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Native Antigen Inc denv2 ns1 hexamer

Phylogenetic tree of Taiwan <t>DENV2</t> strains from 1995 to 2015 based on the DENV2 <t>NS1</t> full-length sequence. The maximum likelihood phylogenetic tree was constructed using the IQ-TREE program with 1000 bootstrap replications. The sequences of DENV2 Taiwan strains from 1995 to 2014 were collected from GenBank while the 2015 DENV2 outbreak strains were previously sequenced with the Illumina Miseq platform . The 2015 Taiwan outbreak strains were marked in red, the Taiwan DENV2 strains from 1995 to 2014 were marked in orange, and the global reference strains were marked in black. Virus names were shown as country, accession number, and reported year of each sequence. Numbers on nodes were bootstrap support value exceeding 75%

Denv2 Ns1 Hexamer, supplied by Native Antigen Inc, used in various techniques. Bioz Stars score: 94/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/denv2 ns1 hexamer/product/Native Antigen Inc
Average 94 stars, based on 18 article reviews

denv2 ns1 hexamer - by Bioz Stars, 2026-05

94/100 stars

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1) Product Images from "A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway"

Article Title: A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway

Journal: Journal of Biomedical Science

doi: 10.1186/s12929-024-01116-4

Phylogenetic tree of Taiwan DENV2 strains from 1995 to 2015 based on the DENV2 NS1 full-length sequence. The maximum likelihood phylogenetic tree was constructed using the IQ-TREE program with 1000 bootstrap replications. The sequences of DENV2 Taiwan strains from 1995 to 2014 were collected from GenBank while the 2015 DENV2 outbreak strains were previously sequenced with the Illumina Miseq platform . The 2015 Taiwan outbreak strains were marked in red, the Taiwan DENV2 strains from 1995 to 2014 were marked in orange, and the global reference strains were marked in black. Virus names were shown as country, accession number, and reported year of each sequence. Numbers on nodes were bootstrap support value exceeding 75%

Figure Legend Snippet: Phylogenetic tree of Taiwan DENV2 strains from 1995 to 2015 based on the DENV2 NS1 full-length sequence. The maximum likelihood phylogenetic tree was constructed using the IQ-TREE program with 1000 bootstrap replications. The sequences of DENV2 Taiwan strains from 1995 to 2014 were collected from GenBank while the 2015 DENV2 outbreak strains were previously sequenced with the Illumina Miseq platform . The 2015 Taiwan outbreak strains were marked in red, the Taiwan DENV2 strains from 1995 to 2014 were marked in orange, and the global reference strains were marked in black. Virus names were shown as country, accession number, and reported year of each sequence. Numbers on nodes were bootstrap support value exceeding 75%

Techniques Used: Sequencing, Construct, Virus

Phylogenetic tree of DENV2 strains of Asian countries from 1995 to 2019 based on the DENV2 NS1 full-length sequence. The maximum likelihood phylogenetic tree was constructed using the IQ-TREE program with 1000 bootstrap replications. The sequences of DENV2 of Asian countries from 1995 to 2019 were collected from GenBank while the 2015 DENV2 outbreak strains were previously sequenced with the Illumina Miseq platform . The 2015 Taiwan outbreak strains were marked in red, the global reference strains were marked in black, and the DENV2 strains of Asian countries from the other countries were marked in different colors. Virus names were shown as country, accession number, and reported year of each sequence. Numbers on nodes were bootstrap support value exceeding 75%. TW: Taiwan; CN: China; IN: India; ID: Indonesia; SG: Singapore; MY: Malaysia; TH: Thailand; VN: Vietnam; PH: Philippines; KH: Cambodia; LA: Laos

Figure Legend Snippet: Phylogenetic tree of DENV2 strains of Asian countries from 1995 to 2019 based on the DENV2 NS1 full-length sequence. The maximum likelihood phylogenetic tree was constructed using the IQ-TREE program with 1000 bootstrap replications. The sequences of DENV2 of Asian countries from 1995 to 2019 were collected from GenBank while the 2015 DENV2 outbreak strains were previously sequenced with the Illumina Miseq platform . The 2015 Taiwan outbreak strains were marked in red, the global reference strains were marked in black, and the DENV2 strains of Asian countries from the other countries were marked in different colors. Virus names were shown as country, accession number, and reported year of each sequence. Numbers on nodes were bootstrap support value exceeding 75%. TW: Taiwan; CN: China; IN: India; ID: Indonesia; SG: Singapore; MY: Malaysia; TH: Thailand; VN: Vietnam; PH: Philippines; KH: Cambodia; LA: Laos

