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[PMID]:28467275
[Au] Autor:Dos Santos PF; Mansur DS
[Ad] Endereço:Departament of Microbiology, Immunology and Parasitology, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina , Santa Catarina, Brazil .
[Ti] Título:Beyond ISGlylation: Functions of Free Intracellular and Extracellular ISG15.
[So] Source:J Interferon Cytokine Res;37(6):246-253, 2017 Jun.
[Is] ISSN:1557-7465
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ISG15 is a ubiquitin-like type I IFN-stimulated protein of 15 kDa and is one of the most prominently expressed proteins in viral infections. ISG15 is widely known to be involved in a process called ISGylation, where it binds to over 150 targets from a variety of classes of proteins including central immune signaling pathways such as those mediated by NFκB, JNK, and IRF-3. However, ISG15 also exists in a free form that can act intra- or extracellularly. In vitro and in vivo evidences suggest that free ISG15 play different roles in several cellular processes, from cancer and defense against viral infections to activation of immune cells such as lymphocytes, monocytes, and NK cells. This review discusses the roles of free intracellular and secreted ISG15 approaching questions yet to be answered about the mechanism of action of this protein.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Citocinas/imunologia
Interferon gama/imunologia
Transdução de Sinais/imunologia
Ubiquitinas/imunologia
Viroses/imunologia
[Mh] Termos MeSH secundário: Infecções Bacterianas/genética
Infecções Bacterianas/microbiologia
Citocinas/genética
Regulação da Expressão Gênica
Seres Humanos
Fator Regulador 3 de Interferon/genética
Fator Regulador 3 de Interferon/imunologia
Interferon Tipo I/genética
Interferon Tipo I/imunologia
Interferon gama/genética
Monócitos/imunologia
Monócitos/microbiologia
Monócitos/virologia
Neutrófilos/imunologia
Neutrófilos/microbiologia
Neutrófilos/virologia
Linfócitos T/imunologia
Linfócitos T/microbiologia
Linfócitos T/virologia
Ubiquitinas/genética
Viroses/genética
Viroses/virologia
eIF-2 Quinase/genética
eIF-2 Quinase/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (Interferon Type I); 0 (Ubiquitins); 60267-61-0 (ISG15 protein, human); 82115-62-6 (Interferon-gamma); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1089/jir.2016.0103


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[PMID]:27770702
[Au] Autor:Mishra P; Dixit U; Pandey AK; Upadhyay A; Pandey VN
[Ad] Endereço:Department of Microbiology, Biochemistry, and Molecular Genetics, Rutgers New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA.
[Ti] Título:Modulation of HCV replication and translation by ErbB3 binding protein1 isoforms.
[So] Source:Virology;500:35-49, 2017 01.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We recently identified a cell-factor, ErbB3 binding protein 1 (Ebp-1), which specifically interacts with the viral RNA genome and modulates HCV replication and translation. Ebp1 has two isoforms, p48, and p42, that result from differential splicing. We found that both isoforms interact with HCV proteins NS5A and NS5B, as well as cell-factor PKR. The p48 isoform, which localizes in the cytoplasm and nuclei, promoted HCV replication, whereas the shorter p42 isoform, which resides exclusively in the cytoplasm, strongly inhibited HCV replication. Transient expression of individual isoforms in Ebp1-knockdown MH14 cells confirmed that the p48 isoform promotes HCV replication, while the p42 isoform inhibits it. We found that Ebp1-p42 significantly enhanced autophosphorylation of PKR, while Ebp1-p48 isoform strongly inhibited it. We propose that modulation of autophosphorylation of PKR by p48 isoform is an important mechanism whereby the HCV virus escapes innate antiviral immune responses by circumventing p42-mediated inhibition of its replication.
