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  1 / 6810 MEDLINE  
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[PMID]:29430664
[Au] Autor:Budzynska PM; Kyläniemi MK; Lassila O; Nera KP; Alinikula J
[Ad] Endereço:Department of Medical Microbiology and Immunology, Institute of Biomedicine, University of Turku, Turku, Finland.
[Ti] Título:BLIMP-1 is insufficient to induce antibody secretion in the absence of IRF4 in DT40 cells.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Differentiation of B cells into antibody-secreting cells (ASCs), plasmablasts and plasma cells is regulated by a network of transcription factors. Within this network, factors including PAX5 and BCL6 prevent ASC differentiation and maintain the B cell phenotype. In contrast, BLIMP-1 and high IRF4 expression promote plasma cell differentiation. BLIMP-1 is thought to induce immunoglobulin secretion, whereas IRF4 is needed for the survival of ASCs. The role of IRF4 in the regulation of antibody secretion has remained controversial. To study the role of IRF4 in the regulation of antibody secretion, we have created a double knockout (DKO) DT40 B cell line deficient in both IRF4 and BCL6. Although BCL6-deficient DT40 B cell line had upregulated BLIMP-1 expression and secreted antibodies, the DKO cell line did not. Even enforced BLIMP-1 expression in DKO cells or IRF4-deficient cells could not induce IgM secretion while in WT DT40 cells, it could. However, enforced IRF4 expression in DKO cells induced strong IgM secretion. Our findings support a model where IRF4 expression in addition to BLIMP-1 expression is required to induce robust antibody secretion.
[Mh] Termos MeSH primário: Anticorpos/imunologia
Formação de Anticorpos/genética
Proteínas Aviárias/genética
Linfócitos B/imunologia
Fatores Reguladores de Interferon/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
[Mh] Termos MeSH secundário: Animais
Linfócitos B/citologia
Diferenciação Celular/imunologia
Linhagem Celular
Proliferação Celular
Galinhas
Técnicas de Inativação de Genes
Imunoglobulina M/biossíntese
Imunoglobulina M/imunologia
Fator de Transcrição PAX5/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/imunologia
Proteínas Proto-Oncogênicas c-bcl-6/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Avian Proteins); 0 (IRF4 protein, Gallus gallus); 0 (Immunoglobulin M); 0 (Interferon Regulatory Factors); 0 (PAX5 Transcription Factor); 0 (Proto-Oncogene Proteins c-bcl-6); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[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:180213
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12646


  2 / 6810 MEDLINE  
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[PMID]:28468914
[Au] Autor:Engel C; Brügmann G; Lambing S; Mühlenbeck LH; Marx S; Hagen C; Horváth D; Goldeck M; Ludwig J; Herzner AM; Drijfhout JW; Wenzel D; Coch C; Tüting T; Schlee M; Hornung V; Hartmann G; Van den Boorn JG
[Ad] Endereço:Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, Bonn, Germany.
[Ti] Título:RIG-I Resists Hypoxia-Induced Immunosuppression and Dedifferentiation.
[So] Source:Cancer Immunol Res;5(6):455-467, 2017 Jun.
[Is] ISSN:2326-6074
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A hypoxic tumor microenvironment is linked to poor prognosis. It promotes tumor cell dedifferentiation and metastasis and desensitizes tumor cells to type-I IFN, chemotherapy, and irradiation. The cytoplasmic immunoreceptor retinoic acid-inducible gene-I (RIG-I) is ubiquitously expressed in tumor cells and upon activation by 5'-triphosphate RNA (3pRNA) drives the induction of type I IFN and immunogenic cell death. Here, we analyzed the impact of hypoxia on the expression of RIG-I in various human and murine tumor and nonmalignant cell types and further investigated its function in hypoxic murine melanoma. 3pRNA-inducible RIG-I-expression was reduced in hypoxic melanoma cells compared with normoxic controls, a phenomenon that depended on the hypoxia-associated transcription factor HIF1α. Still, RIG-I functionality was conserved in hypoxic melanoma cells, whereas responsiveness to recombinant type-I IFN was abolished, due to hypoxia-induced loss of type I IFN receptor expression. Likewise, RIG-I activation in hypoxic melanoma cells, but not exposure to recombinant IFNα, provoked melanocyte antigen-specific CD8 T-cell and NK-cell attack. Scavenging of hypoxia-induced reactive oxygen species by vitamin C restored the inducible expression of RIG-I under hypoxia , boosted anti-melanoma NK- and CD8 T-cell attack, and augmented 3pRNA antitumor efficacy These results demonstrate that RIG-I remains operational under hypoxia and that RIG-I function is largely insensitive to lower cell surface expression of the IFNα receptor. RIG-I function could be fortified under hypoxia by the combined use of 3pRNA with antioxidants. .
