Review



shifnar1  (Santa Cruz Biotechnology)


Bioz Verified Symbol Santa Cruz Biotechnology is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 93
      Buy from Supplier

    Structured Review

    Santa Cruz Biotechnology shifnar1
    A. HCC827 cells were stably infected with lentivirus control shRNA (shCtrl) or shRNA for IFNAR1 lentivirus and silencing was confirmed by Western blot. Silenced clones were studied in AlamarBlue cell survival assays following erlotinib exposure for 72h. Cells with stable silencing of IFNAR1 (clone #3) or control shRNA were subcutaneously injected into 8 nude mice per group. The rate of tumor formation was 5–8 per group as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was administered orally at 6.25 mg/kg/day. Tumor sizes were monitored as described in the Methods section. Representative tumor images are shown. B. A similar experiment was performed with A549 xenografts <t>(shIFNAR1</t> clone #2). Eight nude mice were injected per group and the rate of tumor formation was 5–8 as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was used at 100 mg/kg/d. C. HCC4190 EGFR mutant PDX was subcutaneously implanted on NOD-SCID mice. Eight nude mice were implanted per group and the rate of tumor formation was 7–8 as shown in the Source_Data_Fig.7 (n=7–8). Mice were orally treated with 6.25 mg/kg/day erlotinib and/or i.p. injected with 2 mg/kg/day anifrolumab, a monoclonal IFNAR1 antibody. D. A similar PDX experiment was performed with HCC4087, which harbor mutant KRAS and wild-type EGFR. Eight nude mice were injected per group and all 8 mice formed tumors (n=8). Erlotinib was used at a dose of 100 mg/kg/d. E. KRAS LSL-G12D transgenic mice were generated as in the Methods section, and randomly divided into 4 groups (n=3–4 as the number of dots), receiving vehicle, oral erlotinib of 100 mg/kg/day, i.p. injection of mouse anti-mouse IFNAR1 antibody at 3 mg/kg/day, and combination administration of erlotinib plus IFNAR1 antibody for 28 continuous days. Bi-weekly MRI scanning was used to monitor tumor growth. Tumor sizes were calculated by ImageJ. Representative MRI images are shown, n=3–4 as indicated by the number of dots (mice). The tumors grow as diffuse lung opacities and “H” refers to heart. Data (A-E, in vivo) refers to mean ± S.E.M. of tumor sizes (n as above), *: p<0.05, **:p<0.01, ***:p<0.001, by two-way ANOVA adjusted by Bonferroni’s. For in vitro experiments (A-B), n=3 technical replicates, representative of 3 independent repeats with similar results. Western blots are cropped and representative of three independent repeated experiments with similar results. Uncropped are in Source_Data_Fig.7. Numerical source data for the experiments in this figure can be found in Source_Data_Fig.7.
    Shifnar1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/shifnar1/IFN-%CE%B1%2F%CE%B2R%CE%B1+siRNA/pmc07706867-785-21-13
    Average 93 stars, based on 9 article reviews
    shifnar1 - by Bioz Stars, 2026-09
    93/100 stars

    Images

    1) Product Images from "EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer"