Techniques Used: Sequencing, Construct, Virus

K272R mutant virus replicated faster than WT virus in type I IFN producing cells. A Schematic diagram of NS1 amino acid mutations of Taiwan 2015 DENV2 outbreak strains. The red region represents the NS1 protein of DENV2. The stars indicate the amino acid substitutions isolated from the 2015 Taiwan dengue outbreak. B Production of DENV2-EGFP rg viruses containing each amino acid substitution in BHK-21 cells. The fluorescent images were captured under 10 × magnification of fluorescent microscope. C , D Growth kinetics of each rg virus in C A549 cells and D Vero cells. E Viral competition assay of each rg virus in Vero cells. Vero cells were infected with WT virus, mutant viruses or 1:1 mixture of WT and each mutant, then each group of viruses were passaged up to P5. Sanger sequencing was performed to determine the dominant variant at P1 and P5. All data are representative data from at least two independent experiments with comparable results and plotted as mean ± SEM with *p < 0.05 and ns, p > 0.05 by two-way ANOVA. WT: wildtype

Figure Legend Snippet: K272R mutant virus replicated faster than WT virus in type I IFN producing cells. A Schematic diagram of NS1 amino acid mutations of Taiwan 2015 DENV2 outbreak strains. The red region represents the NS1 protein of DENV2. The stars indicate the amino acid substitutions isolated from the 2015 Taiwan dengue outbreak. B Production of DENV2-EGFP rg viruses containing each amino acid substitution in BHK-21 cells. The fluorescent images were captured under 10 × magnification of fluorescent microscope. C , D Growth kinetics of each rg virus in C A549 cells and D Vero cells. E Viral competition assay of each rg virus in Vero cells. Vero cells were infected with WT virus, mutant viruses or 1:1 mixture of WT and each mutant, then each group of viruses were passaged up to P5. Sanger sequencing was performed to determine the dominant variant at P1 and P5. All data are representative data from at least two independent experiments with comparable results and plotted as mean ± SEM with *p < 0.05 and ns, p > 0.05 by two-way ANOVA. WT: wildtype

Techniques Used: Mutagenesis, Virus, Isolation, Microscopy, Competitive Binding Assay, Infection, Sequencing, Variant Assay

K272R mutant promoted higher secretion of soluble NS1. A , B A549 cells infected with K272R mutant or WT virus at or MOI 0.01 or MOI 0.1 for the indicated time points. C 293 T cells were transfected with 1 µg or 2 µg of plasmid overexpressing NS1-K272R or NS1-WT. A – C NS1 concentration in culture supernatants were measured by ELISA. All data are representative data from at least two independent experiments with ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05 and ns, p > 0.05 by two-way ANOVA

Figure Legend Snippet: K272R mutant promoted higher secretion of soluble NS1. A , B A549 cells infected with K272R mutant or WT virus at or MOI 0.01 or MOI 0.1 for the indicated time points. C 293 T cells were transfected with 1 µg or 2 µg of plasmid overexpressing NS1-K272R or NS1-WT. A – C NS1 concentration in culture supernatants were measured by ELISA. All data are representative data from at least two independent experiments with ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05 and ns, p > 0.05 by two-way ANOVA

Techniques Used: Mutagenesis, Infection, Virus, Transfection, Plasmid Preparation, Concentration Assay, Enzyme-linked Immunosorbent Assay

K272R amino acid substitution contributed to immune evasion from antiviral response. A – C A549 cells were infected with K272R mutant virus or WT virus at MOI 0.1 for 72 h followed by IFN-α treatment (1000 IU/mL) for 6 h. Quantitative RT-PCR analysis of ISGs (A) IFIT1 , (B) ISG15 , and C MxA were performed. D Immunoassay of extracts of 293 T cells transfected with 1 µg or 2 µg of plasmid overexpressing NS1-K272R or NS1-WT. (E–H) 293 T cells transfected with E , F 1 µg or G , H 2 µg of plasmids overexpressing NS1-K272R and NS1-WT, followed by IFN-α treatment (1000 IU/mL) for 6 h. Quantitative RT-PCR analysis of ISGs E , G IFIT1 and F , H ISG15 were performed. I , J STAT1 phosphorylation status was analyzed by western blot analysis. I A549 cells extracts with K272R mutant virus or WT virus infection at MOI 0.5 for 72 h and J 293 T cells were transfected with 2 µg of vector control, overexpressing NS1-WT and K272R mutant plasmids followed by IFN-α treatment (2000 IU/mL) for 1 h. The phosphorylated STAT1 protein expression was detected K A549 cells were infected with K272R mutant virus or WT virus at MOI 0.01 for 72 h and quantitative RT-PCR analysis of SOCS3 was performed. All data are representative data from at least two independent experiments with ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05 by one-way ANOVA. UT: untreated; VC: vector control

