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[PMID]:29287889
[Au] Autor:Cesca F; Bettella E; Polli R; Cama E; Scimemi P; Santarelli R; Murgia A
[Ad] Endereço:Laboratory of Molecular Genetics of Neurodevelopment, Department of Women's and Children's Health, University of Padova, Italy.
[Ti] Título:A novel mutation of the EYA4 gene associated with post-lingual hearing loss in a proband is co-segregating with a novel PAX3 mutation in two congenitally deaf family members.
[So] Source:Int J Pediatr Otorhinolaryngol;104:88-93, 2018 Jan.
[Is] ISSN:1872-8464
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: This work was aimed at establishing the molecular etiology of hearing loss in a 9-year old girl with post-lingual non-syndromic mild sensorineural hearing loss with a complex family history of clinically heterogeneous deafness. METHODS: The proband's DNA was subjected to NGS analysis of a 59-targeted gene panel, with the use of the Ion Torrent PGM platform. Conventional Sanger sequencing was used for segregation analysis in all the affected relatives. The proband and all the other hearing impaired members of the family underwent a thorough clinical and audiological evaluation. RESULTS: A new likely pathogenic mutation in the EYA4 gene (c.1154C > T; p.Ser385Leu) was identified in the proband and in her 42-year-old father with post-lingual non-syndromic profound sensorineural hearing loss. The EYA4 mutation was also found in the proband's grandfather and uncle, both showing clinical features of Waardenburg syndrome type 1. A novel pathogenic splice-site mutation (c.321+1G > A) of the PAX3 gene was found to co-segregate with the EYA4 mutation in these two subjects. CONCLUSION: The identified novel EYA4 mutation can be considered responsible of the hearing loss observed in the proband and her father, while a dual molecular diagnosis was reached in the relatives co-segregating the EYA4 and the PAX3 mutations. In these two subjects the DFNA10 phenotype was masked by Waardenburg syndrome. The use of NGS targeted gene-panel, in combination with an extensive clinical and audiological examination led us to identify the genetic cause of the hearing loss in members of a family in which different forms of autosomal dominant deafness segregate. These results provide precise and especially important prognostic and follow-up information for the future audiologic management in the youngest affected member.
[Mh] Termos MeSH primário: Surdez/genética
Perda Auditiva Neurossensorial/genética
Fator de Transcrição PAX3/genética
Transativadores/genética
Síndrome de Waardenburg/genética
[Mh] Termos MeSH secundário: Adulto
Audiometria
Criança
Família
Feminino
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Mutação
Linhagem
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EYA4 protein, human); 0 (PAX3 Transcription Factor); 0 (PAX3 protein, human); 0 (Trans-Activators)
[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:171231
[St] Status:MEDLINE


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[PMID]:28466892
[Au] Autor:Bondí R; Longo F; Messina M; D'Angelo F; Visca P; Leoni L; Rampioni G
[Ad] Endereço:Department of Science, University Roma Tre, Rome, Italy. giordano.rampioni@uniroma3.it.
[Ti] Título:The multi-output incoherent feedforward loop constituted by the transcriptional regulators LasR and RsaL confers robustness to a subset of quorum sensing genes in Pseudomonas aeruginosa.
[So] Source:Mol Biosyst;13(6):1080-1089, 2017 Jun 01.
