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stt3a promoter  (Addgene inc)


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    Addgene inc stt3a promoter
    Figure 3. SARS-CoV-2 induces N-glycosylation through <t>NF-kB/STT3A</t> axis. (a) Locus compare plot for the comparison between the STT3A eQTLs and the GWAS result, the COVID-19 A2 analysis for patients with severe respiratory symptoms via COVID-19 Host Genetics Initiative (COVID-19-HGI) project. The points are colored based on linkage disequilibrium (LD) bins. rs201008304, the indel variant in strong LD with the lead STT3A eQTL, is the top and most significant SNP in COVID-19 A2 analysis. (b) The eQTL plot for the association between STT3A variant types [A/A (n = 437), A/AT (n = 46), and AT/AT (n = 0)] expression and rs201008304 in cells-cultured fibroblasts was queried from the GTEx. (c) Forest plot shows the risk of rs201008304 in different COVID-19 phenotypes, originally from the summarized statistic results. (d) Representative data of immunohistochemistry staining of STT3A (red cells) and N protein in lung tissues of AAV-Ctrl and AAV-hACE2 mice infected by SARS-CoV2 at 5 dpi. Images were captured at 40x objective lens magnification. Scale bar, 100 mm. Three randomly selected STT3A/nuclei expression fields in lung tissues were exported from CaseViewer software (3DHistech) and quantified by the HistoQuant plugin in QuantCenter (3DHistech). Statistical method: t test, *p < 0.05, (n = 3). (e) Western blotting of S protein in Vero E6 cells after knockdown of STT3A or STT3B. Circle, g-spike; arrow, ng-spike. (f) ChIP analysis of enrichment of NF-kB in STT3A promoters after SARS-CoV-2 infection for 1 d. The enrichment levels were analyzed by RT-qPCR and shown as the per- centage of input. Statistical method: two-way ANOVA, Tukey post hoc tests, ***p < 0.001 (n = 3 with mean § SD shown).
    Stt3a Promoter, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 59 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stt3a promoter/product/Addgene inc
    Average 93 stars, based on 59 article reviews
    stt3a promoter - by Bioz Stars, 2026-03
    93/100 stars

    Images

    1) Product Images from "Targeting conserved N-glycosylation blocks SARS-CoV-2 variant infection in vitro."

    Article Title: Targeting conserved N-glycosylation blocks SARS-CoV-2 variant infection in vitro.

