells; basic fibroblast growth factor in the OCM-1 cells; and placenta growth factor in both cell lines. Among the pro-inflammatory proteins, monocyte chemotactic protein-1 and interleukin-8 were expressed in both untreated cell lines and both were significantly reduced when treated with nicotinamide. Conclusions:: Results from this in vitro model suggest that nicotinamide may have anti-inflammatory and anti-angiogenic properties, which may open the possibility of using it as a chemopreventive agent for uveal melanoma; however, further studies including animal models are warranted.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Anti-Inflamatórios/farmacologia
Citocinas/efeitos dos fármacos
Melanoma/metabolismo
Niacinamida/farmacologia
Neoplasias Uveais/metabolismo
[Mh] Termos MeSH secundário: Angiopoietina-2/metabolismo
Linhagem Celular Tumoral
Quimiocina CCL2/efeitos dos fármacos
Citocinas/metabolismo
Fator de Crescimento Epidérmico/efeitos dos fármacos
Fator 2 de Crescimento de Fibroblastos/efeitos dos fármacos
Seres Humanos
Interleucina-8/efeitos dos fármacos
Melanoma/irrigação sanguínea
Fator de Crescimento Placentário/efeitos dos fármacos
Ribonuclease Pancreático/efeitos dos fármacos
Neoplasias Uveais/irrigação sanguínea
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Angiopoietin-2); 0 (Anti-Inflammatory Agents); 0 (Chemokine CCL2); 0 (Cytokines); 0 (Interleukin-8); 103107-01-3 (Fibroblast Growth Factor 2); 144589-93-5 (Placenta Growth Factor); 25X51I8RD4 (Niacinamide); 62229-50-9 (Epidermal Growth Factor); EC 3.1.27.- (angiogenin); EC 3.1.27.5 (Ribonuclease, Pancreatic)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


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[PMID]:28542243
[Au] Autor:Luitz MP; Barth A; Crevenna AH; Bomblies R; Lamb DC; Zacharias M
[Ad] Endereço:Department Physik, T38, Technische Universität München, 85748 Garching, Germany.
[Ti] Título:Covalent dye attachment influences the dynamics and conformational properties of flexible peptides.
[So] Source:PLoS One;12(5):e0177139, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fluorescence spectroscopy techniques like Förster resonance energy transfer (FRET) and fluorescence correlation spectroscopy (FCS) have become important tools for the in vitro and in vivo investigation of conformational dynamics in biomolecules. These methods rely on the distance-dependent quenching of the fluorescence signal of a donor fluorophore either by a fluorescent acceptor fluorophore (FRET) or a non-fluorescent quencher, as used in FCS with photoinduced electron transfer (PET). The attachment of fluorophores to the molecule of interest can potentially alter the molecular properties and may affect the relevant conformational states and dynamics especially of flexible biomolecules like intrinsically disordered proteins (IDP). Using the intrinsically disordered S-peptide as a model system, we investigate the impact of terminal fluorescence labeling on the molecular properties. We perform extensive molecular dynamics simulations on the labeled and unlabeled peptide and compare the results with in vitro PET-FCS measurements. Experimental and simulated timescales of end-to-end fluctuations were found in excellent agreement. Comparison between simulations with and without labels reveal that the π-stacking interaction between the fluorophore labels traps the conformation of S-peptide in a single dominant state, while the unlabeled peptide undergoes continuous conformational rearrangements. Furthermore, we find that the open to closed transition rate of S-peptide is decreased by at least one order of magnitude by the fluorophore attachment. Our approach combining experimental and in silico methods provides a benchmark for the simulations and reveals the significant effect that fluorescence labeling can have on the conformational dynamics of small biomolecules, at least for inherently flexible short peptides. The presented protocol is not only useful for comparing PET-FCS experiments with simulation results but provides a strategy to minimize the influence on molecular properties when chosing labeling positions for fluorescence experiments.
[Mh] Termos MeSH primário: Corantes Fluorescentes/química
Compostos Heterocíclicos de 4 ou mais Anéis/química
Fragmentos de Peptídeos/química
Ribonuclease Pancreático/química
[Mh] Termos MeSH secundário: Dicroísmo Circular
Elasticidade
Conformação Molecular
Simulação de Dinâmica Molecular
Espectrometria de Fluorescência
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atto655); 0 (Fluorescent Dyes); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (Peptide Fragments); 0 (ribonuclease A S-peptide); EC 3.1.27.5 (Ribonuclease, Pancreatic)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177139


  10 / 3472 MEDLINE  
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[PMID]:28398546
[Au] Autor:Batot G; Michalska K; Ekberg G; Irimpan EM; Joachimiak G; Jedrzejczak R; Babnigg G; Hayes CS; Joachimiak A; Goulding CW
[Ad] Endereço:Department of Molecular Biology & Biochemistry, University of California Irvine, Irvine, CA 92697, USA.
[Ti] Título:The CDI toxin of Yersinia kristensenii is a novel bacterial member of the RNase A superfamily.
[So] Source:Nucleic Acids Res;45(9):5013-5025, 2017 May 19.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Contact-dependent growth inhibition (CDI) is an important mechanism of inter-bacterial competition found in many Gram-negative pathogens. CDI+ cells express cell-surface CdiA proteins that bind neighboring bacteria and deliver C-terminal toxin domains (CdiA-CT) to inhibit target-cell growth. CDI+ bacteria also produce CdiI immunity proteins, which specifically neutralize cognate CdiA-CT toxins to prevent self-inhibition. Here, we present the crystal structure of the CdiA-CT/CdiIYkris complex from Yersinia kristensenii ATCC 33638. CdiA-CTYkris adopts the same fold as angiogenin and other RNase A paralogs, but the toxin does not share sequence similarity with these nucleases and lacks the characteristic disulfide bonds of the superfamily. Consistent with the structural homology, CdiA-CTYkris has potent RNase activity in vitro and in vivo. Structure-guided mutagenesis reveals that His175, Arg186, Thr276 and Tyr278 contribute to CdiA-CTYkris activity, suggesting that these residues participate in substrate binding and/or catalysis. CdiIYkris binds directly over the putative active site and likely neutralizes toxicity by blocking access to RNA substrates. Significantly, CdiA-CTYkris is the first non-vertebrate protein found to possess the RNase A superfamily fold, and homologs of this toxin are associated with secretion systems in many Gram-negative and Gram-positive bacteria. These observations suggest that RNase A-like toxins are commonly deployed in inter-bacterial competition.
[Mh] Termos MeSH primário: Toxinas Bacterianas/química
Endorribonucleases/química
Ribonuclease Pancreático/química
Yersinia/enzimologia
[Mh] Termos MeSH secundário: Toxinas Bacterianas/metabolismo
Cristalografia por Raios X
Modelos Moleculares
Conformação Proteica
RNA/metabolismo
Ribonuclease Pancreático/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Toxins); 0 (CDI toxin, Yersinia kristensenii); 63231-63-0 (RNA); EC 3.1.- (Endoribonucleases); EC 3.1.27.5 (Ribonuclease, Pancreatic)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx230



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