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3prna synthesis megashortscript t7 transcription kit  (Thermo Fisher)


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    Thermo Fisher 3prna synthesis megashortscript t7 transcription kit
    Therapeutic stimulation of tumor cell–intrinsic RIG-I/MAVS signaling sensitizes tumor cells to CAR T-cell–mediated apoptosis. A–E, WT or Mavs − / − B16-EpCAM tumor cells were transfected with <t>3pRNA</t> 24 hours prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. A and B, Tumor cells were sorted 24 hours after coculture for bulk RNA extraction. Relative expression of Puma and Bid ( A ) as well as Fas and Trailr2 ( B ) in B16-EpCAM cells. Data are normalized to unstim. B16 cells. C–E, Apoptosis induction ( C ), cleavage of caspase-3 ( D ), and viability ( E ) in B16-EpCAM cells by flow cytometry. All data are mean ± SEM of n = 3 to 6 replicates. F, B16-EpCAM cells were treated with 3pRNA as described above and were subsequently cocultured with either WT or Mavs − / − CAR T cells. Apoptosis induction in B16-EpCAM cells by flow cytometry is presented as mean ± SEM of n = 3 to 4 replicates. G, Different EGFR-expressing human tumor cell lines were transfected with 3pRNA for 24 hours prior to exposure to EGFR CAR or UTD T cells. Apoptosis induction in tumor cells by flow cytometry is presented as mean ± SEM of n = 3 replicates. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated.
    3prna Synthesis Megashortscript T7 Transcription Kit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/3prna synthesis megashortscript t7 transcription kit/product/Thermo Fisher
    Average 90 stars, based on 1 article reviews
    3prna synthesis megashortscript t7 transcription kit - by Bioz Stars, 2026-06
    90/100 stars

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    1) Product Images from "Targeting Intracellular Innate RNA-Sensing Systems Overcomes Resistance to CAR T-cell Therapy in Solid Tumors"

    Article Title: Targeting Intracellular Innate RNA-Sensing Systems Overcomes Resistance to CAR T-cell Therapy in Solid Tumors

    Journal: Cancer Research

    doi: 10.1158/0008-5472.CAN-24-3425

    Therapeutic stimulation of tumor cell–intrinsic RIG-I/MAVS signaling sensitizes tumor cells to CAR T-cell–mediated apoptosis. A–E, WT or Mavs − / − B16-EpCAM tumor cells were transfected with 3pRNA 24 hours prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. A and B, Tumor cells were sorted 24 hours after coculture for bulk RNA extraction. Relative expression of Puma and Bid ( A ) as well as Fas and Trailr2 ( B ) in B16-EpCAM cells. Data are normalized to unstim. B16 cells. C–E, Apoptosis induction ( C ), cleavage of caspase-3 ( D ), and viability ( E ) in B16-EpCAM cells by flow cytometry. All data are mean ± SEM of n = 3 to 6 replicates. F, B16-EpCAM cells were treated with 3pRNA as described above and were subsequently cocultured with either WT or Mavs − / − CAR T cells. Apoptosis induction in B16-EpCAM cells by flow cytometry is presented as mean ± SEM of n = 3 to 4 replicates. G, Different EGFR-expressing human tumor cell lines were transfected with 3pRNA for 24 hours prior to exposure to EGFR CAR or UTD T cells. Apoptosis induction in tumor cells by flow cytometry is presented as mean ± SEM of n = 3 replicates. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated.
    Figure Legend Snippet: Therapeutic stimulation of tumor cell–intrinsic RIG-I/MAVS signaling sensitizes tumor cells to CAR T-cell–mediated apoptosis. A–E, WT or Mavs − / − B16-EpCAM tumor cells were transfected with 3pRNA 24 hours prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. A and B, Tumor cells were sorted 24 hours after coculture for bulk RNA extraction. Relative expression of Puma and Bid ( A ) as well as Fas and Trailr2 ( B ) in B16-EpCAM cells. Data are normalized to unstim. B16 cells. C–E, Apoptosis induction ( C ), cleavage of caspase-3 ( D ), and viability ( E ) in B16-EpCAM cells by flow cytometry. All data are mean ± SEM of n = 3 to 6 replicates. F, B16-EpCAM cells were treated with 3pRNA as described above and were subsequently cocultured with either WT or Mavs − / − CAR T cells. Apoptosis induction in B16-EpCAM cells by flow cytometry is presented as mean ± SEM of n = 3 to 4 replicates. G, Different EGFR-expressing human tumor cell lines were transfected with 3pRNA for 24 hours prior to exposure to EGFR CAR or UTD T cells. Apoptosis induction in tumor cells by flow cytometry is presented as mean ± SEM of n = 3 replicates. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated.