[Mh] Termos MeSH primário: Hepacivirus/fisiologia
Hepatite C/virologia
Replicação Viral
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Replicação do DNA
Hepacivirus/genética
Hepatite C/genética
Hepatite C/metabolismo
Seres Humanos
Queratina-20/genética
Queratina-20/metabolismo
Fosforilação
Biossíntese de Proteínas
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
eIF-2 Quinase/genética
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (KRT20 protein, human); 0 (Keratin-20); 0 (Protein Isoforms); EC 2.7.11.1 (EIF2AK2 protein, human); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180303
[Lr] Data última revisão:
180303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE


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[PMID]:29317203
[Au] Autor:Liu T; Duan W; Nizigiyimana P; Gao L; Liao Z; Xu B; Liu L; Lei M
[Ad] Endereço:Department of Endocrinology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China; Department of Endocrinology, Haikou People's Hospital, Haikou, Hainan, 570208, China.
[Ti] Título:Alpha-mangostin attenuates diabetic nephropathy in association with suppression of acid sphingomyelianse and endoplasmic reticulum stress.
[So] Source:Biochem Biophys Res Commun;496(2):394-400, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Diabetic nephropathy is a common complication of diabetes, but there are currently few treatment options. The aim of this study was to gain insight into the effect of alpha-mangostin on diabetic nephropathy and possible related mechanisms. METHODS: Goto-Kakizaki rats were used as a diabetic model and received alpha-mangostin or desipramine treatment with normal saline as a control. Ten age-matched Sprague Dawley rats were used as normal controls and treated with normal saline. At week 12, blood glucose, albuminuria, apoptosis and renal pathologic changes were assessed. Protein levels for acid sphingomyelinase, glucose-regulated protein 78, phosphorylated PKR-like ER-resident kinase, activated transcription factor 4, CCAAT/enhancer-binding protein, homologous protein), and cleaved-caspase12 were measured. RESULTS: The level of acid sphingomyelinase was significantly increased, and ER stress was activated in diabetic rat kidneys when compared to the control animals. When acid sphingomyelinase was inhibited by alpha-mangostin, the expression of ER stress-related proteins was down-regulated in association with decreased levels of diabetic kidney injury. CONCLUSIONS: Alpha-mangostin, an acid sphingomyelinase inhibitor plays a protective role in diabetic neuropathy by relieving ER stress induced-renal cell apoptosis.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Nefropatias Diabéticas/tratamento farmacológico
Inibidores Enzimáticos/farmacologia
Substâncias Protetoras/farmacologia
Esfingomielina Fosfodiesterase/antagonistas & inibidores
Xantonas/farmacologia
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/genética
Fator 4 Ativador da Transcrição/metabolismo
Albuminúria/genética
Albuminúria/metabolismo
Albuminúria/patologia
Albuminúria/prevenção & controle
Animais
Apoptose/efeitos dos fármacos
Glicemia/metabolismo
Caspase 12/genética
Caspase 12/metabolismo
Desipramina/farmacologia
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/patologia
Nefropatias Diabéticas/induzido quimicamente
Nefropatias Diabéticas/genética
Nefropatias Diabéticas/patologia
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Regulação da Expressão Gênica
Proteínas de Choque Térmico/genética
Proteínas de Choque Térmico/metabolismo
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/patologia
Masculino
Ratos
Ratos Sprague-Dawley
Esfingomielina Fosfodiesterase/genética
Esfingomielina Fosfodiesterase/metabolismo
Estreptozocina
eIF-2 Quinase/genética
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Atf4 protein, rat); 0 (Blood Glucose); 0 (Enzyme Inhibitors); 0 (Heat-Shock Proteins); 0 (Hspa5 protein, rat); 0 (Protective Agents); 0 (Xanthones); 145891-90-3 (Activating Transcription Factor 4); 5W494URQ81 (Streptozocin); EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (eIF-2 Kinase); EC 3.1.4.- (acid sphingomyelinase-1); EC 3.1.4.12 (Sphingomyelin Phosphodiesterase); EC 3.4.22.- (Casp12 protein, rat); EC 3.4.22.- (Caspase 12); TG537D343B (Desipramine); U6RIV93RU1 (mangostin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE


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[PMID]:29227599
[Au] Autor:Minchenko OH; Kryvdiuk IV; Riabovol OO; Minchenko DO; Danilovskyi SV; Ratushna OO
[Ti] Título:Inhibition of IRE1 modifies the hypoxic regulation of GADD family gene expressions in U87 glioma cells.