[Is] ISSN:1742-2051
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Quorum sensing (QS) is an intercellular communication system which controls virulence-related phenotypes in the human pathogen Pseudomonas aeruginosa. LasR is the QS receptor protein which responds to the signal molecule N-(3-oxododecanoyl)homoserine lactone (3OC -HSL) and promotes signal production by increasing the transcription of the 3OC -HSL synthase gene, lasI. LasR also activates the expression of other genes, including rsaL, coding for the RsaL protein which acts as a transcriptional repressor of lasI. Direct gene activation and RsaL-mediated gene repression, both exerted by LasR on the expression of the output gene lasI, generate a regulatory network motif known as the type 1 incoherent feedforward loop (IFFL-1) that governs 3OC -HSL production. In addition to lasI, RsaL directly represses a set of LasR-activated genes; hence, the IFFL-1 generated by LasR and RsaL is a multi-output IFFL-1. Here we demonstrate that the multi-output IFFL-1 constituted by LasR and RsaL confers robustness with respect to fluctuations in the levels of LasR to the phenotypes controlled by both these transcriptional regulators (e.g. 3OC -HSL synthesis and pyocyanin production). In contrast, other virulence-related phenotypes controlled by LasR but not by RsaL (e.g. elastase and protease production) are sensitive to changes in LasR levels. Overall, the multi-output IFFL-1 generated by LasR and RsaL splits the QS regulon into two distinct sub-regulons with different robustness with respect to LasR fluctuations. This emerging regulatory property enhances the phenotypic plasticity of P. aeruginosa, thus contributing to its adaptation to changing environments.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Pseudomonas aeruginosa/metabolismo
Pseudomonas aeruginosa/fisiologia
Percepção de Quorum
Proteínas Repressoras/metabolismo
Transativadores/metabolismo
[Mh] Termos MeSH secundário: 4-Butirolactona/análogos & derivados
4-Butirolactona/metabolismo
Proteínas de Bactérias/genética
Regulação da Expressão Gênica
Homosserina/análogos & derivados
Homosserina/metabolismo
Proteínas Repressoras/genética
Transativadores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (LasR protein, Pseudomonas aeruginosa); 0 (N-(3-oxododecanoyl)homoserine lactone); 0 (Repressor Proteins); 0 (Trans-Activators); 0 (rsaL protein, Pseudomonas aeruginosa); 1192-20-7 (homoserine lactone); 6KA95X0IVO (Homoserine); OL659KIY4X (4-Butyrolactone)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1039/c7mb00040e


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[PMID]:28453780
[Au] Autor:Billings LK; Jablonski KA; Warner AS; Cheng YC; McAteer JB; Tipton L; Shuldiner AR; Ehrmann DA; Manning AK; Dabelea D; Franks PW; Kahn SE; Pollin TI; Knowler WC; Altshuler D; Florez JC; Diabetes Prevention Program Research Group
[Ad] Endereço:Diabetes Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114.
[Ti] Título:Variation in Maturity-Onset Diabetes of the Young Genes Influence Response to Interventions for Diabetes Prevention.
[So] Source:J Clin Endocrinol Metab;102(8):2678-2689, 2017 Aug 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Variation in genes that cause maturity-onset diabetes of the young (MODY) has been associated with diabetes incidence and glycemic traits. Objectives: This study aimed to determine whether genetic variation in MODY genes leads to differential responses to insulin-sensitizing interventions. Design and Setting: This was a secondary analysis of a multicenter, randomized clinical trial, the Diabetes Prevention Program (DPP), involving 27 US academic institutions. We genotyped 22 missense and 221 common variants in the MODY-causing genes in the participants in the DPP. Participants and Interventions: The study included 2806 genotyped DPP participants randomized to receive intensive lifestyle intervention (n = 935), metformin (n = 927), or placebo (n = 944). Main Outcome Measures: Association of MODY genetic variants with diabetes incidence at a median of 3 years and measures of 1-year ß-cell function, insulinogenic index, and oral disposition index. Analyses were stratified by treatment group for significant single-nucleotide polymorphism × treatment interaction (Pint < 0.05). Sequence kernel association tests examined the association between an aggregate of rare missense variants and insulinogenic traits. Results: After 1 year, the minor allele of rs3212185 (HNF4A) was associated with improved ß-cell function in the metformin and lifestyle groups but not the placebo group; the minor allele of rs6719578 (NEUROD1) was associated with an increase in insulin secretion in the metformin group but not in the placebo and lifestyle groups. Conclusions: These results provide evidence that genetic variation among MODY genes may influence response to insulin-sensitizing interventions.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Diabetes Mellitus Tipo 2/genética
