Only in Titles

           Search results for: Mouse Anti-Simian Virus 5   

paperclip

#29031073   2017/10/14 Save this To Up

Discovery of novel diarylpyrazolylquinoline derivatives as potent anti-dengue virus agents.

A number of diarylpyrazolylquinoline derivatives were synthesized and evaluated for their anti-dengue virus (DENV) activity. Among them, 6-fluoro-2-(1-(4-fluorophenyl)-3- (4-methoxyphenyl)-1H-pyrazol-5-yl)quinoline (11c), 2-[1,3-bis(4-methoxyphenyl)-1H-pyrazol- 5-yl]-6-fluoroquinoline (12c), and 4-[5-(6-fluoroquinolin-2-yl)-3-(4-methoxyphenyl)-1H-pyrazol- 1-yl]benzenesulfonamide (13c) exhibited approximately 10-folds more active anti-DENV-2 activity (IC50 of 1.36, 1.09 and 0.81 μM, respectively) than that of ribavirin (IC50 = 12.61 μM). Compound 13c was also potent inhibited other sero-types of DENV. It reduced DENV replication in both viral protein and mRNA levels, and no significant cell cytotoxicity was detected, with greater than 50% viability of Huh-7-DV-Fluc cells at a concentration of 200 μM. Furthermore, compound 13c can effectively protect mice from DENV infection by reducing disease symptoms and mortality of DENV-infected mice. It represents a potential antiviral agent to block DENV replication in vitro and in vivo. Structural optimization of the initial lead compound, 13c, and the detailed molecular mechanism of action are ongoing.

2722 related Products with: Discovery of novel diarylpyrazolylquinoline derivatives as potent anti-dengue virus agents.

Mouse Anti-Dengue Virus A Mouse Anti-Dengue Virus A Mouse Anti-Dengue Virus T Anti-Dengue Virus Antibod Anti Dengue Virus anti Adenovirus E11 IgG2a anti Adenovirus C11 IgG2a Viral antibodies, anti-R anti Rotavirus p42 IgG2a anti TGE IgG1 (monoclonal Monoclonal antibody Anti anti CD16 monoclonal anti

Related Pathways

paperclip

#29030319   2017/10/14 Save this To Up

Coordination of different complexes to copper(II) and cobalt(III) metal centers enhances Zika virus and dengue virus loads in both arthropod cells and human keratinocytes.

Trace elements such as copper and cobalt have been associated with virus-host interactions. However, studies to show the effect of conjugation of copper(II) or cobalt(III) metal centers to thiosemicarbazone ligand(s) derived from either food additives or mosquito repellent such as 2-acetylethiazole or citral, respectively, on Zika virus (ZIKV) or dengue virus (serotype 2; DENV2) infections have not been explored. In this study, we show that four compounds comprising of thiosemicarbazone ligand derived from 2-acetylethiazole viz., (E)-N-ethyl-2-[1-(thiazol-2-yl)ethylidene]hydrazinecarbothioamide (acetylethTSC) (compound 1), a copper(II) complex with acetylethTSC as a ligand (compound 2), a thiosemicarbazone ligand-derived from citral (compound 3) and a cobalt(III) complex with a citral-thiosemicarbazone ligand- (compound 4) increased DENV2 and ZIKV replication in both mosquito C6/36 cells and human keratinocytes (HaCaT cells). Treatment of both cell lines with compounds 2 or 4 showed increased dengue viral titers at all three tested doses. Enhanced dengue viral plaque formation was also noted at the tested dose of 100μM, suggesting higher production of infectious viral particles. Treatment with the compounds 2 or 4 enhanced ZIKV and DENV2 RNA levels in HeLa cell line and primary cultures of mouse bone marrow derived dendritic cells. Also, pre- or post treatments with conjugated compound 2 or 4 showed higher loads of ZIKV or DENV2 envelope (E) protein in HaCaT cells. No changes in loads of E-protein were found in ZIKV-infected C6/36 cells, when compounds were treated after infection. In addition, we tested bis(1,10-phenanthroline)copper(II) chloride ([Cu(phen)2]Cl2, (compound 5) and tris(1,10-phenanthroline)cobalt(III) chloride ([Co(phen)3]Cl3, (compound 6) that also showed enhanced DENV2 loads. Also, we found that copper(II) chloride dehydrate (CuCl2·2H2O) or cobalt(II) chloride hexahydrate (CoCl2·6H2O) alone had no effects as "free" cations. Taken together, these findings suggest that use of Cu(II) or Co(III) conjugation to organic compounds, in insect repellents and/or food additives could enhance DENV2/ZIKV loads in human cells and perhaps induce pathogenesis in infected individuals or individuals pre-exposed to such conjugated complexes.