    Techniques Used: Transfection, Control, RNA Extraction, Expressing, Flow Cytometry

    Tumor-intrinsic MAVS signaling induces susceptibility to CAR T-cell killing via soluble factors and auto-/paracrine IFN signaling that can spread to bystander tumor cells. A, B16-EpCAM cells were pretreated with anti-IFNaR1 blocking antibody before 3pRNA transfection and subsequent coculture with anti-EpCAM CAR or UTD T cells. Apoptosis induction in tumor cells after 24 hours was determined by flow cytometry. Data are mean ± SEM of n = 3 replicates. B, WT or Mavs − / − B16-EpCAM cells were either directly transfected with 3pRNA or exposed to conditioned culture medium from 3pRNA-activated WT B16-EpCAM cells. Relative expression of Puma , Bid , and Ifnb1 in bystander B16-EpCAM cells was determined by RT-PCR. Data were normalized to unstimulated (unstim.) B16 cells and are mean ± SEM of n = 3 replicates. C, WT or Mavs − / − B16-EpCAM cells were exposed to anti-EpCAM CAR or UTD T cells in the presence of conditioned culture medium from 3pRNA-activated WT B16-EpCAM cells. Apoptosis induction by flow cytometry is presented as mean ± SEM of n = 6 replicates. All data are representative of or pooled from at least two independent experiments.
    Figure Legend Snippet: Tumor-intrinsic MAVS signaling induces susceptibility to CAR T-cell killing via soluble factors and auto-/paracrine IFN signaling that can spread to bystander tumor cells. A, B16-EpCAM cells were pretreated with anti-IFNaR1 blocking antibody before 3pRNA transfection and subsequent coculture with anti-EpCAM CAR or UTD T cells. Apoptosis induction in tumor cells after 24 hours was determined by flow cytometry. Data are mean ± SEM of n = 3 replicates. B, WT or Mavs − / − B16-EpCAM cells were either directly transfected with 3pRNA or exposed to conditioned culture medium from 3pRNA-activated WT B16-EpCAM cells. Relative expression of Puma , Bid , and Ifnb1 in bystander B16-EpCAM cells was determined by RT-PCR. Data were normalized to unstimulated (unstim.) B16 cells and are mean ± SEM of n = 3 replicates. C, WT or Mavs − / − B16-EpCAM cells were exposed to anti-EpCAM CAR or UTD T cells in the presence of conditioned culture medium from 3pRNA-activated WT B16-EpCAM cells. Apoptosis induction by flow cytometry is presented as mean ± SEM of n = 6 replicates. All data are representative of or pooled from at least two independent experiments.

    Techniques Used: Blocking Assay, Transfection, Flow Cytometry, Expressing, Reverse Transcription Polymerase Chain Reaction

    Therapeutically activated tumor-intrinsic RIG-I/MAVS signaling imprints a cytolytic phenotype on CAR T cells. A and B, B16-EpCAM tumor cells were transfected with 3pRNA prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. Expression of CD69, IFNγ, and granzyme B ( A ) and Fas ligand (FasL; B ) on T cells was measured by flow cytometry 24 hours after coculture. Data are mean ± SEM of n = 6 replicates. C, Anti-EpCAM CAR or UTD T cells were cocultured with 3pRNA-treated WT or Mavs − / − B16-EpCAM for 24 hours before rechallenge with steady-state WT B16-EpCAM cells. Apoptosis induction in initial and rechallenge B16 cells was determined by flow cytometry. All data are mean ± SEM of n = 6 replicates. D, Anti-EpCAM CAR T cells were exposed to conditioned culture medium from RIG-I–treated B16-EpCAM cells. Expression of CD25, PD-1, CD69, and granzyme B on CAR T cells is presented as mean ± SEM of n = 3 replicates. E, Apoptosis induction in 3pRNA-treated B16-EpCAM cells 24 hours after coculture with WT or Ifnar1 − / − anti-EpCAM CAR or UTD T cells. Data are mean ± SEM of n = 4 replicates. F, Heatmap showing the relative release of cytokines and chemokines from B16-EpCAM, Panc02-EpCAM, and MG846-MSLN cells in response to RIG-I activation. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated. C, Created in BioRender. Soliman, N. (2025) https://BioRender.com/l0n2a28 .
    Figure Legend Snippet: Therapeutically activated tumor-intrinsic RIG-I/MAVS signaling imprints a cytolytic phenotype on CAR T cells. A and B, B16-EpCAM tumor cells were transfected with 3pRNA prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. Expression of CD69, IFNγ, and granzyme B ( A ) and Fas ligand (FasL; B ) on T cells was measured by flow cytometry 24 hours after coculture. Data are mean ± SEM of n = 6 replicates. C, Anti-EpCAM CAR or UTD T cells were cocultured with 3pRNA-treated WT or Mavs − / − B16-EpCAM for 24 hours before rechallenge with steady-state WT B16-EpCAM cells. Apoptosis induction in initial and rechallenge B16 cells was determined by flow cytometry. All data are mean ± SEM of n = 6 replicates. D, Anti-EpCAM CAR T cells were exposed to conditioned culture medium from RIG-I–treated B16-EpCAM cells. Expression of CD25, PD-1, CD69, and granzyme B on CAR T cells is presented as mean ± SEM of n = 3 replicates. E, Apoptosis induction in 3pRNA-treated B16-EpCAM cells 24 hours after coculture with WT or Ifnar1 − / − anti-EpCAM CAR or UTD T cells. Data are mean ± SEM of n = 4 replicates. F, Heatmap showing the relative release of cytokines and chemokines from B16-EpCAM, Panc02-EpCAM, and MG846-MSLN cells in response to RIG-I activation. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated. C, Created in BioRender. Soliman, N. (2025) https://BioRender.com/l0n2a28 .