Terapia por Exercício
Fator 4 Nuclear de Hepatócito/genética
Programas de Redução de Peso
[Mh] Termos MeSH secundário: Diabetes Mellitus Tipo 2/prevenção & controle
Variação Genética
Glucoquinase/genética
Fator 1-alfa Nuclear de Hepatócito/genética
Fator 1-beta Nuclear de Hepatócito/genética
Proteínas de Homeodomínio/genética
Seres Humanos
Metformina/uso terapêutico
Mutação de Sentido Incorreto
Polimorfismo de Nucleotídeo Único
Comportamento de Redução do Risco
Transativadores/genética
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (HNF1A protein, human); 0 (HNF1B protein, human); 0 (HNF4A protein, human); 0 (Hepatocyte Nuclear Factor 1-alpha); 0 (Hepatocyte Nuclear Factor 4); 0 (Homeodomain Proteins); 0 (NEUROD1 protein, human); 0 (Trans-Activators); 0 (pancreatic and duodenal homeobox 1 protein); 138674-15-4 (Hepatocyte Nuclear Factor 1-beta); 9100L32L2N (Metformin); EC 2.7.1.2 (Glucokinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-3429


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[PMID]:29295976
[Au] Autor:Liu CY; Zhang YH; Li RB; Zhou LY; An T; Zhang RC; Zhai M; Huang Y; Yan KW; Dong YH; Ponnusamy M; Shan C; Xu S; Wang Q; Zhang YH; Zhang J; Wang K
[Ad] Endereço:Center for Developmental Cardiology, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266021, China.
[Ti] Título:LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription.
[So] Source:Nat Commun;9(1):29, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H O and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.
[Mh] Termos MeSH primário: Autofagia/genética
Infarto do Miocárdio/genética
Proteínas Nucleares/genética
RNA Longo não Codificante/genética
Transativadores/genética
Ativação Transcricional
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Camundongos
Infarto do Miocárdio/patologia
Traumatismo por Reperfusão Miocárdica/genética
Traumatismo por Reperfusão Miocárdica/metabolismo
Miócitos Cardíacos/metabolismo
Proteínas Nucleares/metabolismo
Ligação Proteica
Interferência de RNA
RNA Longo não Codificante/metabolismo
Transativadores/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Proteins); 0 (RNA, Long Noncoding); 0 (Trans-Activators); 0 (Tumor Suppressor Protein p53); 0 (myocardin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02280-y


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[PMID]:29302027
[Au] Autor:Campbell M; Watanabe T; Nakano K; Davis RR; Lyu Y; Tepper CG; Durbin-Johnson B; Fujimuro M; Izumiya Y
[Ad] Endereço:Department of Dermatology, School of Medicine, University of California Davis (UC Davis), Sacramento, CA, 95817, USA.
[Ti] Título:KSHV episomes reveal dynamic chromatin loop formation with domain-specific gene regulation.
[So] Source:Nat Commun;9(1):49, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The three-dimensional structure of chromatin organized by genomic loops facilitates RNA polymerase II access to distal promoters. The Kaposi's sarcoma-associated herpesvirus (KSHV) lytic transcriptional program is initiated by a single viral transactivator, K-Rta. Here we report the KSHV genomic structure and its relationship with K-Rta recruitment sites using Capture Hi-C analyses. High-resolution 3D viral genomic maps identify a number of direct physical, long-range, and dynamic genomic interactions. Mutant KSHV chromosomes harboring point mutations in the K-Rta responsive elements (RE) significantly attenuate not only the directly proximate downstream gene, but also distal gene expression in a domain-specific manner. Genomic loops increase in the presence of K-Rta, while abrogation of K-Rta binding impairs the formation of inducible genomic loops, decreases the expression of genes networked through the looping, and diminishes KSHV replication. Our study demonstrates that genomic architectural dynamics plays an essential role in herpesvirus gene expression.