1034 related Products with: Coordination of different complexes to copper(II) and cobalt(III) metal centers enhances Zika virus and dengue virus loads in both arthropod cells and human keratinocytes.

Human Epstein-Barr Virus Rabbit Anti-Human Androge Rabbit Anti-Human Androge Macrophage Colony Stimula Macrophage Colony Stimula Rabbit Anti-Human Androge Goat Anti-Human Androgen CAR,CAR,Constitutive acti Dengue Virus General type FIV Core Ag, recombinant Recombinant Human Androge Avian Influenza virus H5N

Related Pathways

paperclip

#29023813   2017/10/12 Save this To Up

Dual catenin loss in murine liver causes tight junctional deregulation and progressive intrahepatic cholestasis.

β-Catenin, the downstream effector of the Wnt signaling, plays important roles in hepatic development, regeneration and tumorigenesis. However, its role at hepatocyte adherens junctions (AJ) is relatively poorly understood, chiefly due to spontaneous compensation by γ-catenin. Here, we simultaneously ablate β- and γ-catenin expression in mouse liver by interbreeding β-catenin-γ-catenin double-floxed mice and albumin-cre transgenic mice. Double knockout mice (DKO) show failure to thrive, impaired hepatocyte differentiation, cholemia, ductular reaction, progressive cholestasis, inflammation, fibrosis and tumorigenesis, which was associated with deregulation of tight junctions (TJ) and bile acid transporters, leading to early morbidity and mortality, a phenotype reminiscent of Progressive Familial Intrahepatic Cholestasis (PFIC). To address the mechanism, we specifically and temporally eliminated both catenins from hepatocytes using adeno-associated virus-8 carrying cre-recombinase under the thyroid-binding globulin promoter (AAV8-TBG-Cre). This led to a time-dependent breach of blood bile barrier associated with sequential disruption of AJ and TJ verified by ultrastructural imaging and intravital microscopy, which revealed unique para-cellular leaks around individual hepatocytes allowing mixing of blood and bile, and leakage of blood from one sinusoid to another. Molecular analysis identified sequential losses of E-cadherin, occludin, claudin-3 and claudin-5 due to enhanced proteasomal degradation, and of claudin-2, a β-catenin transcriptional target, which was also validated in vitro. In conclusion, we report partially redundant function of catenins at AJ in regulating TJ and contributing to blood bile barrier. Furthermore, concomitant hepatic loss of β- and γ-catenin disrupts structural and functional integrity of AJ and TJ via transcriptional and posttranslational mechanisms. Mice with dual catenin loss develop progressive intrahepatic cholestasis, and hence provides a unique model to study diseases like PFIC. This article is protected by copyright. All rights reserved.

1026 related Products with: Dual catenin loss in murine liver causes tight junctional deregulation and progressive intrahepatic cholestasis.

Alkaline Phospatase (ALP) Zearalenone Mycotoxins EL Liver disease spectrum ti Liver carcinoma and norma Liver carcinoma and norma Liver carcinoma and norma Colon cancer, metastasize Goat Anti-Human Catenin a Goat Anti-Human Dual oxid GI cancer (esophageal, ga AccuPower DualStar qPCR P AccuPower DualStar qPCR P

Related Pathways

paperclip

#29022386   2017/10/12 Save this To Up

Bacillus toyonensis improves immune response in the mice vaccinated with recombinant antigen of bovine herpesvirus type 5.