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer

    Journal: Nature cancer

    doi: 10.1038/s43018-020-0048-0

    A. HCC827 cells were stably infected with lentivirus control shRNA (shCtrl) or shRNA for IFNAR1 lentivirus and silencing was confirmed by Western blot. Silenced clones were studied in AlamarBlue cell survival assays following erlotinib exposure for 72h. Cells with stable silencing of IFNAR1 (clone #3) or control shRNA were subcutaneously injected into 8 nude mice per group. The rate of tumor formation was 5–8 per group as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was administered orally at 6.25 mg/kg/day. Tumor sizes were monitored as described in the Methods section. Representative tumor images are shown. B. A similar experiment was performed with A549 xenografts (shIFNAR1 clone #2). Eight nude mice were injected per group and the rate of tumor formation was 5–8 as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was used at 100 mg/kg/d. C. HCC4190 EGFR mutant PDX was subcutaneously implanted on NOD-SCID mice. Eight nude mice were implanted per group and the rate of tumor formation was 7–8 as shown in the Source_Data_Fig.7 (n=7–8). Mice were orally treated with 6.25 mg/kg/day erlotinib and/or i.p. injected with 2 mg/kg/day anifrolumab, a monoclonal IFNAR1 antibody. D. A similar PDX experiment was performed with HCC4087, which harbor mutant KRAS and wild-type EGFR. Eight nude mice were injected per group and all 8 mice formed tumors (n=8). Erlotinib was used at a dose of 100 mg/kg/d. E. KRAS LSL-G12D transgenic mice were generated as in the Methods section, and randomly divided into 4 groups (n=3–4 as the number of dots), receiving vehicle, oral erlotinib of 100 mg/kg/day, i.p. injection of mouse anti-mouse IFNAR1 antibody at 3 mg/kg/day, and combination administration of erlotinib plus IFNAR1 antibody for 28 continuous days. Bi-weekly MRI scanning was used to monitor tumor growth. Tumor sizes were calculated by ImageJ. Representative MRI images are shown, n=3–4 as indicated by the number of dots (mice). The tumors grow as diffuse lung opacities and “H” refers to heart. Data (A-E, in vivo) refers to mean ± S.E.M. of tumor sizes (n as above), *: p<0.05, **:p<0.01, ***:p<0.001, by two-way ANOVA adjusted by Bonferroni’s. For in vitro experiments (A-B), n=3 technical replicates, representative of 3 independent repeats with similar results. Western blots are cropped and representative of three independent repeated experiments with similar results. Uncropped are in Source_Data_Fig.7. Numerical source data for the experiments in this figure can be found in Source_Data_Fig.7.
    Figure Legend Snippet: A. HCC827 cells were stably infected with lentivirus control shRNA (shCtrl) or shRNA for IFNAR1 lentivirus and silencing was confirmed by Western blot. Silenced clones were studied in AlamarBlue cell survival assays following erlotinib exposure for 72h. Cells with stable silencing of IFNAR1 (clone #3) or control shRNA were subcutaneously injected into 8 nude mice per group. The rate of tumor formation was 5–8 per group as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was administered orally at 6.25 mg/kg/day. Tumor sizes were monitored as described in the Methods section. Representative tumor images are shown. B. A similar experiment was performed with A549 xenografts (shIFNAR1 clone #2). Eight nude mice were injected per group and the rate of tumor formation was 5–8 as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was used at 100 mg/kg/d. C. HCC4190 EGFR mutant PDX was subcutaneously implanted on NOD-SCID mice. Eight nude mice were implanted per group and the rate of tumor formation was 7–8 as shown in the Source_Data_Fig.7 (n=7–8). Mice were orally treated with 6.25 mg/kg/day erlotinib and/or i.p. injected with 2 mg/kg/day anifrolumab, a monoclonal IFNAR1 antibody. D. A similar PDX experiment was performed with HCC4087, which harbor mutant KRAS and wild-type EGFR. Eight nude mice were injected per group and all 8 mice formed tumors (n=8). Erlotinib was used at a dose of 100 mg/kg/d. E. KRAS LSL-G12D transgenic mice were generated as in the Methods section, and randomly divided into 4 groups (n=3–4 as the number of dots), receiving vehicle, oral erlotinib of 100 mg/kg/day, i.p. injection of mouse anti-mouse IFNAR1 antibody at 3 mg/kg/day, and combination administration of erlotinib plus IFNAR1 antibody for 28 continuous days. Bi-weekly MRI scanning was used to monitor tumor growth. Tumor sizes were calculated by ImageJ. Representative MRI images are shown, n=3–4 as indicated by the number of dots (mice). The tumors grow as diffuse lung opacities and “H” refers to heart. Data (A-E, in vivo) refers to mean ± S.E.M. of tumor sizes (n as above), *: p<0.05, **:p<0.01, ***:p<0.001, by two-way ANOVA adjusted by Bonferroni’s. For in vitro experiments (A-B), n=3 technical replicates, representative of 3 independent repeats with similar results. Western blots are cropped and representative of three independent repeated experiments with similar results. Uncropped are in Source_Data_Fig.7. Numerical source data for the experiments in this figure can be found in Source_Data_Fig.7.

    Techniques Used: Stable Transfection, Infection, shRNA, Western Blot, Clone Assay, Injection, Mutagenesis, Transgenic Assay, Generated, In Vivo, In Vitro

    Related Articles

    Stable Transfection:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    shRNA:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    Infection:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    Western Blot:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    Clone Assay:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    Injection:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    Mutagenesis:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    Transgenic Assay:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    Generated:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    In Vivo:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).

    In Vitro:

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer
    Article Snippet: LPS (19661), TBK1 inhibitor BX795, and EGFR inhibitor erlotinib and afatinib for in vitro studies were obtained from Cayman Chemical (Ann Arbor, MI).