[Mh] Termos MeSH primário: Hipóxia/metabolismo
Tolerância Imunológica
Melanoma/metabolismo
Receptores do Ácido Retinoico/metabolismo
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Ácido Ascórbico/farmacologia
Linhagem Celular
Linhagem Celular Tumoral
Feminino
Técnicas de Inativação de Genes
Seres Humanos
Camundongos Endogâmicos C57BL
RNA/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Receptores do Ácido Retinoico/genética
Baço/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (RARRES3 protein, human); 0 (Reactive Oxygen Species); 0 (Receptors, Retinoic Acid); 63231-63-0 (RNA); PQ6CK8PD0R (Ascorbic Acid)
[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:170505
[St] Status:MEDLINE
[do] DOI:10.1158/2326-6066.CIR-16-0129-T


  3 / 6810 MEDLINE  
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[PMID]:29317620
[Au] Autor:Blum CF; Heramvand N; Khonsari AS; Kollmann M
[Ad] Endereço:Institute for Mathematical Modeling of Biological Systems, Heinrich-Heine University of Düsseldorf, Universitätsstraße 1, 40225, Düsseldorf, Germany.
[Ti] Título:Experimental noise cutoff boosts inferability of transcriptional networks in large-scale gene-deletion studies.
[So] Source:Nat Commun;9(1):133, 2018 01 09.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Generating a comprehensive map of molecular interactions in living cells is difficult and great efforts are undertaken to infer molecular interactions from large-scale perturbation experiments. Here, we develop the analytical and numerical tools to quantify the fundamental limits for inferring transcriptional networks from gene knockout screens and introduce a network inference method that is unbiased with respect to measurement noise and scalable to large network sizes. We show that network asymmetry, knockout coverage and measurement noise are central determinants that limit prediction accuracy, whereas the knowledge about gene-specific variability among biological replicates can be used to eliminate noise-sensitive nodes and thereby boost the performance of network inference algorithms.
[Mh] Termos MeSH primário: Algoritmos
Biologia Computacional/métodos
Deleção de Genes
Redes Reguladoras de Genes
[Mh] Termos MeSH secundário: Perfilação da Expressão Gênica
Técnicas de Inativação de Genes/métodos
Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Saccharomyces cerevisiae Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02489-x


  4 / 6810 MEDLINE  
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[PMID]:29231924
[Au] Autor:Sakamoto T; Yoshiki M; Sakamoto H
[Ad] Endereço:Ushimado Marine Institute, Faculty of Science, Okayama University, Setouchi 701-4303, Japan.
[Ti] Título:The mineralocorticoid receptor knockout in medaka is further validated by glucocorticoid receptor compensation.
[So] Source:Sci Data;4:170189, 2017 12 12.
[Is] ISSN:2052-4463
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To study the critical role of mineralocorticoid signalling, we generated a constitutive mineralocorticoid receptor (MR)-knockout (KO) medaka as the first adult-viable MR-KO animal. This KO medaka displayed abnormal behaviours affected by visual stimuli. In contrast, the loss of MR did not result in overt phenotypic changes in osmoregulation, despite the well-known osmoregulatory functions of MR in mammals. Since glucocorticoid receptor (GR) has been suggested to compensate for loss of MR, we examined expression of duplicated GRs with markedly different ligand sensitivities, in various tissues. qRT-PCR results revealed that the absence of MR induced GR1 in the brain and eyes, but not in osmoregulatory organs. This reinforces the important functions of glucocorticoid signalling, but the minor role of mineralocorticoid signalling, in fish osmoregulation. Because both 11-deoxycorticosterone (DOC) and cortisol are ligands for MR, whereas GRs are specific to cortisol, GR1 signalling may compensate for the absence of cortisol-MR, rather than that of DOC-MR. Thus, this GR expression suggests that our MR-KO model can be used specifically to characterize DOC-MR signalling.