Probiotics modulate the immune response and can increase the effectiveness of vaccines. Bacillus toyonensis is widely used as a probiotic in animal feed. The aim of this study was to assess the effects of B. toyonensis administration on the immune response to an experimental recombinant vaccine against bovine herpesvirus type 5 (BoHV-5) in mice. Mice were vaccinated with BoHV-5 recombinant glycoprotein D and supplemented with the probiotic B. toyonensis in two regimes: one group received the probiotic only during seven days prior to the initial vaccination while the second group was given the probiotic throughout the experimental period of seven weeks. Animals supplemented with probiotic B. toyonensis in two regimes showed an increase in total immunoglobulin (Ig)G, IgG1 and IgG2a levels in serum, in addition to higher titres of antibodies capable of neutralising the BoHV-5 virus than non-supplemented animals (P<0.05). Splenocytes from the supplemented mice had higher mRNA transcription levels of cytokines interleukin (IL)-4 and IL-12. These results show that the use of this probiotic may significantly contribute to the response elicited by recombinant vaccines, especially those that rely on increasing antibody and cell-mediated immune responses for efficacy. Further, the data support an immunomodulatory effect for probiotic B. toyonensis and imply that enhance effect on the immune response against a BoHV-5 recombinant vaccine in mice.

1445 related Products with: Bacillus toyonensis improves immune response in the mice vaccinated with recombinant antigen of bovine herpesvirus type 5.

Recombinant Chikungunya W Bovine prolactin-induced Recombinant Hemagglutinin Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant

Related Pathways

paperclip

#29021303   2017/10/12 Save this To Up

A single intramuscular dose of a plant-made virus-like-particle vaccine elicits a balanced humoral and cellular response and protects young and aged mice from influenza H1N1 challenge despite a modest/absent humoral response.

Background: Virus-like-particle (VLP) influenza vaccines can be given intramuscularly (IM) or intranasally (IN) and may have advantages over split-virion formulations in the elderly. We tested a plant-made VLP vaccine candidate bearing the viral hemagglutinin (HA) delivered either IM or IN in young and aged mice. Methods: Young adult (5-8 weeks) and aged (16-20 months) female BALB/c mice received a single 3μg dose based on HA (A/California/07/2009 H1N1) content of a plant-made H1-VLP (IM or IN), split-virion vaccine (IM) or left naïve. After vaccination, humoral and splenocyte responses were assessed and some mice were challenged. Results: Both VLP and split vaccines given IM protected 100% of the young animals but the VLP group lost the least weight, and had stronger humoral and cellular responses. Compared to split vaccine recipients, aged animals vaccinated IM with VLP were more likely to survive challenge (80% vs. 60%). Lung viral load post-challenge was lowest in the VLP IM groups. Mice vaccinated with VLP IN made little detectable immune responses but survival was significantly increased. Conclusion: In both age groups, IM administration of the H1-VLP vaccine elicited more balanced humoral and cellular responses and provided better protection from homologous challenge than the split-virion vaccine.

2370 related Products with: A single intramuscular dose of a plant-made virus-like-particle vaccine elicits a balanced humoral and cellular response and protects young and aged mice from influenza H1N1 challenge despite a modest/absent humoral response.

CAR,CAR,Constitutive acti Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac 5α-N-Acetyl-2'H-androst- 5α-N-Acetyl-2'H-androst-

Related Pathways

paperclip

#29019980   2017/10/11 Save this To Up

Radically truncated MeCP2 rescues Rett syndrome-like neurological defects.

Heterozygous mutations in the X-linked MECP2 gene cause the neurological disorder Rett syndrome. The methyl-CpG-binding protein 2 (MeCP2) protein is an epigenetic reader whose binding to chromatin primarily depends on 5-methylcytosine. Functionally, MeCP2 has been implicated in several cellular processes on the basis of its reported interaction with more than 40 binding partners, including transcriptional co-repressors (for example, the NCoR/SMRT complex), transcriptional activators, RNA, chromatin remodellers, microRNA-processing proteins and splicing factors. Accordingly, MeCP2 has been cast as a multi-functional hub that integrates diverse processes that are essential in mature neurons. At odds with the concept of broad functionality, missense mutations that cause Rett syndrome are concentrated in two discrete clusters coinciding with interaction sites for partner macromolecules: the methyl-CpG binding domain and the NCoR/SMRT interaction domain. Here we test the hypothesis that the single dominant function of MeCP2 is to physically connect DNA with the NCoR/SMRT complex, by removing almost all amino-acid sequences except the methyl-CpG binding and NCoR/SMRT interaction domains. We find that mice expressing truncated MeCP2 lacking both the N- and C-terminal regions (approximately half of the native protein) are phenotypically near-normal; and those expressing a minimal MeCP2 additionally lacking a central domain survive for over one year with only mild symptoms. This minimal protein is able to prevent or reverse neurological symptoms when introduced into MeCP2-deficient mice by genetic activation or virus-mediated delivery to the brain. Thus, despite evolutionary conservation of the entire MeCP2 protein sequence, the DNA and co-repressor binding domains alone are sufficient to avoid Rett syndrome-like defects and may therefore have therapeutic utility.