    Similar Products

    hepg2 cd81 shifn β shifnar1  (ATCC)
    99
    ATCC hepg2 cd81 shifn β shifnar1
    Hepg2 Cd81 Shifn β Shifnar1, supplied by ATCC, 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/product/shifnar1/Hep+G2/pmc03624324-409-8-25
    Average 99 stars, based on 1 article reviews
    hepg2 cd81 shifn β shifnar1 - by Bioz Stars, 2026-09
    99/100 stars
    		  Buy from Supplier
    shifnar1  (Santa Cruz Biotechnology)
    93
    Santa Cruz Biotechnology shifnar1
    A. HCC827 cells were stably infected with lentivirus control shRNA (shCtrl) or shRNA for IFNAR1 lentivirus and silencing was confirmed by Western blot. Silenced clones were studied in AlamarBlue cell survival assays following erlotinib exposure for 72h. Cells with stable silencing of IFNAR1 (clone #3) or control shRNA were subcutaneously injected into 8 nude mice per group. The rate of tumor formation was 5–8 per group as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was administered orally at 6.25 mg/kg/day. Tumor sizes were monitored as described in the Methods section. Representative tumor images are shown. B. A similar experiment was performed with A549 xenografts <t>(shIFNAR1</t> clone #2). Eight nude mice were injected per group and the rate of tumor formation was 5–8 as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was used at 100 mg/kg/d. C. HCC4190 EGFR mutant PDX was subcutaneously implanted on NOD-SCID mice. Eight nude mice were implanted per group and the rate of tumor formation was 7–8 as shown in the Source_Data_Fig.7 (n=7–8). Mice were orally treated with 6.25 mg/kg/day erlotinib and/or i.p. injected with 2 mg/kg/day anifrolumab, a monoclonal IFNAR1 antibody. D. A similar PDX experiment was performed with HCC4087, which harbor mutant KRAS and wild-type EGFR. Eight nude mice were injected per group and all 8 mice formed tumors (n=8). Erlotinib was used at a dose of 100 mg/kg/d. E. KRAS LSL-G12D transgenic mice were generated as in the Methods section, and randomly divided into 4 groups (n=3–4 as the number of dots), receiving vehicle, oral erlotinib of 100 mg/kg/day, i.p. injection of mouse anti-mouse IFNAR1 antibody at 3 mg/kg/day, and combination administration of erlotinib plus IFNAR1 antibody for 28 continuous days. Bi-weekly MRI scanning was used to monitor tumor growth. Tumor sizes were calculated by ImageJ. Representative MRI images are shown, n=3–4 as indicated by the number of dots (mice). The tumors grow as diffuse lung opacities and “H” refers to heart. Data (A-E, in vivo) refers to mean ± S.E.M. of tumor sizes (n as above), *: p<0.05, **:p<0.01, ***:p<0.001, by two-way ANOVA adjusted by Bonferroni’s. For in vitro experiments (A-B), n=3 technical replicates, representative of 3 independent repeats with similar results. Western blots are cropped and representative of three independent repeated experiments with similar results. Uncropped are in Source_Data_Fig.7. Numerical source data for the experiments in this figure can be found in Source_Data_Fig.7.
    Shifnar1, supplied by Santa Cruz Biotechnology, 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/product/shifnar1/IFN-%CE%B1%2F%CE%B2R%CE%B1+siRNA/pmc07706867-785-21-13
    Average 93 stars, based on 1 article reviews
    shifnar1 - by Bioz Stars, 2026-09
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    A. HCC827 cells were stably infected with lentivirus control shRNA (shCtrl) or shRNA for IFNAR1 lentivirus and silencing was confirmed by Western blot. Silenced clones were studied in AlamarBlue cell survival assays following erlotinib exposure for 72h. Cells with stable silencing of IFNAR1 (clone #3) or control shRNA were subcutaneously injected into 8 nude mice per group. The rate of tumor formation was 5–8 per group as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was administered orally at 6.25 mg/kg/day. Tumor sizes were monitored as described in the Methods section. Representative tumor images are shown. B. A similar experiment was performed with A549 xenografts (shIFNAR1 clone #2). Eight nude mice were injected per group and the rate of tumor formation was 5–8 as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was used at 100 mg/kg/d. C. HCC4190 EGFR mutant PDX was subcutaneously implanted on NOD-SCID mice. Eight nude mice were implanted per group and the rate of tumor formation was 7–8 as shown in the Source_Data_Fig.7 (n=7–8). Mice were orally treated with 6.25 mg/kg/day erlotinib and/or i.p. injected with 2 mg/kg/day anifrolumab, a monoclonal IFNAR1 antibody. D. A similar PDX experiment was performed with HCC4087, which harbor mutant KRAS and wild-type EGFR. Eight nude mice were injected per group and all 8 mice formed tumors (n=8). Erlotinib was used at a dose of 100 mg/kg/d. E. KRAS LSL-G12D transgenic mice were generated as in the Methods section, and randomly divided into 4 groups (n=3–4 as the number of dots), receiving vehicle, oral erlotinib of 100 mg/kg/day, i.p. injection of mouse anti-mouse IFNAR1 antibody at 3 mg/kg/day, and combination administration of erlotinib plus IFNAR1 antibody for 28 continuous days. Bi-weekly MRI scanning was used to monitor tumor growth. Tumor sizes were calculated by ImageJ. Representative MRI images are shown, n=3–4 as indicated by the number of dots (mice). The tumors grow as diffuse lung opacities and “H” refers to heart. Data (A-E, in vivo) refers to mean ± S.E.M. of tumor sizes (n as above), *: p<0.05, **:p<0.01, ***:p<0.001, by two-way ANOVA adjusted by Bonferroni’s. For in vitro experiments (A-B), n=3 technical replicates, representative of 3 independent repeats with similar results. Western blots are cropped and representative of three independent repeated experiments with similar results. Uncropped are in Source_Data_Fig.7. Numerical source data for the experiments in this figure can be found in Source_Data_Fig.7.