[Mh] Termos MeSH primário: Oryzias/metabolismo
Receptores de Glucocorticoides/metabolismo
Receptores de Mineralocorticoides/genética
[Mh] Termos MeSH secundário: Animais
Técnicas de Inativação de Genes
Oryzias/genética
[Pt] Tipo de publicação:DATASET; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Glucocorticoid); 0 (Receptors, Mineralocorticoid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1038/sdata.2017.189


  5 / 6810 MEDLINE  
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[PMID]:27776915
[Au] Autor:Mendler M; Riedinger C; Schlotterer A; Volk N; Fleming T; Herzig S; Nawroth PP; Morcos M
[Ad] Endereço:Department of Medicine 1 and Clinical Chemistry, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany. Electronic address: michael.mendler@med.uni-heidelberg.de.
[Ti] Título:Reduction in ins-7 gene expression in non-neuronal cells of high glucose exposed Caenorhabditis elegans protects from reactive metabolites, preserves neuronal structure and head motility, and prolongs lifespan.
[So] Source:J Diabetes Complications;31(2):304-310, 2017 Feb.
[Is] ISSN:1873-460X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Glucose derived metabolism generates reactive metabolites affecting the neuronal system and lifespan in C. elegans. Here, the role of the insulin homologue ins-7 and its downstream effectors in the generation of high glucose induced neuronal damage and shortening of lifespan was studied. RESULTS: In C. elegans high glucose conditions induced the expression of the insulin homologue ins-7. Abrogating ins-7 under high glucose conditions in non-neuronal cells decreased reactive oxygen species (ROS)-formation and accumulation of methylglyoxal derived advanced glycation endproducts (AGEs), prevented structural neuronal damage and normalised head motility and lifespan. The restoration of lifespan by decreased ins-7 expression was dependent on the concerted action of sod-3 and glod-4 coding for the homologues of iron-manganese superoxide dismutase and glyoxalase 1, respectively. CONCLUSIONS: Under high glucose conditions mitochondria-mediated oxidative stress and glycation are downstream targets of ins-7. This impairs the neuronal system and longevity via a non-neuronal/neuronal crosstalk by affecting sod-3 and glod-4, thus giving further insight into the pathophysiology of diabetic complications.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/antagonistas & inibidores
Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Glucose/envenenamento
Lactoilglutationa Liase/metabolismo
Estresse Oxidativo
Hormônios Peptídicos/antagonistas & inibidores
Superóxido Dismutase/metabolismo
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Caenorhabditis elegans/enzimologia
Caenorhabditis elegans/crescimento & desenvolvimento
Proteínas de Caenorhabditis elegans/agonistas
Proteínas de Caenorhabditis elegans/genética
Retroalimentação Fisiológica
Técnicas de Silenciamento de Genes
Técnicas de Inativação de Genes
Produtos Finais de Glicação Avançada/metabolismo
Lactoilglutationa Liase/antagonistas & inibidores
Lactoilglutationa Liase/genética
Longevidade
Mutação
Neuroproteção
Concentração Osmolar
Hormônios Peptídicos/agonistas
Hormônios Peptídicos/genética
Hormônios Peptídicos/metabolismo
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/antagonistas & inibidores
Superóxido Dismutase/genética
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Glycation End Products, Advanced); 0 (Ins-7 protein, C elegans); 0 (Peptide Hormones); 0 (Reactive Oxygen Species); EC 1.15.1.1 (Sod-3 protein, C elegans); EC 1.15.1.1 (Superoxide Dismutase); EC 4.4.1.5 (Lactoylglutathione Lyase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  6 / 6810 MEDLINE  
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[PMID]:28449103
[Au] Autor:Li H; Pei W; Vergarajauregui S; Zerfas PM; Raben N; Burgess SM; Puertollano R
[Ad] Endereço:Cell Biology and Physiology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
[Ti] Título:Novel degenerative and developmental defects in a zebrafish model of mucolipidosis type IV.