[So] Source:Ukr Biochem J;88(2):25-34, 2016 Mar-Apr.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:We have studied hypoxic regulation of the expression of genes encoded GADD (growth arrest and DNA damage) family proteins in U87 glioma cells in relation to inhibition of IRE1 (inositol requiring enzyme-1), which controls cell proliferation and tumor growth as a central mediator of endoplasmic reticulum stress. We have shown that hypoxia up-regulates the expression of GADD34, GADD45A, GADD45B, and GADD153 genes, which are related to cell proliferation and apoptosis, in control (transfected by empty vector) glioma cells in gene specific manner. At the same time, the expression level of EIF2AK 1 (eukaryotic translation initiation factor 2-alpha kinase 1) and AI FM1 (apoptosis inducing factor, mitochondria associated 1) genes in these cells is down-regulated upon hypoxic condition. It was also shown that inhibition of ІRE1 signaling enzyme function in U87 glioma cells enhances the effect of hypoxia on these genes expression, except EIF2AK 1 and AI FM1 genes. Furthermore, the expression of all studied genes in ІRE1 knockdown cells is significantly decreased upon normoxic condition, except GADD45B gene, which expression level is strongly up-regulated. Therefore, the expression level of genes encoding GADD34, GADD45A, GADD45B, GADD153, EIF2AK 1, and AI FM1 is affected by hypoxia and by inhibition of IRE1-mediated endoplasmic reticulum stress signaling in gene specific manner and correlates with suppression of glioma cell proliferation upon inhibition of the IRE1 enzyme function.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/genética
Estresse do Retículo Endoplasmático/genética
Endorribonucleases/genética
Regulação Neoplásica da Expressão Gênica
Neuroglia/metabolismo
Proteínas Nucleares/genética
Proteína Fosfatase 1/genética
Proteínas Serina-Treonina Quinases/genética
[Mh] Termos MeSH secundário: Antígenos de Diferenciação/genética
Antígenos de Diferenciação/metabolismo
Apoptose/genética
Fator de Indução de Apoptose/genética
Fator de Indução de Apoptose/metabolismo
Proteínas de Ciclo Celular/metabolismo
Hipóxia Celular
Linhagem Celular Tumoral
Proliferação Celular
Endorribonucleases/deficiência
Técnicas de Silenciamento de Genes
Seres Humanos
Neuroglia/patologia
Proteínas Nucleares/metabolismo
Plasmídeos/química
Plasmídeos/metabolismo
Proteína Fosfatase 1/metabolismo
Proteínas Serina-Treonina Quinases/deficiência
Transdução de Sinais
Fator de Transcrição CHOP/genética
Fator de Transcrição CHOP/metabolismo
Transfecção
eIF-2 Quinase/genética
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIFM1 protein, human); 0 (Antigens, Differentiation); 0 (Apoptosis Inducing Factor); 0 (Cell Cycle Proteins); 0 (DDIT3 protein, human); 0 (GADD45A protein, human); 0 (GADD45B protein, human); 0 (Nuclear Proteins); 147336-12-7 (Transcription Factor CHOP); EC 2.7.11.1 (EIF2AK1 protein, human); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (eIF-2 Kinase); EC 3.1.- (Endoribonucleases); EC 3.1.3.16 (PPP1R15A protein, human); EC 3.1.3.16 (Protein Phosphatase 1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.02.025


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[PMID]:29220654
[Au] Autor:Guan BJ; van Hoef V; Jobava R; Elroy-Stein O; Valasek LS; Cargnello M; Gao XH; Krokowski D; Merrick WC; Kimball SR; Komar AA; Koromilas AE; Wynshaw-Boris A; Topisirovic I; Larsson O; Hatzoglou M
[Ad] Endereço:Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44106, USA.
[Ti] Título:A Unique ISR Program Determines Cellular Responses to Chronic Stress.