[Mh] Termos MeSH primário: Regulação Viral da Expressão Gênica
Genoma Viral/genética
Herpesvirus Humano 8/genética
Plasmídeos/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Linhagem Celular Tumoral
Cercopithecus aethiops
Seres Humanos
Transativadores/genética
Células Vero
Proteínas Virais/genética
Latência Viral/genética
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Trans-Activators); 0 (Viral Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02089-9


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[PMID]:28460481
[Au] Autor:Kang HJ; Chung DH; Sung CO; Yoo SH; Yu E; Kim N; Lee SH; Song JY; Kim CJ; Choi J
[Ad] Endereço:Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
[Ti] Título:SHP2 is induced by the HBx-NF-κB pathway and contributes to fibrosis during human early hepatocellular carcinoma development.
[So] Source:Oncotarget;8(16):27263-27276, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The non-receptor tyrosine phosphatase SHP2 has scaffolding functions in signal transduction cascades downstream of growth receptors. A recent study suggested that SHP2 acts as a tumor suppressor during hepatocellular carcinoma (HCC) development. Herein we examined whether SHP2 links the HBx-NF-κB pathway to EGFR signaling during HCC development. The overexpression of HBx or NF-κB led to increased SHP2 expression via NF-κB binding to the Shp2 promoter. EGF treatment induced ERK activation as well as the rapid assembly of SHP2, EGFR, and Gab1. Upon LPS stimulation, NF-κB-SHP2-ERK activation and phosphorylated STAT3 levels exhibited a negative correlation in vitro. By contrast, in patients with HBV-associated HCC, NF-κB-SHP2-ERK and IL-6-JAK-STAT3 pathway activity levels were concomitantly higher in adjacent non-neoplastic tissues than in HCC tissues. The immunohistochemical analysis of 162 tissues of patients with HCC revealed that SHP2 levels were significantly higher in non-neoplastic background tissues than in corresponding HCC tissues and considerably increased in background liver tissues with advanced fibrosis (P < 0.001). SHP2 expression increased gradually from normal liver to chronic hepatitis, cirrhosis, and background liver with a dysplastic nodule, but was decreased or lost in dysplastic nodules and HCC. This is the first report to describe the existence of the HBx-NF-κB-SHP2 pathway, linking HBV infection to the EGFR-RAS-RAF-MAPK pathway in the liver. SHP2 depletion from the negative crosstalk between NF-κB and STAT3 accelerates HCC development.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/etiologia
Carcinoma Hepatocelular/metabolismo
Neoplasias Hepáticas/etiologia
Neoplasias Hepáticas/metabolismo
NF-kappa B/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma Hepatocelular/patologia
Carcinoma Hepatocelular/cirurgia
Linhagem Celular Tumoral
Feminino
Fibrose
Regulação Neoplásica da Expressão Gênica
Vírus da Hepatite B/fisiologia
Seres Humanos
Cirrose Hepática/etiologia
Cirrose Hepática/metabolismo
Cirrose Hepática/patologia
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas/cirurgia
Masculino
Meia-Idade
Modelos Biológicos
Gradação de Tumores
Estadiamento de Neoplasias
Regiões Promotoras Genéticas
Ligação Proteica
Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Proteínas ras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (STAT3 Transcription Factor); 0 (Trans-Activators); 0 (hepatitis B virus X protein); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15930


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[PMID]:28456021
[Au] Autor:Lupey-Green LN; Moquin SA; Martin KA; McDevitt SM; Hulse M; Caruso LB; Pomerantz RT; Miranda JL; Tempera I
[Ad] Endereço:Fels Institute for Cancer Research & Molecular Biology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.
[Ti] Título:PARP1 restricts Epstein Barr Virus lytic reactivation by binding the BZLF1 promoter.
