superscript iii first strand synthesis supermix kit Search Results


  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 99
    Thermo Fisher superscript iii first strand synthesis supermix kit
    Superscript Iii First Strand Synthesis Supermix Kit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/superscript iii first strand synthesis supermix kit/product/Thermo Fisher
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    superscript iii first strand synthesis supermix kit - by Bioz Stars, 2021-04
    99/100 stars
      Buy from Supplier

    99
    Thermo Fisher qrt pcr kit
    SPARCS expression is inducible and triggers positive feedback amplification. ( a ) Isotype control versus PD-L1 or CD44 surface expression on H69AR cells ± 200 ng/mL 24 h IFNγ stimulation (representative of n= 3 biological replicates). ( b ) Schematic of IFNγ pulse treatment (200 ng/mL) of H69 or H69AR cells. ( c ) <t>qRT-PCR</t> of MLT1C49 in H69 and H69AR cells ± 200 ng/mL IFNγ pulse – 24 h chase. Mean ± s.e.m of n=3 biological replicates shown (Two-way ANOVA; Sidak’s multiple comparisons tests). ( d ) ATAC-seq insertion tracks of H69 and H69AR cells around TRIM22 , TRIM38 and PD-L1 . Differentially accessible regions indicated with arrows. ( e ) Immunoblot of EZH2 and β-actin in H69, H69M and H69AR cells. ( f ) Log-2 fold change cytokine/chemokine differences between EZH2i treated H69 cells after IFNγ pulse, EZH2i treated cells, and IFNγ pulsed H69 cells relative to untreated control cells. *same as H69M-PD-L1 high cytokine profile in Fig. 1f . ( g ) Log-2 fold change comparison of IFNγ induced expression of SPARCS ERVs in EZH2i treated H69 cells versus H69AR cells. ( h ) qRT-PCR of 36B4 control, MLT1C49 , MLT1J and MLT1A in H69AR cells + 10 min IFNγ pulse - 24 h chase. RNA was treated with RNase A and immunoprecipitated with anti-dsRNA J2 antibody, values normalized against beta-actin. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( i ) Immunoblot of pTBK1, TBK1, pIRF3, IRF3, pSTAT1, STAT1 and β-actin levels in H69 and H69AR cells ± 200 ng/mL IFNγ 10 min pulse - 24 h chase. ( j ) qRT-PCR of MLT1C49 , IFN-β and CXCL10 in H69AR cells ± 10 min IFN-γ pulse - 24 h chase. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( k ) qRT-PCR and ELISA of CXCL10 in sgCTRL and sgMAVS-H69AR cells 72 h following Poly(I:C) transfection. Mean ± s.e.m of n=2 biological replicates shown (Unpaired two-tailed Student’s t test). ( l ) Log-2 fold change cytokine/chemokine differences in CM between CRISPR-H69AR cells after 10 min IFNγ 10 ng/mL pulse relative to sgCTRL cells (Scramble). ( m ) CXCL10 ELISA in Scramble, STING KO, MAVS KO and dKO H69AR CM following 10 min IFNγ 10 ng/mL pulse and chase for 3 days. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( n ) Photograph of representative excised tumors from sgCTRL and sgMAVS H69AR cells and tumor volumes measurements after 38 days of injection. Each data point represents mean ± s.e.m. tumor volumes (n=6 in sgCTRL group and n=6 in sgMAVS group; Two-way ANOVA; Sidak’s multiple comparisons tests). *p
    Qrt Pcr Kit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/qrt pcr kit/product/Thermo Fisher
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    qrt pcr kit - by Bioz Stars, 2021-04
    99/100 stars
      Buy from Supplier