    Journal: EBioMedicine

    doi: 10.1016/j.ebiom.2021.103712

    Figure 3. SARS-CoV-2 induces N-glycosylation through NF-kB/STT3A axis. (a) Locus compare plot for the comparison between the STT3A eQTLs and the GWAS result, the COVID-19 A2 analysis for patients with severe respiratory symptoms via COVID-19 Host Genetics Initiative (COVID-19-HGI) project. The points are colored based on linkage disequilibrium (LD) bins. rs201008304, the indel variant in strong LD with the lead STT3A eQTL, is the top and most significant SNP in COVID-19 A2 analysis. (b) The eQTL plot for the association between STT3A variant types [A/A (n = 437), A/AT (n = 46), and AT/AT (n = 0)] expression and rs201008304 in cells-cultured fibroblasts was queried from the GTEx. (c) Forest plot shows the risk of rs201008304 in different COVID-19 phenotypes, originally from the summarized statistic results. (d) Representative data of immunohistochemistry staining of STT3A (red cells) and N protein in lung tissues of AAV-Ctrl and AAV-hACE2 mice infected by SARS-CoV2 at 5 dpi. Images were captured at 40x objective lens magnification. Scale bar, 100 mm. Three randomly selected STT3A/nuclei expression fields in lung tissues were exported from CaseViewer software (3DHistech) and quantified by the HistoQuant plugin in QuantCenter (3DHistech). Statistical method: t test, *p < 0.05, (n = 3). (e) Western blotting of S protein in Vero E6 cells after knockdown of STT3A or STT3B. Circle, g-spike; arrow, ng-spike. (f) ChIP analysis of enrichment of NF-kB in STT3A promoters after SARS-CoV-2 infection for 1 d. The enrichment levels were analyzed by RT-qPCR and shown as the per- centage of input. Statistical method: two-way ANOVA, Tukey post hoc tests, ***p < 0.001 (n = 3 with mean § SD shown).
    Figure Legend Snippet: Figure 3. SARS-CoV-2 induces N-glycosylation through NF-kB/STT3A axis. (a) Locus compare plot for the comparison between the STT3A eQTLs and the GWAS result, the COVID-19 A2 analysis for patients with severe respiratory symptoms via COVID-19 Host Genetics Initiative (COVID-19-HGI) project. The points are colored based on linkage disequilibrium (LD) bins. rs201008304, the indel variant in strong LD with the lead STT3A eQTL, is the top and most significant SNP in COVID-19 A2 analysis. (b) The eQTL plot for the association between STT3A variant types [A/A (n = 437), A/AT (n = 46), and AT/AT (n = 0)] expression and rs201008304 in cells-cultured fibroblasts was queried from the GTEx. (c) Forest plot shows the risk of rs201008304 in different COVID-19 phenotypes, originally from the summarized statistic results. (d) Representative data of immunohistochemistry staining of STT3A (red cells) and N protein in lung tissues of AAV-Ctrl and AAV-hACE2 mice infected by SARS-CoV2 at 5 dpi. Images were captured at 40x objective lens magnification. Scale bar, 100 mm. Three randomly selected STT3A/nuclei expression fields in lung tissues were exported from CaseViewer software (3DHistech) and quantified by the HistoQuant plugin in QuantCenter (3DHistech). Statistical method: t test, *p < 0.05, (n = 3). (e) Western blotting of S protein in Vero E6 cells after knockdown of STT3A or STT3B. Circle, g-spike; arrow, ng-spike. (f) ChIP analysis of enrichment of NF-kB in STT3A promoters after SARS-CoV-2 infection for 1 d. The enrichment levels were analyzed by RT-qPCR and shown as the per- centage of input. Statistical method: two-way ANOVA, Tukey post hoc tests, ***p < 0.001 (n = 3 with mean § SD shown).

    Techniques Used: Glycoproteomics, Comparison, Variant Assay, Expressing, Cell Culture, Immunohistochemistry, Staining, Infection, Software, Western Blot, Knockdown, Quantitative RT-PCR

    Figure 4. Impairment of STT3A compromises SARS-CoV-2 infectivity. (a) Luciferase assay was used to monitor the infection rate of pseudovirions generated from shSTT3A or shSTT3B HEK293T cells in HEK293T-ACE2 cells. Expression of spike in pseudovirus produced from shSTT3A and shSTT3B. Statistical method: one-way ANOVA, Tukey post hoc tests. **p < 0.01 (n = 3 with mean § SD shown). (b) Western blot analysis of N protein expression in A549-ACE2 cells infected with SARS-CoV-2 generated from control, shSTT3A or shSTT3B Vero E6 cells (left panel). N protein intensity was quantified by ImageJ (right panel). (c) Western blot analysis of spike and N protein expression in DMSO and NGI-1 treated SARS-CoV-2 infected Vero E6 cells. (d) Representative immunofluorescence images of N protein expression in DMSO and NGI-1 treated Vero E6 cell after SARS-CoV-2 infection. Scale bar, 100 mm. (e) SARS-CoV-2 neutralization IC50 of NGI-1 in Vero E6. Vero E6 cells was pretreated with NGI-1 1 h ahead at the indicated doses prior to SARS-CoV-2 infection (red). Cell viability of Vero E6 cells following NGI-1 treatment determined by MTT assay (black). Data shown are means § SD from representative triplicates. (f) Luciferase activity was measured at 48 h to determine SARS-CoV-2, Alpha, and Beta variants pseudoviral infectivity in DMSO and NGI-1 treated HEK293T-ACE2; Data shown are means § SD from represen- tative triplicates.
    Figure Legend Snippet: Figure 4. Impairment of STT3A compromises SARS-CoV-2 infectivity. (a) Luciferase assay was used to monitor the infection rate of pseudovirions generated from shSTT3A or shSTT3B HEK293T cells in HEK293T-ACE2 cells. Expression of spike in pseudovirus produced from shSTT3A and shSTT3B. Statistical method: one-way ANOVA, Tukey post hoc tests. **p < 0.01 (n = 3 with mean § SD shown). (b) Western blot analysis of N protein expression in A549-ACE2 cells infected with SARS-CoV-2 generated from control, shSTT3A or shSTT3B Vero E6 cells (left panel). N protein intensity was quantified by ImageJ (right panel). (c) Western blot analysis of spike and N protein expression in DMSO and NGI-1 treated SARS-CoV-2 infected Vero E6 cells. (d) Representative immunofluorescence images of N protein expression in DMSO and NGI-1 treated Vero E6 cell after SARS-CoV-2 infection. Scale bar, 100 mm. (e) SARS-CoV-2 neutralization IC50 of NGI-1 in Vero E6. Vero E6 cells was pretreated with NGI-1 1 h ahead at the indicated doses prior to SARS-CoV-2 infection (red). Cell viability of Vero E6 cells following NGI-1 treatment determined by MTT assay (black). Data shown are means § SD from representative triplicates. (f) Luciferase activity was measured at 48 h to determine SARS-CoV-2, Alpha, and Beta variants pseudoviral infectivity in DMSO and NGI-1 treated HEK293T-ACE2; Data shown are means § SD from represen- tative triplicates.