[So] Source:Virology;507:220-230, 2017 07.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Epstein Barr virus (EBV) genome persists in infected host cells as a chromatinized episome and is subject to chromatin-mediated regulation. Binding of the host insulator protein CTCF to the EBV genome has an established role in maintaining viral latency type, and in other herpesviruses, loss of CTCF binding at specific regions correlates with viral reactivation. Here, we demonstrate that binding of PARP1, an important cofactor of CTCF, at the BZLF1 lytic switch promoter restricts EBV reactivation. Knockdown of PARP1 in the Akata-EBV cell line significantly increases viral copy number and lytic protein expression. Interestingly, CTCF knockdown has no effect on viral reactivation, and CTCF binding across the EBV genome is largely unchanged following reactivation. Moreover, EBV reactivation attenuates PARP activity, and Zta expression alone is sufficient to decrease PARP activity. Here we demonstrate a restrictive function of PARP1 in EBV lytic reactivation.
[Mh] Termos MeSH primário: Infecções por Vírus Epstein-Barr/enzimologia
Infecções por Vírus Epstein-Barr/virologia
Herpesvirus Humano 4/fisiologia
Poli(ADP-Ribose) Polimerase-1/metabolismo
Regiões Promotoras Genéticas
Transativadores/genética
Ativação Viral
[Mh] Termos MeSH secundário: Linhagem Celular
Infecções por Vírus Epstein-Barr/genética
Regulação Viral da Expressão Gênica
Herpesvirus Humano 4/genética
Interações Hospedeiro-Patógeno
Seres Humanos
Poli(ADP-Ribose) Polimerase-1/genética
Ligação Proteica
Transativadores/metabolismo
Latência Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (BZLF1 protein, Herpesvirus 4, Human); 0 (Trans-Activators); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180304
[Lr] Data última revisão:
180304
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29385169
[Au] Autor:Bissa M; Forlani G; Zanotto C; Tosi G; De Giuli Morghen C; Accolla RS; Radaelli A
[Ad] Endereço:Department of Pharmacological and Biomolecular Sciences, University of Milan, via Balzaretti 9, Milan, Italy.
[Ti] Título:Fowlpoxvirus recombinants coding for the CIITA gene increase the expression of endogenous MHC-II and Fowlpox Gag/Pro and Env SIV transgenes.
[So] Source:PLoS One;13(1):e0190869, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A complete eradication of an HIV infection has never been achieved by vaccination and the search for new immunogens that can induce long-lasting protective responses is ongoing. Avipoxvirus recombinants are host-restricted for replication to avian species and they do not have the undesired side effects induced by vaccinia recombinants. In particular, Fowlpox (FP) recombinants can express transgenes over long periods and can induce protective immunity in mammals, mainly due to CD4-dependent CD8+ T cells. In this context, the class II transactivator (CIITA) has a pivotal role in triggering the adaptive immune response through induction of the expression of class-II major histocompatibility complex molecule (MHC-II), that can present antigens to CD4+ T helper cells. Here, we report on construction of novel FPgp and FPenv recombinants that express the highly immunogenic SIV Gag-pro and Env structural antigens. Several FP-based recombinants, with single or dual genes, were also developed that express CIITA, driven from H6 or SP promoters. These recombinants were used to infect CEF and Vero cells in vitro and determine transgene expression, which was evaluated by real-time PCR and Western blotting. Subcellular localisation of the different proteins was evaluated by confocal microscopy, whereas HLA-DR or MHC-II expression was measured by flow cytometry. Fowlpox recombinants were also used to infect syngeneic T/SA tumour cells, then injected into Balb/c mice to elicit MHC-II immune response and define the presentation of the SIV transgene products in the presence or absence of FPCIITA. Antibodies to Env were measured by ELISA. Our data show that the H6 promoter was more efficient than SP to drive CIITA expression and that CIITA can enhance the levels of the gag/pro and env gene products only when infection is performed by FP single recombinants. Also, CIITA expression is higher when carried by FP single recombinants than when combined with FPgp or FPenv constructs and can induce HLA-DR cell surface expression. However, in-vivo experiments did not show any significant increase in the humoral response. As CIITA already proved to elicit immunogenicity by improving antigen presentation, further in-vivo experiments should be performed to increase the immune responses. The use of prime/boost immunisation protocols and the oral administration route of the recombinants may enhance the immunogenicity of Env peptides presented by MHC-II and provide CD4+ T-cell stimulation.