    Image Search Results


    SPARCS expression is inducible and triggers positive feedback amplification. ( a ) Isotype control versus PD-L1 or CD44 surface expression on H69AR cells ± 200 ng/mL 24 h IFNγ stimulation (representative of n= 3 biological replicates). ( b ) Schematic of IFNγ pulse treatment (200 ng/mL) of H69 or H69AR cells. ( c ) qRT-PCR of MLT1C49 in H69 and H69AR cells ± 200 ng/mL IFNγ pulse – 24 h chase. Mean ± s.e.m of n=3 biological replicates shown (Two-way ANOVA; Sidak’s multiple comparisons tests). ( d ) ATAC-seq insertion tracks of H69 and H69AR cells around TRIM22 , TRIM38 and PD-L1 . Differentially accessible regions indicated with arrows. ( e ) Immunoblot of EZH2 and β-actin in H69, H69M and H69AR cells. ( f ) Log-2 fold change cytokine/chemokine differences between EZH2i treated H69 cells after IFNγ pulse, EZH2i treated cells, and IFNγ pulsed H69 cells relative to untreated control cells. *same as H69M-PD-L1 high cytokine profile in Fig. 1f . ( g ) Log-2 fold change comparison of IFNγ induced expression of SPARCS ERVs in EZH2i treated H69 cells versus H69AR cells. ( h ) qRT-PCR of 36B4 control, MLT1C49 , MLT1J and MLT1A in H69AR cells + 10 min IFNγ pulse - 24 h chase. RNA was treated with RNase A and immunoprecipitated with anti-dsRNA J2 antibody, values normalized against beta-actin. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( i ) Immunoblot of pTBK1, TBK1, pIRF3, IRF3, pSTAT1, STAT1 and β-actin levels in H69 and H69AR cells ± 200 ng/mL IFNγ 10 min pulse - 24 h chase. ( j ) qRT-PCR of MLT1C49 , IFN-β and CXCL10 in H69AR cells ± 10 min IFN-γ pulse - 24 h chase. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( k ) qRT-PCR and ELISA of CXCL10 in sgCTRL and sgMAVS-H69AR cells 72 h following Poly(I:C) transfection. Mean ± s.e.m of n=2 biological replicates shown (Unpaired two-tailed Student’s t test). ( l ) Log-2 fold change cytokine/chemokine differences in CM between CRISPR-H69AR cells after 10 min IFNγ 10 ng/mL pulse relative to sgCTRL cells (Scramble). ( m ) CXCL10 ELISA in Scramble, STING KO, MAVS KO and dKO H69AR CM following 10 min IFNγ 10 ng/mL pulse and chase for 3 days. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( n ) Photograph of representative excised tumors from sgCTRL and sgMAVS H69AR cells and tumor volumes measurements after 38 days of injection. Each data point represents mean ± s.e.m. tumor volumes (n=6 in sgCTRL group and n=6 in sgMAVS group; Two-way ANOVA; Sidak’s multiple comparisons tests). *p

    Journal: Nature medicine

    Article Title: Tumor innate immunity primed by specific interferon-stimulated endogenous retroviruses