1725 related Products with: Radically truncated MeCP2 rescues Rett syndrome-like neurological defects.

MECP2 oral-facial-digital syndr Goat Anti-Human Wiskott-A Rabbit Anti-Toxic Shock S Rabbit Anti-Toxic Shock S

Related Pathways

paperclip

#29016934   2017/10/10 Save this To Up

microRNA-7 upregulates death receptor 5 and primes resistant brain tumors to caspase-mediated apoptosis.

MicroRNAs (miRs) are known to play a pivotal role in tumorigenesis, controlling cell proliferation and apoptosis. In this study, we investigated the potential of miR-7 to prime resistant tumor cells to apoptosis in glioblastoma (GBM).

1604 related Products with: microRNA-7 upregulates death receptor 5 and primes resistant brain tumors to caspase-mediated apoptosis.

Androgen Receptor (Phosph Androgen Receptor (Phosph Androgen Receptor (Ab 650 PDGF Receptor â (Ab 751) AZD-3514 Mechanisms: Andr ∆2-Androstene-1α,17β- Androst-16-en-3-ol C19H30 (5α)-Androst-2-en-17-one (5α)-Androstane-3,11,17- 4-Benzyloxy-3-methoxy-tol p Toluenesulfinic acid so Cell Strainers 70μm Cell

Related Pathways

paperclip

#28993710   2017/10/10 Save this To Up

Dose-dependent expression of claudin-5 is a modifying factor in schizophrenia.

Schizophrenia is a neurodevelopmental disorder that affects up to 1% of the general population. Various genes show associations with schizophrenia and a very weak nominal association with the tight junction protein, claudin-5, has previously been identified. Claudin-5 is expressed in endothelial cells forming part of the blood-brain barrier (BBB). Furthermore, schizophrenia occurs in 30% of individuals with 22q11 deletion syndrome (22q11DS), a population who are haploinsufficient for the claudin-5 gene. Here, we show that a variant in the claudin-5 gene is weakly associated with schizophrenia in 22q11DS, leading to 75% less claudin-5 being expressed in endothelial cells. We also show that targeted adeno-associated virus-mediated suppression of claudin-5 in the mouse brain results in localized BBB disruption and behavioural changes. Using an inducible 'knockdown' mouse model, we further link claudin-5 suppression with psychosis through a distinct behavioural phenotype showing impairments in learning and memory, anxiety-like behaviour and sensorimotor gating. In addition, these animals develop seizures and die after 3-4 weeks of claudin-5 suppression, reinforcing the crucial role of claudin-5 in normal neurological function. Finally, we show that anti-psychotic medications dose-dependently increase claudin-5 expression in vitro and in vivo while aberrant, discontinuous expression of claudin-5 in the brains of schizophrenic patients post mortem was observed compared to age-matched controls. Together, these data suggest that BBB disruption may be a modifying factor in the development of schizophrenia and that drugs directly targeting the BBB may offer new therapeutic opportunities for treating this disorder.Molecular Psychiatry advance online publication, 10 October 2017; doi:10.1038/mp.2017.156.

1976 related Products with: Dose-dependent expression of claudin-5 is a modifying factor in schizophrenia.

Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Factor VlllC antibody, Mo Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep Rabbit Anti-factor VIII(F Rabbit Anti-Integrin beta Rabbit Anti-factor VIII(F Rabbit Anti-Integrin β2 Rabbit Anti-Integrin alph Rabbit Anti-Insulin Recep

Related Pathways

  •  
  • No related Items
paperclip

#28989973   2017/10/09 Save this To Up

Cloning, Assembly, and Modification of the Primary Human Cytomegalovirus Isolate Toledo by Yeast-Based Transformation-Associated Recombination.