[So] Source:Hum Mol Genet;26(14):2701-2718, 2017 07 15.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mucolipidosis type IV (MLIV) is a lysosomal storage disease characterized by neurologic and ophthalmologic abnormalities. There is currently no effective treatment. MLIV is caused by mutations in MCOLN1, a lysosomal cation channel from the transient receptor potential (TRP) family. In this study, we used genome editing to knockout the two mcoln1 genes present in Danio rerio (zebrafish). Our model successfully reproduced the retinal and neuromuscular defects observed in MLIV patients, indicating that this model is suitable for studying the disease pathogenesis. Importantly, our model revealed novel insights into the origins and progression of the MLIV pathology, including the contribution of autophagosome accumulation to muscle dystrophy and the role of mcoln1 in embryonic development, hair cell viability and cellular maintenance. The generation of a MLIV model in zebrafish is particularly relevant given the suitability of this organism for large-scale in vivo drug screening, thus providing unprecedented opportunities for therapeutic discovery.
[Mh] Termos MeSH primário: Mucolipidoses/genética
Canais de Receptores Transientes de Potencial/genética
Proteínas de Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Autofagossomos/metabolismo
Modelos Animais de Doenças
Técnicas de Inativação de Genes
Mucolipidoses/metabolismo
Mucolipidoses/patologia
Mutação
Canais de Receptores Transientes de Potencial/metabolismo
Peixe-Zebra
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (MCOLN1.1 protein, zebrafish); 0 (Transient Receptor Potential Channels); 0 (Zebrafish Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180225
[Lr] Data última revisão:
180225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx158


  7 / 6810 MEDLINE  
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[PMID]:29365376
[Au] Autor:Fang Y; Xu C; Li DW; Wang ZL; Zhang L; Wu P; Wang ZZ; Du H; Li WF; Liao ZS
[Ad] Endereço:First Clinical Institute, Wenzhou Medical University, Wenzhou 325000, China.
[Ti] Título:[Tumor-secreted vascular endothelial growth factor A increases the pulmonary metastasis from nasopharyngeal carcinoma].
[So] Source:Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi;53(1):27-33, 2018 Jan 07.
[Is] ISSN:1673-0860
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Vascular endothelial growth factor A (VEGFA) was investigated as the key protein which might promote the specific metastasis progress of nasopharyngeal carcinoma. Sixteen specimens of pulmonary metastasis carcinoma and counterparts in primary nasopharyngeal carcinoma tissue were collected from patients. The expression of VEGFA through immunohistochemistry was investigated.VEGFA was knocked down by siRNA in two cell lines of nasopharyngeal carcinoma (CNE-1 and 5-8F), MTT and Transwell test were used to explore the role of VEGFA in praxiology. Then shRNA was used to cultivate the stable CNE-1 cell line with down-regulated-expression of VEGFA. The nude mice models were built through tail vein injection of specific nasopharyngeal carcinoma cells, and lungs were collected to perform further metastasis analysis. Previous genetic studies showed that VEGFA had higher expression in metastasis tissue, and the result was validated in the present study using immunohistochemistry. The percentage of positive cells was 84.8% in pulmonary metastasis group, 51.5% in primary tissue group ( =8.639, <0.05), average optical density was 0.154 in pulmonary metastasis group, 0.061 in primary tissue group ( =18.791, <0.05). Low expression of VEGFA inhibited cell viability of optical density value of CNE-1 in siRNA gourp was 0.715, 0.902 in control group ( =7.274, <0.05); 5-8F in siRNA group was 0.715, 0.935 in control group ( =7.751, <0.05). Number counting suppressed migration of CNE-1 in siRNA group was 52 per high-power lens, 124 per high-power lens in control group ( =29.380, <0.05), 5-8F in siRNA group was 65 per high-power lens, 155 per high-power lens in control group ( =18.181, <0.05). Number counting invasion of CNE-1 in siRNA gourp was 38 per high-power lens, 86 per high-power lens in control group ( =27.665, <0.05), 5-8F in siRNA group was 52 per high-power lens, 116 per high-power lens in control group ( =40.972, <0.05) in vitro. Furthermore, knock-down of VEGFA in nasopharyngeal carcinoma reduced the pulmonary metastasis . Number counting of tumor volumes in shRNA group was 2.4, and 11.0 in control group ( =6.143, <0.05); average optical density of immunohistochemistry in shRNA group was 0.033, and 0.176 in control group ( =15.734, <0.05). Results above reveal the overexpression of VEGFA in nasopharyngeal carcinoma can facilitate the pulmonary metastasis. Targeting VEGFA may provide a new biomarker of clinical study.