    doi: 10.1038/s41591-018-0116-5

    Figure Lengend Snippet: SPARCS expression is inducible and triggers positive feedback amplification. ( a ) Isotype control versus PD-L1 or CD44 surface expression on H69AR cells ± 200 ng/mL 24 h IFNγ stimulation (representative of n= 3 biological replicates). ( b ) Schematic of IFNγ pulse treatment (200 ng/mL) of H69 or H69AR cells. ( c ) qRT-PCR of MLT1C49 in H69 and H69AR cells ± 200 ng/mL IFNγ pulse – 24 h chase. Mean ± s.e.m of n=3 biological replicates shown (Two-way ANOVA; Sidak’s multiple comparisons tests). ( d ) ATAC-seq insertion tracks of H69 and H69AR cells around TRIM22 , TRIM38 and PD-L1 . Differentially accessible regions indicated with arrows. ( e ) Immunoblot of EZH2 and β-actin in H69, H69M and H69AR cells. ( f ) Log-2 fold change cytokine/chemokine differences between EZH2i treated H69 cells after IFNγ pulse, EZH2i treated cells, and IFNγ pulsed H69 cells relative to untreated control cells. *same as H69M-PD-L1 high cytokine profile in Fig. 1f . ( g ) Log-2 fold change comparison of IFNγ induced expression of SPARCS ERVs in EZH2i treated H69 cells versus H69AR cells. ( h ) qRT-PCR of 36B4 control, MLT1C49 , MLT1J and MLT1A in H69AR cells + 10 min IFNγ pulse - 24 h chase. RNA was treated with RNase A and immunoprecipitated with anti-dsRNA J2 antibody, values normalized against beta-actin. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( i ) Immunoblot of pTBK1, TBK1, pIRF3, IRF3, pSTAT1, STAT1 and β-actin levels in H69 and H69AR cells ± 200 ng/mL IFNγ 10 min pulse - 24 h chase. ( j ) qRT-PCR of MLT1C49 , IFN-β and CXCL10 in H69AR cells ± 10 min IFN-γ pulse - 24 h chase. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( k ) qRT-PCR and ELISA of CXCL10 in sgCTRL and sgMAVS-H69AR cells 72 h following Poly(I:C) transfection. Mean ± s.e.m of n=2 biological replicates shown (Unpaired two-tailed Student’s t test). ( l ) Log-2 fold change cytokine/chemokine differences in CM between CRISPR-H69AR cells after 10 min IFNγ 10 ng/mL pulse relative to sgCTRL cells (Scramble). ( m ) CXCL10 ELISA in Scramble, STING KO, MAVS KO and dKO H69AR CM following 10 min IFNγ 10 ng/mL pulse and chase for 3 days. Mean ± s.e.m of n=3 biological replicates shown (Unpaired two-tailed Student’s t test). ( n ) Photograph of representative excised tumors from sgCTRL and sgMAVS H69AR cells and tumor volumes measurements after 38 days of injection. Each data point represents mean ± s.e.m. tumor volumes (n=6 in sgCTRL group and n=6 in sgMAVS group; Two-way ANOVA; Sidak’s multiple comparisons tests). *p

    Article Snippet: After extraction, 1 μg total RNA was used to generate cDNA with the SuperScript III First-Strand Synthesis SuperMix for qRT-PCR kit, which includes both oligo-dT and random primers (Thermo Fisher Scientific, Waltham, MA).

    Techniques: Expressing, Amplification, Quantitative RT-PCR, Immunoprecipitation, Two Tailed Test, Enzyme-linked Immunosorbent Assay, Transfection, CRISPR, Injection