[Mh] Termos MeSH primário: Genes Virais
Complexo Principal de Histocompatibilidade/genética
Proteínas Nucleares/genética
Poxviridae/genética
Recombinação Genética
Vírus da Imunodeficiência Símia/genética
Transativadores/genética
Transgenes
[Mh] Termos MeSH secundário: Vacinas contra a AIDS/genética
Vacinas contra a AIDS/imunologia
Animais
Western Blotting
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Linhagem Celular
Embrião de Galinha
Ensaio de Imunoadsorção Enzimática
Infecções por HIV/imunologia
Infecções por HIV/prevenção & controle
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Microscopia Confocal
Regiões Promotoras Genéticas
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AIDS Vaccines); 0 (MHC class II transactivator protein); 0 (Nuclear Proteins); 0 (Trans-Activators)
[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:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190869


  9 / 43581 MEDLINE  
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[PMID]:29222050
[Au] Autor:Li N; Cao M; Yi S; Cheng J; Wang L; Tao Y; Wu D; Peng J; Zhang M; Qi P; Zhao J
[Ad] Endereço:Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610065, Sichuan, PR China.
[Ti] Título:Effects of the RNA-binding protein, KSRP, on innate immune response against Helicobacter pylori infection in mice.
[So] Source:Biochem Biophys Res Commun;495(2):1573-1579, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Helicobacter pylori (H. pylori) contributes to various gastric diseases such as chronic gastritis, gastric ulcer, and gastric carcinoma. Host innate immune response against the pathogen plays a significant role in elimination of pathogen infection. Importantly, pathogen elimination is closely related to numerous inflammatory-related genes that participate in complex biological response of cells to harmful stimuli. Here we studied effects of the KH-type splicing regulatory protein (KSRP), a RNA-binding protein, on innate immune response against H. pylori infection. We found that H. pylori infection downregulated KSRP expression directly, and that KSRP overexpression repressed upregulation of CXCL-2 expression induced by H. pylori and facilitated H. pylori proliferation in vitro. Similarly, KSRP overexpression in H. pylori mice also facilitated H. pylori proliferation and colonization, and induced more severe gastric mucosal damage. Intriguingly, CXCL-2 and HMOX-1 were upregulated in H. pylori infected mice after KSRP overexpression. This difference in expression of these genes implicated that KSRP was closely associated with and directly participated in the innate immune response against H. pylori. These results were beneficial for understanding the in vivo function of KSRP on innate immune response against pathogen infection.
[Mh] Termos MeSH primário: Infecções por Helicobacter/imunologia
Helicobacter pylori
Proteínas de Ligação a RNA/imunologia
Transativadores/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Quimiocina CXCL2/genética
Regulação para Baixo
Feminino
Gastrite/genética
Gastrite/imunologia
Gastrite/patologia
Infecções por Helicobacter/genética
Infecções por Helicobacter/patologia
Helicobacter pylori/genética
Helicobacter pylori/imunologia
Helicobacter pylori/patogenicidade
Heme Oxigenase-1/genética
Seres Humanos
Imunidade Inata/genética
Masculino
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos BALB C
Proteínas de Ligação a RNA/genética
Receptor 2 Toll-Like/genética
Transativadores/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCL2 protein, human); 0 (Chemokine CXCL2); 0 (Cxcl2 protein, mouse); 0 (KHSRP protein, human); 0 (KSRP protein, mouse); 0 (Membrane Proteins); 0 (RNA-Binding Proteins); 0 (TLR2 protein, human); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); 0 (Trans-Activators); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse)
[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:171210
[St] Status:MEDLINE


  10 / 43581 MEDLINE  
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[PMID]:28935584
[Au] Autor:Liu C; Jia X; Zou Z; Wang X; Wang Y; Zhang Z
[Ad] Endereço:Key Laboratory of Healthy Mariculture for the East China Sea, Ministry of Agriculture, Fisheries College, Jimei University, Xiamen 361021, China.