[Mh] Termos MeSH primário: Carcinoma/secundário
Carcinoma/secreção
Neoplasias Pulmonares/secundário
Neoplasias Nasofaríngeas/patologia
Neoplasias Nasofaríngeas/secreção
Fator A de Crescimento do Endotélio Vascular/secreção
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo
Técnicas de Inativação de Genes
Seres Humanos
Imuno-Histoquímica
Camundongos
Camundongos Nus
RNA Interferente Pequeno
Fator A de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1673-0860.2018.01.006


  8 / 6810 MEDLINE  
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[PMID]:29339069
[Au] Autor:Liu H; Sui T; Liu D; Liu T; Chen M; Deng J; Xu Y; Li Z
[Ad] Endereço:Jilin Provincial Key Laboratory of Animal Embryo Engineering, Jilin University, Changchun 130062, China.
[Ti] Título:Multiple homologous genes knockout (KO) by CRISPR/Cas9 system in rabbit.
[So] Source:Gene;647:261-267, 2018 Mar 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The CRISPR/Cas9 system is a highly efficient and convenient genome editing tool, which has been widely used for single or multiple gene mutation in a variety of organisms. Disruption of multiple homologous genes, which have similar DNA sequences and gene function, is required for the study of the desired phenotype. In this study, to test whether the CRISPR/Cas9 system works on the mutation of multiple homologous genes, a single guide RNA (sgRNA) targeting three fucosyltransferases encoding genes (FUT1, FUT2 and SEC1) was designed. As expected, triple gene mutation of FUT1, FUT2 and SEC1 could be achieved simultaneously via a sgRNA mediated CRISPR/Cas9 system. Besides, significantly reduced serum fucosyltransferases enzymes activity was also determined in those triple gene mutation rabbits. Thus, we provide the first evidence that multiple homologous genes knockout (KO) could be achieved efficiently by a sgRNA mediated CRISPR/Cas9 system in mammals, which could facilitate the genotype to phenotype studies of homologous genes in future.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas/genética
Mutação/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Repetições Palindrômicas Curtas Agrupadas e Regularmente Espaçadas/genética
Fucosiltransferases/genética
Técnicas de Inativação de Genes/métodos
Fenótipo
RNA Guia/genética
Coelhos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Guide); EC 2.4.1.- (Fucosyltransferases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


  9 / 6810 MEDLINE  
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[PMID]:28465214
[Au] Autor:Guo J; Wang Y; Li B; Huang S; Chen Y; Guo X; Xiao D
[Ad] Endereço:Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education College of Biotechnology, Tianjin University of Science Technology, Tianjin, 300457, China.
[Ti] Título:Development of a one-step gene knock-out and knock-in method for metabolic engineering of Aureobasidium pullulans.
[So] Source:J Biotechnol;251:145-150, 2017 Jun 10.
[Is] ISSN:1873-4863
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Aureobasidium pullulans is an increasingly attractive host for bio-production of pullulan, heavy oil, polymalic acid, and a large spectrum of extracellular enzymes. To date, genetic manipulation of A. pullulans mainly relies on time-consuming conventional restriction enzyme digestion and ligation methods. In this study, we present a one-step homologous recombination-based method for rapid genetic manipulation in A. pullulans. Overlaps measuring >40bp length and 10µg DNA segments for homologous recombination provided maximum benefits to transformation of A. pullulans. This optimized method was successfully applied to PKSIII gene (encodes polyketide synthase) knock-out and gltP gene (encodes glycolipid transfer protein) knock-in. After disruption of PKSIII gene, secretion of melanin decreased slightly. The melanin purified from disruptant showed lower reducing capacity compared with that of the parent strain, leading to a decrease in exopolysaccharide production. Knock-in of gltP gene resulted in at least 4.68-fold increase in heavy oil production depending on the carbon source used, indicating that gltP can regulate heavy oil synthesis in A. pullulans.