    Discovery of an IFN-inducible subclass of ERVs. ( a ) Immunoblot of pTBK1, TBK1, IKKε, pIRF3, pERK, ERK, pAKT, AKT and tubulin levels in H69 and H69M cells after 24 or 72 h culture. ( b ) Log-2 fold change cytokine/chemokine differences between H69M/H69 CM. ( c ) H E and pTBK1 IHC of a patient-derived SCLC brain metastasis. Scale bar indicates 20 μm. ( d ) Isotype control versus PD-L1 or CD44 surface expression on H69 and H69M cells ± 200 ng/mL 24 h IFNγ stimulation (representative of n=3 biological replicates). ( e ) Immunoblot of pTBK1, TBK1, pERK, ERK, pAKT, AKT and β-actin levels in H69, H69M, H69M-PD-L1 low , and H69M-PD-L1 high cells. ( f ) Log-2 fold change cytokine/chemokines differences between H69M-PD-L1 high or H69M-PD-L1 low /H69 CM. ( g ) qRT-PCR of ERVs in H69M-PD-L1 high normalized to H69M-PD-L1 low cells. Numeric values on each bar represent the fold change in expression of a DNMT regulated ERV enriched panel 11 , 12 of previously published ERVs. Error bars are mean ± s.e.m of n=3 biological replicates. TRIM22 promoter and antisense orientation of MLT1C49 in the 3′UTR are represented below the qRT-PCR graph. ( h ) qRT-PCR of CXCL10 and CCL2 in H69M PD-L1 low cells transfected with pLX-307-GFP control or pLX_307-MLT1C49 construct for 72h. Mean ± s.e.m of n=3 biological replicates shown. ( i ) qRT-PCR of CXCL10 and CCL2 in H69M PD-L1 high cells transfected with scrambled negative control siRNA or siRNAs specific for MLT1C49. Mean ± s.e.m of n=3 biological replicates shown. ( j ) Overlap of 3′UTR antisense ERVs with H69M upregulated genes (log-2 fold change relative to H69 > 2) and table showing the fold change in expression of these genes/ERVs in H69M-PD-L1 high normalized to H69M-PD-L1 low cells. ( k ) Immunoblot of STING, MAVS, pTBK1, TBK1, pIRF3, IRF3, E-Cadherin, Vimentin and β-actin levels in H69M cells after CRISPR mediated deletion of MAVS and/or STING. ( l ) Log-2 fold change cytokine/chemokine differences in CM from H69M cells after CRISPR mediated deletion of MAVS and/or STING compared to sgCTRL (Scramble). ( m ) CXCL10 Luminex absolute levels (pg/mL) in Scramble, STING KO, MAVS KO and double KO (dKO) H69M cells. Mean ± s.e.m of n=2 biological replicates shown. *p

    Journal: Nature medicine

    Article Title: Tumor innate immunity primed by specific interferon-stimulated endogenous retroviruses

    doi: 10.1038/s41591-018-0116-5

    Figure Lengend Snippet: Discovery of an IFN-inducible subclass of ERVs. ( a ) Immunoblot of pTBK1, TBK1, IKKε, pIRF3, pERK, ERK, pAKT, AKT and tubulin levels in H69 and H69M cells after 24 or 72 h culture. ( b ) Log-2 fold change cytokine/chemokine differences between H69M/H69 CM. ( c ) H E and pTBK1 IHC of a patient-derived SCLC brain metastasis. Scale bar indicates 20 μm. ( d ) Isotype control versus PD-L1 or CD44 surface expression on H69 and H69M cells ± 200 ng/mL 24 h IFNγ stimulation (representative of n=3 biological replicates). ( e ) Immunoblot of pTBK1, TBK1, pERK, ERK, pAKT, AKT and β-actin levels in H69, H69M, H69M-PD-L1 low , and H69M-PD-L1 high cells. ( f ) Log-2 fold change cytokine/chemokines differences between H69M-PD-L1 high or H69M-PD-L1 low /H69 CM. ( g ) qRT-PCR of ERVs in H69M-PD-L1 high normalized to H69M-PD-L1 low cells. Numeric values on each bar represent the fold change in expression of a DNMT regulated ERV enriched panel 11 , 12 of previously published ERVs. Error bars are mean ± s.e.m of n=3 biological replicates. TRIM22 promoter and antisense orientation of MLT1C49 in the 3′UTR are represented below the qRT-PCR graph. ( h ) qRT-PCR of CXCL10 and CCL2 in H69M PD-L1 low cells transfected with pLX-307-GFP control or pLX_307-MLT1C49 construct for 72h. Mean ± s.e.m of n=3 biological replicates shown. ( i ) qRT-PCR of CXCL10 and CCL2 in H69M PD-L1 high cells transfected with scrambled negative control siRNA or siRNAs specific for MLT1C49. Mean ± s.e.m of n=3 biological replicates shown. ( j ) Overlap of 3′UTR antisense ERVs with H69M upregulated genes (log-2 fold change relative to H69 > 2) and table showing the fold change in expression of these genes/ERVs in H69M-PD-L1 high normalized to H69M-PD-L1 low cells. ( k ) Immunoblot of STING, MAVS, pTBK1, TBK1, pIRF3, IRF3, E-Cadherin, Vimentin and β-actin levels in H69M cells after CRISPR mediated deletion of MAVS and/or STING. ( l ) Log-2 fold change cytokine/chemokine differences in CM from H69M cells after CRISPR mediated deletion of MAVS and/or STING compared to sgCTRL (Scramble). ( m ) CXCL10 Luminex absolute levels (pg/mL) in Scramble, STING KO, MAVS KO and double KO (dKO) H69M cells. Mean ± s.e.m of n=2 biological replicates shown. *p