Genetic engineering of cytomegalovirus (CMV) currently relies on generating a bacterial artificial chromosome (BAC) by introducing a bacterial origin of replication into the viral genome using in vivo recombination in virally infected tissue culture cells. However, this process is inefficient, results in adaptive mutations, and involves deletion of viral genes to avoid oversized genomes when inserting the BAC cassette. Moreover, BAC technology does not permit the simultaneous manipulation of multiple genome loci and cannot be used to construct synthetic genomes. To overcome these limitations, we adapted synthetic biology tools to clone CMV genomes in Saccharomyces cerevisiae. Using an early passage of the human CMV isolate Toledo, we first applied transformation-associated recombination (TAR) to clone 16 overlapping fragments covering the entire Toledo genome in Saccharomyces cerevisiae. Then, we assembled these fragments by TAR in a stepwise process until the entire genome was reconstituted in yeast. Since next-generation sequence analysis revealed that the low-passage-number isolate represented a mixture of parental and fibroblast-adapted genomes, we selectively modified individual DNA fragments of fibroblast-adapted Toledo (Toledo-F) and again used TAR assembly to recreate parental Toledo (Toledo-P). Linear, full-length HCMV genomes were transfected into human fibroblasts to recover virus. Unlike Toledo-F, Toledo-P displayed characteristics of primary isolates, including broad cellular tropism in vitro and the ability to establish latency and reactivation in humanized mice. Our novel strategy thus enables de novo cloning of CMV genomes, more-efficient genome-wide engineering, and the generation of viral genomes that are partially or completely derived from synthetic DNA. IMPORTANCE The genomes of large DNA viruses, such as human cytomegalovirus (HCMV), are difficult to manipulate using current genetic tools, and at this time, it is not possible to obtain, molecular clones of CMV without extensive tissue culture. To overcome these limitations, we used synthetic biology tools to capture genomic fragments from viral DNA and assemble full-length genomes in yeast. Using an early passage of the HCMV isolate Toledo containing a mixture of wild-type and tissue culture-adapted virus. we directly cloned the majority sequence and recreated the minority sequence by simultaneous modification of multiple genomic regions. Thus, our novel approach provides a paradigm to not only efficiently engineer HCMV and other large DNA viruses on a genome-wide scale but also facilitates the cloning and genetic manipulation of primary isolates and provides a pathway to generating entirely synthetic genomes.

1234 related Products with: Cloning, Assembly, and Modification of the Primary Human Cytomegalovirus Isolate Toledo by Yeast-Based Transformation-Associated Recombination.

Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Primary antibody BRCA1 ( Primary antibody eIF2β Primary antibody Histone Rabbit Anti-Human Androge Rabbit Anti-Human Androge Primary antibody NMDANR2 Primary antibody PKM1 An Primary antibody Keratin Primary antibody NAC1 An Primary antibody ABCA1 A

Related Pathways

paperclip

#28989018   2017/10/09 Save this To Up

Optimization of a Vaginal Suppository Formulation to Deliver SHetA2 as a Novel Treatment for Cervical Dysplasia.

Cervical dysplasia induced by the human papilloma virus (HPV) unpredictably progresses to cervical cancer. Therapeutic options are invasive and affect the patient's quality of life. SHetA2 has demonstrated therapeutic efficacy against human and murine HPV- induced tumors, but its oral bioavailability is <1%. An optimized vaginal suppository formulation can deliver SHetA2 in sufficient doses to prevent cervical dysplasia. The quality by design (QbD) approach was employed to optimize the suppository formulation consisting of cocoa butter as base with 5% Kolliphor and 40% SHetA2. The suppository had a content uniformity of 105.44±0.42%, melted in <8 minutes and had a complete release of SHetA2 in water. Administration of the suppository to mice achieved cervix concentrations that were significantly higher than the SHetA2 therapeutic concentration, with the maximum concentration (Cmax-cervix = 336.78 μg/g) being more than 100-fold the therapeutic SHetA2concentration. Furthermore, the levels of cyclin D1 protein decreased 9-fold indicating a correlation of drug concentrations with the pharmacodynamic endpoint. These proof-of-concept studies suggest that the SHetA2 optimized vaginal suppository formulation may have a potential use in the prevention of cervical dysplasia, but detailed efficacy studies are required to confirm this assumption.

1533 related Products with: Optimization of a Vaginal Suppository Formulation to Deliver SHetA2 as a Novel Treatment for Cervical Dysplasia.

Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri Glucose Assay With the La Cultrex In Vitro Angiogen ENZYMATIC ASSAY KITS (CH Endothelial Tube Formatio QuantiChrom™ Formaldehy QuantiChrom™ Formaldehy Human Antithrombin III to Human Plasminogen Total A Total Human tPA Functiona Total Human uPA Antigen A

Related Pathways

  •  
  • No related Items