[So] Source:Mol Cell;68(5):885-900.e6, 2017 Dec 07.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The integrated stress response (ISR) is a homeostatic mechanism induced by endoplasmic reticulum (ER) stress. In acute/transient ER stress, decreased global protein synthesis and increased uORF mRNA translation are followed by normalization of protein synthesis. Here, we report a dramatically different response during chronic ER stress. This chronic ISR program is characterized by persistently elevated uORF mRNA translation and concurrent gene expression reprogramming, which permits simultaneous stress sensing and proteostasis. The program includes PERK-dependent switching to an eIF3-dependent translation initiation mechanism, resulting in partial, but not complete, translational recovery, which, together with transcriptional reprogramming, selectively bolsters expression of proteins with ER functions. Coordination of transcriptional and translational reprogramming prevents ER dysfunction and inhibits "foamy cell" development, thus establishing a molecular basis for understanding human diseases associated with ER dysfunction.
[Mh] Termos MeSH primário: Estresse do Retículo Endoplasmático
Fator de Iniciação 3 em Eucariotos/metabolismo
Fibroblastos/metabolismo
Biossíntese de Proteínas
RNA Mensageiro/biossíntese
Transcrição Genética
eIF-2 Quinase/metabolismo
[Mh] Termos MeSH secundário: Animais
Reprogramação Celular
Fator de Iniciação 3 em Eucariotos/genética
Fibroblastos/patologia
Células HEK293
Seres Humanos
Camundongos
Fases de Leitura Aberta
Fenótipo
Proteostase
Interferência de RNA
RNA Mensageiro/genética
Transdução de Sinais
Fatores de Tempo
Transfecção
eIF-2 Quinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Eukaryotic Initiation Factor-3); 0 (RNA, Messenger); EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


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[PMID]:28450289
[Au] Autor:Gulland A
[Ad] Endereço:London.
[Ti] Título:Sixty seconds on . . . a cure for dementia.
[So] Source:BMJ;357:j1978, 2017 04 27.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Demência/terapia
Doenças Neurodegenerativas/terapia
[Mh] Termos MeSH secundário: Animais
Encéfalo/citologia
Encéfalo/patologia
Morte Celular/fisiologia
Seres Humanos
Camundongos
Modelos Animais
Doenças Neurodegenerativas/fisiopatologia
Fatores de Tempo
eIF-2 Quinase/antagonistas & inibidores
eIF-2 Quinase/uso terapêutico
eIF-2 Quinase/toxicidade
[Pt] Tipo de publicação:NEWS
[Nm] Nome de substância:
EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.j1978


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[PMID]:29053745
[Au] Autor:Dzananovic E; Astha; Chojnowski G; Deo S; Booy EP; Padilla-Meier P; McEleney K; Bujnicki JM; Patel TR; McKenna SA
[Ad] Endereço:Department of Chemistry, University of Manitoba, Winnipeg, Manitoba, Canada.
[Ti] Título:Impact of the structural integrity of the three-way junction of adenovirus VAI RNA on PKR inhibition.
[So] Source:PLoS One;12(10):e0186849, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Highly structured RNA derived from viral genomes is a key cellular indicator of viral infection. In response, cells produce the interferon inducible RNA-dependent protein kinase (PKR) that, when bound to viral dsRNA, phosphorylates eukaryotic initiation factor 2α and attenuates viral protein translation. Adenovirus can evade this line of defence through transcription of a non-coding RNA, VAI, an inhibitor of PKR. VAI consists of three base-paired regions that meet at a three-way junction; an apical stem responsible for the interaction with PKR, a central stem required for inhibition, and a terminal stem. Recent studies have highlighted the potential importance of the tertiary structure of the three-way junction to PKR inhibition by enabling interaction between regions of the central and terminal stems. To further investigate the role of the three-way junction, we characterized the binding affinity and inhibitory potential of central stem mutants designed to introduce subtle alterations. These results were then correlated with small-angle X-ray scattering solution studies and computational tertiary structural models. Our results demonstrate that while mutations to the central stem have no observable effect on binding affinity to PKR, mutations that appear to disrupt the structure of the three-way junction prevent inhibition of PKR. Therefore, we propose that instead of simply sequestering PKR, a specific structural conformation of the PKR-VAI complex may be required for inhibition.