    Techniques Used: Infection, Luciferase, Generated, Expressing, Produced, Western Blot, Control, Neutralization, MTT Assay, Activity Assay



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    stt3a promoter  (Addgene inc)
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    Addgene inc stt3a promoter
    Figure 3. SARS-CoV-2 induces N-glycosylation through <t>NF-kB/STT3A</t> axis. (a) Locus compare plot for the comparison between the STT3A eQTLs and the GWAS result, the COVID-19 A2 analysis for patients with severe respiratory symptoms via COVID-19 Host Genetics Initiative (COVID-19-HGI) project. The points are colored based on linkage disequilibrium (LD) bins. rs201008304, the indel variant in strong LD with the lead STT3A eQTL, is the top and most significant SNP in COVID-19 A2 analysis. (b) The eQTL plot for the association between STT3A variant types [A/A (n = 437), A/AT (n = 46), and AT/AT (n = 0)] expression and rs201008304 in cells-cultured fibroblasts was queried from the GTEx. (c) Forest plot shows the risk of rs201008304 in different COVID-19 phenotypes, originally from the summarized statistic results. (d) Representative data of immunohistochemistry staining of STT3A (red cells) and N protein in lung tissues of AAV-Ctrl and AAV-hACE2 mice infected by SARS-CoV2 at 5 dpi. Images were captured at 40x objective lens magnification. Scale bar, 100 mm. Three randomly selected STT3A/nuclei expression fields in lung tissues were exported from CaseViewer software (3DHistech) and quantified by the HistoQuant plugin in QuantCenter (3DHistech). Statistical method: t test, *p < 0.05, (n = 3). (e) Western blotting of S protein in Vero E6 cells after knockdown of STT3A or STT3B. Circle, g-spike; arrow, ng-spike. (f) ChIP analysis of enrichment of NF-kB in STT3A promoters after SARS-CoV-2 infection for 1 d. The enrichment levels were analyzed by RT-qPCR and shown as the per- centage of input. Statistical method: two-way ANOVA, Tukey post hoc tests, ***p < 0.001 (n = 3 with mean § SD shown).
    Stt3a Promoter, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stt3a promoter/product/Addgene inc
    Average 93 stars, based on 1 article reviews
    stt3a promoter - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier

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    Figure 3. SARS-CoV-2 induces N-glycosylation through NF-kB/STT3A axis. (a) Locus compare plot for the comparison between the STT3A eQTLs and the GWAS result, the COVID-19 A2 analysis for patients with severe respiratory symptoms via COVID-19 Host Genetics Initiative (COVID-19-HGI) project. The points are colored based on linkage disequilibrium (LD) bins. rs201008304, the indel variant in strong LD with the lead STT3A eQTL, is the top and most significant SNP in COVID-19 A2 analysis. (b) The eQTL plot for the association between STT3A variant types [A/A (n = 437), A/AT (n = 46), and AT/AT (n = 0)] expression and rs201008304 in cells-cultured fibroblasts was queried from the GTEx. (c) Forest plot shows the risk of rs201008304 in different COVID-19 phenotypes, originally from the summarized statistic results. (d) Representative data of immunohistochemistry staining of STT3A (red cells) and N protein in lung tissues of AAV-Ctrl and AAV-hACE2 mice infected by SARS-CoV2 at 5 dpi. Images were captured at 40x objective lens magnification. Scale bar, 100 mm. Three randomly selected STT3A/nuclei expression fields in lung tissues were exported from CaseViewer software (3DHistech) and quantified by the HistoQuant plugin in QuantCenter (3DHistech). Statistical method: t test, *p < 0.05, (n = 3). (e) Western blotting of S protein in Vero E6 cells after knockdown of STT3A or STT3B. Circle, g-spike; arrow, ng-spike. (f) ChIP analysis of enrichment of NF-kB in STT3A promoters after SARS-CoV-2 infection for 1 d. The enrichment levels were analyzed by RT-qPCR and shown as the per- centage of input. Statistical method: two-way ANOVA, Tukey post hoc tests, ***p < 0.001 (n = 3 with mean § SD shown).

    Journal: EBioMedicine

    Article Title: Targeting conserved N-glycosylation blocks SARS-CoV-2 variant infection in vitro.

    doi: 10.1016/j.ebiom.2021.103712

    Figure Lengend Snippet: Figure 3. SARS-CoV-2 induces N-glycosylation through NF-kB/STT3A axis. (a) Locus compare plot for the comparison between the STT3A eQTLs and the GWAS result, the COVID-19 A2 analysis for patients with severe respiratory symptoms via COVID-19 Host Genetics Initiative (COVID-19-HGI) project. The points are colored based on linkage disequilibrium (LD) bins. rs201008304, the indel variant in strong LD with the lead STT3A eQTL, is the top and most significant SNP in COVID-19 A2 analysis. (b) The eQTL plot for the association between STT3A variant types [A/A (n = 437), A/AT (n = 46), and AT/AT (n = 0)] expression and rs201008304 in cells-cultured fibroblasts was queried from the GTEx. (c) Forest plot shows the risk of rs201008304 in different COVID-19 phenotypes, originally from the summarized statistic results. (d) Representative data of immunohistochemistry staining of STT3A (red cells) and N protein in lung tissues of AAV-Ctrl and AAV-hACE2 mice infected by SARS-CoV2 at 5 dpi. Images were captured at 40x objective lens magnification. Scale bar, 100 mm. Three randomly selected STT3A/nuclei expression fields in lung tissues were exported from CaseViewer software (3DHistech) and quantified by the HistoQuant plugin in QuantCenter (3DHistech). Statistical method: t test, *p < 0.05, (n = 3). (e) Western blotting of S protein in Vero E6 cells after knockdown of STT3A or STT3B. Circle, g-spike; arrow, ng-spike. (f) ChIP analysis of enrichment of NF-kB in STT3A promoters after SARS-CoV-2 infection for 1 d. The enrichment levels were analyzed by RT-qPCR and shown as the per- centage of input. Statistical method: two-way ANOVA, Tukey post hoc tests, ***p < 0.001 (n = 3 with mean § SD shown).

    Article Snippet: The deleted NF-kB binding motif construct had a deletion at bases 363CGTAGTTTCC 353 in the STT3A promoter. pBabe-PuroIkBalpha-mut (RRID:Addgene_15291; Addgene plasmid #15291, Watertown, MA, USA) [21] is a dominant-negative mutant NF-kB inhibitor (IkBaSR) and inhibits NF-kB activity.