    Journal: Nature cancer

    Article Title: EGFR inhibition triggers an adaptive response by co-opting antiviral signaling pathways in lung cancer

    doi: 10.1038/s43018-020-0048-0

    Figure Lengend Snippet: A. HCC827 cells were stably infected with lentivirus control shRNA (shCtrl) or shRNA for IFNAR1 lentivirus and silencing was confirmed by Western blot. Silenced clones were studied in AlamarBlue cell survival assays following erlotinib exposure for 72h. Cells with stable silencing of IFNAR1 (clone #3) or control shRNA were subcutaneously injected into 8 nude mice per group. The rate of tumor formation was 5–8 per group as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was administered orally at 6.25 mg/kg/day. Tumor sizes were monitored as described in the Methods section. Representative tumor images are shown. B. A similar experiment was performed with A549 xenografts (shIFNAR1 clone #2). Eight nude mice were injected per group and the rate of tumor formation was 5–8 as shown in the Source_Data_Fig.7 (n=5–8). Erlotinib was used at 100 mg/kg/d. C. HCC4190 EGFR mutant PDX was subcutaneously implanted on NOD-SCID mice. Eight nude mice were implanted per group and the rate of tumor formation was 7–8 as shown in the Source_Data_Fig.7 (n=7–8). Mice were orally treated with 6.25 mg/kg/day erlotinib and/or i.p. injected with 2 mg/kg/day anifrolumab, a monoclonal IFNAR1 antibody. D. A similar PDX experiment was performed with HCC4087, which harbor mutant KRAS and wild-type EGFR. Eight nude mice were injected per group and all 8 mice formed tumors (n=8). Erlotinib was used at a dose of 100 mg/kg/d. E. KRAS LSL-G12D transgenic mice were generated as in the Methods section, and randomly divided into 4 groups (n=3–4 as the number of dots), receiving vehicle, oral erlotinib of 100 mg/kg/day, i.p. injection of mouse anti-mouse IFNAR1 antibody at 3 mg/kg/day, and combination administration of erlotinib plus IFNAR1 antibody for 28 continuous days. Bi-weekly MRI scanning was used to monitor tumor growth. Tumor sizes were calculated by ImageJ. Representative MRI images are shown, n=3–4 as indicated by the number of dots (mice). The tumors grow as diffuse lung opacities and “H” refers to heart. Data (A-E, in vivo) refers to mean ± S.E.M. of tumor sizes (n as above), *: p<0.05, **:p<0.01, ***:p<0.001, by two-way ANOVA adjusted by Bonferroni’s. For in vitro experiments (A-B), n=3 technical replicates, representative of 3 independent repeats with similar results. Western blots are cropped and representative of three independent repeated experiments with similar results. Uncropped are in Source_Data_Fig.7. Numerical source data for the experiments in this figure can be found in Source_Data_Fig.7.

    Article Snippet: Lentiviruses for establishing stable cell lines used for xenograft experiments were obtained from Santa Cruz Biotechnology (Dallas, TX), including shTBK1(sc-39058-V), shIRF3(sc-35710-V), shIFNAR1(sc-35637-V) Human Lentiviral Particles, and Control shRNA Lentiviral Particles-A(sc-108080).

    Techniques: Stable Transfection, Infection, shRNA, Western Blot, Clone Assay, Injection, Mutagenesis, Transgenic Assay, Generated, In Vivo, In Vitro