[Mh] Termos MeSH primário: Ascomicetos/genética
Ascomicetos/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Transporte/genética
Fermentação
Proteínas Fúngicas/metabolismo
Técnicas de Introdução de Genes
Técnicas de Inativação de Genes
Genes Fúngicos
Glucose/metabolismo
Melaninas/metabolismo
Engenharia Metabólica
Policetídeo Sintases/genética
Recombinação Genética
Xilose/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Fungal Proteins); 0 (Melanins); 0 (lipid transfer protein); 79956-01-7 (Polyketide Synthases); A1TA934AKO (Xylose); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:27777774
[Au] Autor:Van Der Kraak L; Goel G; Ramanan K; Kaltenmeier C; Zhang L; Normolle DP; Freeman GJ; Tang D; Nason KS; Davison JM; Luketich JD; Dhupar R; Lotze MT
[Ad] Endereço:Department of Cardiothoracic Surgery, University of Pittsburgh, Pittsburgh, PA USA.
[Ti] Título:5-Fluorouracil upregulates cell surface B7-H1 (PD-L1) expression in gastrointestinal cancers.
[So] Source:J Immunother Cancer;4:65, 2016.
[Is] ISSN:2051-1426
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Resistance to chemotherapy is a major obstacle in the effective treatment of cancer patients. B7-homolog 1, also known as programmed death ligand-1 (PD-L1), is an immunoregulatory protein that is overexpressed in several human cancers. Interaction of B7-H1 with programmed death 1 (PD-1) prevents T-cell activation and proliferation, sequestering the T-cell receptor from the cell membrane, inducing T-cell apoptosis, thereby leading to cancer immunoresistance. B7-H1 upregulation contributes to chemoresistance in several types of cancer, but little is known with respect to changes associated with 5-fluorouracil (5-FU) or gastrointestinal cancers. METHODS: HCT 116 p53 , HCT 116 p53 colorectal cancer (CRC) and OE33 esophageal adenocarcinoma (EAC) cells were treated with increasing doses of 5-FU (0.5 uM, 5 uM, 50 uM, 500 uM) or interferon gamma (IFN-γ, 10 ng/mL) in culture for 24 h and B7-H1 expression was quantified using flow cytometry and western blot analysis. We also evaluated B7-H1 expression, by immunohistochemistry, in tissue collected prior to and following neoadjuvant therapy in 10 EAC patients. RESULTS: B7-H1 expression in human HCT 116 p53 and HCT 116 p53 CRC cells lines, while low at baseline, can be induced by treatment with 5-FU. OE33 baseline B7-H1 expression exceeded CRC cell maximal expression and could be further increased in a dose dependent manner following 5-FU treatment in the absence of immune cells. We further demonstrate tumor B7-H1 expression in esophageal adenocarcinoma patient-derived pre-treatment biopsies. While B7-H1 expression was not enhanced in post-treatment esophagectomy specimens, this may be due to the limits of immunohistochemical quantification. CONCLUSIONS: B7-H1/PD-L1 expression can be increased following treatment with 5-FU in gastrointestinal cancer cell lines, suggesting alternative mechanisms to classic immune-mediated upregulation. This suggests that combining 5-FU treatment with PD-1/B7-H1 blockade may improve treatment in patients with gastrointestinal adenocarcinoma.
[Mh] Termos MeSH primário: Antimetabólitos Antineoplásicos/farmacologia
Antígeno B7-H1/metabolismo
Membrana Celular/metabolismo
Fluoruracila/farmacologia
Neoplasias Gastrointestinais/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Antígeno B7-H1/genética
Esôfago de Barrett/genética
Esôfago de Barrett/metabolismo
Esôfago de Barrett/patologia
Biópsia
Linhagem Celular Tumoral
Neoplasias Esofágicas/genética
Neoplasias Esofágicas/metabolismo
Neoplasias Esofágicas/patologia
Citometria de Fluxo
Neoplasias Gastrointestinais/tratamento farmacológico
Neoplasias Gastrointestinais/genética
Neoplasias Gastrointestinais/patologia
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Técnicas de Inativação de Genes
Seres Humanos
Imuno-Histoquímica
Interferon gama/farmacologia
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (Tumor Suppressor Protein p53); 82115-62-6 (Interferon-gamma); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1186/s40425-016-0163-8



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