[Ti] Título:VIH from the mud crab is specifically expressed in the eyestalk and potentially regulated by transactivator of Sox9/Oct4/Oct1.
[So] Source:Gen Comp Endocrinol;255:1-11, 2018 Jan 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vitellogenesis-inhibiting hormone (VIH) is known to regulate ovarian maturation by suppressing the synthesis of vitellogenin (Vtg) in crustaceans, which belongs to a member of crustacean hyperglycemic hormone (CHH) family synthesized and secreted from the X-organ/sinus gland complex of eyestalks. In this study, the cDNA, genomic DNA (gDNA) and the 5'-upstream regulatory (promoter region) sequences of VIH gene were obtained by conventional PCR, genome walker and tail-PCR techniques according to our transcriptomic database of Scylla paramamosain. The full-length cDNA of SpVIH is 634bp including 105bp 5'UTR, 151bp 3'UTR and 378bp ORF that encodes a peptide of 125 amino acids. The full length gDNA of SpVIH is 790bp containing two exons and one intron. The 5'-flanking promoter regions of SpVIH we isolated are 3070bp from the translation initiation (ATG) and 2398bp from the predicted transcription initiation (A), which consists of putative core promoter region and multiple potential transcription factor binding sites. SpVIH was only expressed in eyestalk. The expression level of SpVIH in eyestalk of female crab decreased gradually along with the development of ovary. As there is not cell line of crabs available, we chose the mature transfection system HEK293FT cell lines to explore the mechanism of transcription regulation of SpVIH in crabs. Sequential deletion assays using luciferase reporter gene in HEK293FT cells revealed that the possible promoter activity regions (including positive and negative transcription factors binding sites simultaneously) presented between pSpVIH-4 and pSpVIH-6. In order to further identify the crucial transcription factors binding site in this region, the site-directed mutagenesis of Sox9/Oct4/Oct1 binding site of pSpVIH-4 was created. The results demonstrated that the transcriptional activity of pSpVIH-4â–³ decreased significantly (p<0.05). Thus, it is reasonable to deduce that the Sox9/Oct4/Oct1 may be the essential positive transcription factors which regulate the expression of SpVIH.
[Mh] Termos MeSH primário: Braquiúros/metabolismo
Proteínas de Transporte/metabolismo
Olho/metabolismo
Hormônios de Invertebrado/metabolismo
Fator 1 de Transcrição de Octâmero/metabolismo
Fator 3 de Transcrição de Octâmero/metabolismo
Fatores de Transcrição SOX9/metabolismo
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Região 5'-Flanqueadora/genética
Sequência de Aminoácidos
Animais
Sequência de Bases
Proteínas de Transporte/química
Proteínas de Transporte/genética
DNA Complementar/genética
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Células HEK293
Seres Humanos
Hormônios de Invertebrado/química
Hormônios de Invertebrado/genética
Mutação/genética
Ovário/embriologia
Ovário/metabolismo
Filogenia
Regiões Promotoras Genéticas/genética
Análise de Sequência de DNA
Transgenes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (DNA, Complementary); 0 (Invertebrate Hormones); 0 (Octamer Transcription Factor-1); 0 (Octamer Transcription Factor-3); 0 (SOX9 Transcription Factor); 0 (Trans-Activators); 138360-48-2 (vitellogenesis inhibiting hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE



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