    Techniques: Glycoproteomics, Comparison, Variant Assay, Expressing, Cell Culture, Immunohistochemistry, Staining, Infection, Software, Western Blot, Knockdown, Quantitative RT-PCR

    Figure 4. Impairment of STT3A compromises SARS-CoV-2 infectivity. (a) Luciferase assay was used to monitor the infection rate of pseudovirions generated from shSTT3A or shSTT3B HEK293T cells in HEK293T-ACE2 cells. Expression of spike in pseudovirus produced from shSTT3A and shSTT3B. Statistical method: one-way ANOVA, Tukey post hoc tests. **p < 0.01 (n = 3 with mean § SD shown). (b) Western blot analysis of N protein expression in A549-ACE2 cells infected with SARS-CoV-2 generated from control, shSTT3A or shSTT3B Vero E6 cells (left panel). N protein intensity was quantified by ImageJ (right panel). (c) Western blot analysis of spike and N protein expression in DMSO and NGI-1 treated SARS-CoV-2 infected Vero E6 cells. (d) Representative immunofluorescence images of N protein expression in DMSO and NGI-1 treated Vero E6 cell after SARS-CoV-2 infection. Scale bar, 100 mm. (e) SARS-CoV-2 neutralization IC50 of NGI-1 in Vero E6. Vero E6 cells was pretreated with NGI-1 1 h ahead at the indicated doses prior to SARS-CoV-2 infection (red). Cell viability of Vero E6 cells following NGI-1 treatment determined by MTT assay (black). Data shown are means § SD from representative triplicates. (f) Luciferase activity was measured at 48 h to determine SARS-CoV-2, Alpha, and Beta variants pseudoviral infectivity in DMSO and NGI-1 treated HEK293T-ACE2; Data shown are means § SD from represen- tative triplicates.

    Journal: EBioMedicine

    Article Title: Targeting conserved N-glycosylation blocks SARS-CoV-2 variant infection in vitro.

    doi: 10.1016/j.ebiom.2021.103712

    Figure Lengend Snippet: Figure 4. Impairment of STT3A compromises SARS-CoV-2 infectivity. (a) Luciferase assay was used to monitor the infection rate of pseudovirions generated from shSTT3A or shSTT3B HEK293T cells in HEK293T-ACE2 cells. Expression of spike in pseudovirus produced from shSTT3A and shSTT3B. Statistical method: one-way ANOVA, Tukey post hoc tests. **p < 0.01 (n = 3 with mean § SD shown). (b) Western blot analysis of N protein expression in A549-ACE2 cells infected with SARS-CoV-2 generated from control, shSTT3A or shSTT3B Vero E6 cells (left panel). N protein intensity was quantified by ImageJ (right panel). (c) Western blot analysis of spike and N protein expression in DMSO and NGI-1 treated SARS-CoV-2 infected Vero E6 cells. (d) Representative immunofluorescence images of N protein expression in DMSO and NGI-1 treated Vero E6 cell after SARS-CoV-2 infection. Scale bar, 100 mm. (e) SARS-CoV-2 neutralization IC50 of NGI-1 in Vero E6. Vero E6 cells was pretreated with NGI-1 1 h ahead at the indicated doses prior to SARS-CoV-2 infection (red). Cell viability of Vero E6 cells following NGI-1 treatment determined by MTT assay (black). Data shown are means § SD from representative triplicates. (f) Luciferase activity was measured at 48 h to determine SARS-CoV-2, Alpha, and Beta variants pseudoviral infectivity in DMSO and NGI-1 treated HEK293T-ACE2; Data shown are means § SD from represen- tative triplicates.

    Article Snippet: The deleted NF-kB binding motif construct had a deletion at bases 363CGTAGTTTCC 353 in the STT3A promoter. pBabe-PuroIkBalpha-mut (RRID:Addgene_15291; Addgene plasmid #15291, Watertown, MA, USA) [21] is a dominant-negative mutant NF-kB inhibitor (IkBaSR) and inhibits NF-kB activity.

    Techniques: Infection, Luciferase, Generated, Expressing, Produced, Western Blot, Control, Neutralization, MTT Assay, Activity Assay