[Mh] Termos MeSH primário: RNA Viral/fisiologia
eIF-2 Quinase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Mutação
RNA Viral/genética
Espalhamento de Radiação
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Viral); 0 (adenovirus associated RNA); EC 2.7.11.1 (eIF-2 Kinase)
[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:171021
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186849


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[PMID]:28938442
[Au] Autor:Chan SMH; Lau YS; Miller AA; Ku JM; Potocnik S; Ye JM; Woodman OL; Herbert TP
[Ad] Endereço:School of Health and Biomedical Sciences, Royal Melbourne Institute of Technology University, Bundoora, Victoria 3083, Australia.
[Ti] Título:Angiotensin II Causes ß-Cell Dysfunction Through an ER Stress-Induced Proinflammatory Response.
[So] Source:Endocrinology;158(10):3162-3173, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The metabolic syndrome is associated with an increase in the activation of the renin angiotensin system, whose inhibition reduces the incidence of new-onset diabetes. Importantly, angiotensin II (AngII), independently of its vasoconstrictor action, causes ß-cell inflammation and dysfunction, which may be an early step in the development of type 2 diabetes. The aim of this study was to determine how AngII causes ß-cell dysfunction. Islets of Langerhans were isolated from C57BL/6J mice that had been infused with AngII in the presence or absence of taurine-conjugated ursodeoxycholic acid (TUDCA) and effects on endoplasmic reticulum (ER) stress, inflammation, and ß-cell function determined. The mechanism of action of AngII was further investigated using isolated murine islets and clonal ß cells. We show that AngII triggers ER stress, an increase in the messenger RNA expression of proinflammatory cytokines, and promotes ß-cell dysfunction in murine islets of Langerhans both in vivo and ex vivo. These effects were significantly attenuated by TUDCA, an inhibitor of ER stress. We also show that AngII-induced ER stress is required for the increased expression of proinflammatory cytokines and is caused by reactive oxygen species and IP3 receptor activation. These data reveal that the induction of ER stress is critical for AngII-induced ß-cell dysfunction and indicates how therapies that promote ER homeostasis may be beneficial in the prevention of type 2 diabetes.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Estresse do Retículo Endoplasmático/fisiologia
Inflamação/fisiopatologia
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Citocinas/genética
Diabetes Mellitus Tipo 2/etiologia
Diabetes Mellitus Tipo 2/prevenção & controle
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Endorribonucleases/antagonistas & inibidores
Endorribonucleases/genética
Endorribonucleases/fisiologia
Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Glucose/farmacologia
Receptores de Inositol 1,4,5-Trifosfato/fisiologia
Insulinoma
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/fisiopatologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Pancreáticas
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/fisiologia
RNA Interferente Pequeno
Espécies Reativas de Oxigênio/metabolismo
Sistema Renina-Angiotensina/fisiologia
Taurina/farmacologia
Ácido Ursodesoxicólico/farmacologia
eIF-2 Quinase/antagonistas & inibidores
eIF-2 Quinase/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inositol 1,4,5-Trisphosphate Receptors); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (taurine-ursodeoxycholate conjugate); 11128-99-7 (Angiotensin II); 1EQV5MLY3D (Taurine); 724L30Y2QR (Ursodeoxycholic Acid); EC 2.7.11.1 (Ern1 protein, mouse); EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (eIF-2 Kinase); EC 3.1.- (Endoribonucleases); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1879


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[PMID]:28919326
[Au] Autor:Huynh TP; Jancovich JK; Tripuraneni L; Heck MC; Langland JO; Jacobs BL
[Ad] Endereço:School of Life Sciences, and The Biodesign Institute, Center for Infectious Diseases and Vaccinology Arizona State University, Tempe, AZ 85287-5001, USA.