Figure Legend Snippet: K272R amino acid substitution contributed to immune evasion from antiviral response. A – C A549 cells were infected with K272R mutant virus or WT virus at MOI 0.1 for 72 h followed by IFN-α treatment (1000 IU/mL) for 6 h. Quantitative RT-PCR analysis of ISGs (A) IFIT1 , (B) ISG15 , and C MxA were performed. D Immunoassay of extracts of 293 T cells transfected with 1 µg or 2 µg of plasmid overexpressing NS1-K272R or NS1-WT. (E–H) 293 T cells transfected with E , F 1 µg or G , H 2 µg of plasmids overexpressing NS1-K272R and NS1-WT, followed by IFN-α treatment (1000 IU/mL) for 6 h. Quantitative RT-PCR analysis of ISGs E , G IFIT1 and F , H ISG15 were performed. I , J STAT1 phosphorylation status was analyzed by western blot analysis. I A549 cells extracts with K272R mutant virus or WT virus infection at MOI 0.5 for 72 h and J 293 T cells were transfected with 2 µg of vector control, overexpressing NS1-WT and K272R mutant plasmids followed by IFN-α treatment (2000 IU/mL) for 1 h. The phosphorylated STAT1 protein expression was detected K A549 cells were infected with K272R mutant virus or WT virus at MOI 0.01 for 72 h and quantitative RT-PCR analysis of SOCS3 was performed. All data are representative data from at least two independent experiments with ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05 by one-way ANOVA. UT: untreated; VC: vector control

Techniques Used: Infection, Mutagenesis, Virus, Quantitative RT-PCR, Transfection, Plasmid Preparation, Western Blot, Control, Expressing

Schematic diagram of effects of K272R amino acid substitution on the NS1 properties upon viral infection. During K272R mutant virus infection, the NS1-K272R inhibited the phosphorylation of STAT1 protein and downstream expression of ISGs to enhance the K272R mutant replication. Besides, the infection of K272R mutant virus induced more intense phosphorylation of p65 and higher secretion of pro-inflammatory cytokines which may be due to the higher production of sNS1

Figure Legend Snippet: Schematic diagram of effects of K272R amino acid substitution on the NS1 properties upon viral infection. During K272R mutant virus infection, the NS1-K272R inhibited the phosphorylation of STAT1 protein and downstream expression of ISGs to enhance the K272R mutant replication. Besides, the infection of K272R mutant virus induced more intense phosphorylation of p65 and higher secretion of pro-inflammatory cytokines which may be due to the higher production of sNS1

Techniques Used: Infection, Mutagenesis, Virus, Expressing

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Journal: Journal of Biomedical Science

Article Title: A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway

doi: 10.1186/s12929-024-01116-4

Figure Lengend Snippet: Phylogenetic tree of Taiwan DENV2 strains from 1995 to 2015 based on the DENV2 NS1 full-length sequence. The maximum likelihood phylogenetic tree was constructed using the IQ-TREE program with 1000 bootstrap replications. The sequences of DENV2 Taiwan strains from 1995 to 2014 were collected from GenBank while the 2015 DENV2 outbreak strains were previously sequenced with the Illumina Miseq platform . The 2015 Taiwan outbreak strains were marked in red, the Taiwan DENV2 strains from 1995 to 2014 were marked in orange, and the global reference strains were marked in black. Virus names were shown as country, accession number, and reported year of each sequence. Numbers on nodes were bootstrap support value exceeding 75%

Article Snippet: The standard used in this experiment was purchased from the Native Antigen Company, which is DENV2 NS1 hexamer produced in mammalian HEK293 cells with purity higher than 95% determined by sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS-PAGE).

Techniques: Sequencing, Construct, Virus

Journal: Journal of Biomedical Science

Article Title: A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway

doi: 10.1186/s12929-024-01116-4

Figure Lengend Snippet: Phylogenetic tree of DENV2 strains of Asian countries from 1995 to 2019 based on the DENV2 NS1 full-length sequence. The maximum likelihood phylogenetic tree was constructed using the IQ-TREE program with 1000 bootstrap replications. The sequences of DENV2 of Asian countries from 1995 to 2019 were collected from GenBank while the 2015 DENV2 outbreak strains were previously sequenced with the Illumina Miseq platform . The 2015 Taiwan outbreak strains were marked in red, the global reference strains were marked in black, and the DENV2 strains of Asian countries from the other countries were marked in different colors. Virus names were shown as country, accession number, and reported year of each sequence. Numbers on nodes were bootstrap support value exceeding 75%. TW: Taiwan; CN: China; IN: India; ID: Indonesia; SG: Singapore; MY: Malaysia; TH: Thailand; VN: Vietnam; PH: Philippines; KH: Cambodia; LA: Laos