    Article Snippet: After extraction, 1 μg total RNA was used to generate cDNA with the SuperScript III First-Strand Synthesis SuperMix for qRT-PCR kit, which includes both oligo-dT and random primers (Thermo Fisher Scientific, Waltham, MA).

    Techniques: Immunohistochemistry, Derivative Assay, Expressing, Quantitative RT-PCR, Transfection, Construct, Negative Control, CRISPR, Luminex

    Expression of SPARCS-containing genes across cancers. ( a ) ssGSEA of SPARCS-gene containing signature across TCGA (n=3602 tumors) and significantly associated gene sets grouped based on biological annotations. IC = information coefficient. FDR = false discovery rate. ( b ) Intersection of top 1000 genes co-regulated with SPARCS-containing gene signature in TCGA and CCLE datasets. MHC class I pathway genes in top 40 highlighted in red, EMT related genes in blue and immune evasion markers in green. ( c ) Distribution of high versus low SPARCS-containing gene expression by TCGA cancer histology. ( d ) Immunoblot of AXL, MET, Vimentin, STING, MAVS and β-actin levels in cell lines with high, intermediate, or low SPARCS gene signature expression after 72 h culture. ( e ) qRT-PCR of MLT1C49 , CXCL10, PD-L1 and CD44 in SPARCS high and SPARCS low cell lines ± IFNγ 10 min pulse - 24 h chase. p values indicated for comparison of SPARCS high versus SPARCS low groups. Mean ± s.e.m of n=2 biological replicates shown (Two-tailed Mann-Whitney U test). *p

    Journal: Nature medicine

    Article Title: Tumor innate immunity primed by specific interferon-stimulated endogenous retroviruses

    doi: 10.1038/s41591-018-0116-5

    Figure Lengend Snippet: Expression of SPARCS-containing genes across cancers. ( a ) ssGSEA of SPARCS-gene containing signature across TCGA (n=3602 tumors) and significantly associated gene sets grouped based on biological annotations. IC = information coefficient. FDR = false discovery rate. ( b ) Intersection of top 1000 genes co-regulated with SPARCS-containing gene signature in TCGA and CCLE datasets. MHC class I pathway genes in top 40 highlighted in red, EMT related genes in blue and immune evasion markers in green. ( c ) Distribution of high versus low SPARCS-containing gene expression by TCGA cancer histology. ( d ) Immunoblot of AXL, MET, Vimentin, STING, MAVS and β-actin levels in cell lines with high, intermediate, or low SPARCS gene signature expression after 72 h culture. ( e ) qRT-PCR of MLT1C49 , CXCL10, PD-L1 and CD44 in SPARCS high and SPARCS low cell lines ± IFNγ 10 min pulse - 24 h chase. p values indicated for comparison of SPARCS high versus SPARCS low groups. Mean ± s.e.m of n=2 biological replicates shown (Two-tailed Mann-Whitney U test). *p

    Article Snippet: After extraction, 1 μg total RNA was used to generate cDNA with the SuperScript III First-Strand Synthesis SuperMix for qRT-PCR kit, which includes both oligo-dT and random primers (Thermo Fisher Scientific, Waltham, MA).

    Techniques: Expressing, Quantitative RT-PCR, Two Tailed Test, MANN-WHITNEY