[Ti] Título:Characterization of a PKR inhibitor from the pathogenic ranavirus, Ambystoma tigrinum virus, using a heterologous vaccinia virus system.
[So] Source:Virology;511:290-299, 2017 Nov.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ambystoma tigrinum virus (ATV) (family Iridoviridae, genus Ranavirus) was isolated from diseased tiger salamanders (Ambystoma tigrinum stebbinsi) from the San Rafael Valley in southern Arizona, USA in 1996. Genomic sequencing of ATV, as well as other members of the genus, identified an open reading frame that has homology to the eukaryotic translation initiation factor, eIF2α (ATV eIF2α homologue, vIF2αH). Therefore, we asked if the ATV vIF2αH could also inhibit PKR. To test this hypothesis, the ATV vIF2αH was cloned into vaccinia virus (VACV) in place of the well-characterized VACV PKR inhibitor, E3L. Recombinant VACV expressing ATV vIF2αH partially rescued deletion of the VACV E3L gene. Rescue coincided with rapid degradation of PKR in infected cells. These data suggest that the salamander virus, ATV, contains a novel gene that may counteract host defenses, and this gene product may be involved in the presentation of disease caused by this environmentally important pathogen.
[Mh] Termos MeSH primário: Inibidores de Proteínas Quinases/metabolismo
Ranavirus/patogenicidade
Proteínas Recombinantes/metabolismo
Proteínas Virais/metabolismo
Fatores de Virulência/metabolismo
eIF-2 Quinase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Ambystoma/virologia
Animais
Arizona
Expressão Gênica
Vetores Genéticos
Interações Hospedeiro-Patógeno
Evasão da Resposta Imune
Ranavirus/genética
Proteínas Recombinantes/genética
Vírus Vaccinia/genética
Proteínas Virais/genética
Fatores de Virulência/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Recombinant Proteins); 0 (Viral Proteins); 0 (Virulence Factors); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


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[PMID]:28888981
[Au] Autor:Guo Q; Jin S; Hu H; Zhou Y; Yan Y; Zong H; Wang Y; He H; Oh Y; Liu C; Gu N
[Ad] Endereço:School of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
[Ti] Título:Hypoxia in 3T3-L1 adipocytes suppresses adiponectin expression via the PERK and IRE1 unfolded protein response.
[So] Source:Biochem Biophys Res Commun;493(1):346-351, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adiponectin, an adipocytokine produced by adipocytes, functions as an anti-inflammatory and anti-apoptotic substance, while also enhancing insulin sensitivity. Patients or model animals with obesity or diabetes typically present attenuated expression of adiponectin. Moreover, obesity and diabetes are often accompanied with hypoxia in adipose tissue, which may result in endoplasmic reticulum (ER) stress as well as low expression of adiponectin. The purpose of this study was to investigate the specific role of the unfolded protein response (UPR) involved in the low expression of adiponectin induced by hypoxia. Subjecting 3T3-L1 adipocytes to hypoxia significantly reduced adiponectin expression and activated the PERK and IRE1 signaling pathways in a time-dependent manner. The ATF6 signaling pathway showed no obvious changes with hypoxia treatment under a similar time course. Moreover, the down-regulated expression of adiponectin induced by hypoxia was relieved once the PERK and IRE1 signaling pathways were suppressed by the inhibitors GSK2656157 and 4µ8C, respectively. Overall, these data demonstrate that hypoxia can suppress adiponectin expression and activate the PERK and IRE1 signaling pathways in differentiated adipocytes, and this two pathways are involved in the suppression of adiponectin expression induced by hypoxia.
[Mh] Termos MeSH primário: Adiponectina/metabolismo
Proteínas de Membrana/metabolismo
Oxigênio/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Resposta a Proteínas não Dobradas/fisiologia
eIF-2 Quinase/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Animais
Hipóxia Celular/fisiologia
Regulação para Baixo/fisiologia
Camundongos
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Membrane Proteins); EC 2.7.1.- (Ern2 protein, mouse); EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (eIF-2 Kinase); S88TT14065 (Oxygen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170911
[St] Status:MEDLINE



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