Techniques: Sequencing, Construct, Virus

Journal: Journal of Biomedical Science

Article Title: A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway

doi: 10.1186/s12929-024-01116-4

Figure Lengend Snippet: K272R mutant virus replicated faster than WT virus in type I IFN producing cells. A Schematic diagram of NS1 amino acid mutations of Taiwan 2015 DENV2 outbreak strains. The red region represents the NS1 protein of DENV2. The stars indicate the amino acid substitutions isolated from the 2015 Taiwan dengue outbreak. B Production of DENV2-EGFP rg viruses containing each amino acid substitution in BHK-21 cells. The fluorescent images were captured under 10 × magnification of fluorescent microscope. C , D Growth kinetics of each rg virus in C A549 cells and D Vero cells. E Viral competition assay of each rg virus in Vero cells. Vero cells were infected with WT virus, mutant viruses or 1:1 mixture of WT and each mutant, then each group of viruses were passaged up to P5. Sanger sequencing was performed to determine the dominant variant at P1 and P5. All data are representative data from at least two independent experiments with comparable results and plotted as mean ± SEM with *p < 0.05 and ns, p > 0.05 by two-way ANOVA. WT: wildtype

Techniques: Mutagenesis, Virus, Isolation, Microscopy, Competitive Binding Assay, Infection, Sequencing, Variant Assay

Journal: Journal of Biomedical Science

Article Title: A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway

doi: 10.1186/s12929-024-01116-4

Figure Lengend Snippet: K272R mutant promoted higher secretion of soluble NS1. A , B A549 cells infected with K272R mutant or WT virus at or MOI 0.01 or MOI 0.1 for the indicated time points. C 293 T cells were transfected with 1 µg or 2 µg of plasmid overexpressing NS1-K272R or NS1-WT. A – C NS1 concentration in culture supernatants were measured by ELISA. All data are representative data from at least two independent experiments with ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05 and ns, p > 0.05 by two-way ANOVA

Techniques: Mutagenesis, Infection, Virus, Transfection, Plasmid Preparation, Concentration Assay, Enzyme-linked Immunosorbent Assay

Journal: Journal of Biomedical Science

Article Title: A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway

doi: 10.1186/s12929-024-01116-4

Figure Lengend Snippet: K272R amino acid substitution contributed to immune evasion from antiviral response. A – C A549 cells were infected with K272R mutant virus or WT virus at MOI 0.1 for 72 h followed by IFN-α treatment (1000 IU/mL) for 6 h. Quantitative RT-PCR analysis of ISGs (A) IFIT1 , (B) ISG15 , and C MxA were performed. D Immunoassay of extracts of 293 T cells transfected with 1 µg or 2 µg of plasmid overexpressing NS1-K272R or NS1-WT. (E–H) 293 T cells transfected with E , F 1 µg or G , H 2 µg of plasmids overexpressing NS1-K272R and NS1-WT, followed by IFN-α treatment (1000 IU/mL) for 6 h. Quantitative RT-PCR analysis of ISGs E , G IFIT1 and F , H ISG15 were performed. I , J STAT1 phosphorylation status was analyzed by western blot analysis. I A549 cells extracts with K272R mutant virus or WT virus infection at MOI 0.5 for 72 h and J 293 T cells were transfected with 2 µg of vector control, overexpressing NS1-WT and K272R mutant plasmids followed by IFN-α treatment (2000 IU/mL) for 1 h. The phosphorylated STAT1 protein expression was detected K A549 cells were infected with K272R mutant virus or WT virus at MOI 0.01 for 72 h and quantitative RT-PCR analysis of SOCS3 was performed. All data are representative data from at least two independent experiments with ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05 by one-way ANOVA. UT: untreated; VC: vector control

Techniques: Infection, Mutagenesis, Virus, Quantitative RT-PCR, Transfection, Plasmid Preparation, Western Blot, Control, Expressing

Journal: Journal of Biomedical Science

Article Title: A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway

doi: 10.1186/s12929-024-01116-4

Figure Lengend Snippet: Schematic diagram of effects of K272R amino acid substitution on the NS1 properties upon viral infection. During K272R mutant virus infection, the NS1-K272R inhibited the phosphorylation of STAT1 protein and downstream expression of ISGs to enhance the K272R mutant replication. Besides, the infection of K272R mutant virus induced more intense phosphorylation of p65 and higher secretion of pro-inflammatory cytokines which may be due to the higher production of sNS1

Techniques: Infection, Mutagenesis, Virus, Expressing

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