    Techniques Used: Transfection, Control, Expressing, Flow Cytometry, Activation Assay



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    3prna synthesis megashortscript t7 transcription kit  (Thermo Fisher)
    90
    Thermo Fisher 3prna synthesis megashortscript t7 transcription kit
    Therapeutic stimulation of tumor cell–intrinsic RIG-I/MAVS signaling sensitizes tumor cells to CAR T-cell–mediated apoptosis. A–E, WT or Mavs − / − B16-EpCAM tumor cells were transfected with <t>3pRNA</t> 24 hours prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. A and B, Tumor cells were sorted 24 hours after coculture for bulk RNA extraction. Relative expression of Puma and Bid ( A ) as well as Fas and Trailr2 ( B ) in B16-EpCAM cells. Data are normalized to unstim. B16 cells. C–E, Apoptosis induction ( C ), cleavage of caspase-3 ( D ), and viability ( E ) in B16-EpCAM cells by flow cytometry. All data are mean ± SEM of n = 3 to 6 replicates. F, B16-EpCAM cells were treated with 3pRNA as described above and were subsequently cocultured with either WT or Mavs − / − CAR T cells. Apoptosis induction in B16-EpCAM cells by flow cytometry is presented as mean ± SEM of n = 3 to 4 replicates. G, Different EGFR-expressing human tumor cell lines were transfected with 3pRNA for 24 hours prior to exposure to EGFR CAR or UTD T cells. Apoptosis induction in tumor cells by flow cytometry is presented as mean ± SEM of n = 3 replicates. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated.
    3prna Synthesis Megashortscript T7 Transcription Kit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/3prna synthesis megashortscript t7 transcription kit/product/Thermo Fisher
    Average 90 stars, based on 1 article reviews
    3prna synthesis megashortscript t7 transcription kit - by Bioz Stars, 2026-06
    90/100 stars
    		  Buy from Supplier

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    Therapeutic stimulation of tumor cell–intrinsic RIG-I/MAVS signaling sensitizes tumor cells to CAR T-cell–mediated apoptosis. A–E, WT or Mavs − / − B16-EpCAM tumor cells were transfected with 3pRNA 24 hours prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. A and B, Tumor cells were sorted 24 hours after coculture for bulk RNA extraction. Relative expression of Puma and Bid ( A ) as well as Fas and Trailr2 ( B ) in B16-EpCAM cells. Data are normalized to unstim. B16 cells. C–E, Apoptosis induction ( C ), cleavage of caspase-3 ( D ), and viability ( E ) in B16-EpCAM cells by flow cytometry. All data are mean ± SEM of n = 3 to 6 replicates. F, B16-EpCAM cells were treated with 3pRNA as described above and were subsequently cocultured with either WT or Mavs − / − CAR T cells. Apoptosis induction in B16-EpCAM cells by flow cytometry is presented as mean ± SEM of n = 3 to 4 replicates. G, Different EGFR-expressing human tumor cell lines were transfected with 3pRNA for 24 hours prior to exposure to EGFR CAR or UTD T cells. Apoptosis induction in tumor cells by flow cytometry is presented as mean ± SEM of n = 3 replicates. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated.

    Journal: Cancer Research

    Article Title: Targeting Intracellular Innate RNA-Sensing Systems Overcomes Resistance to CAR T-cell Therapy in Solid Tumors

    doi: 10.1158/0008-5472.CAN-24-3425

    Figure Lengend Snippet: Therapeutic stimulation of tumor cell–intrinsic RIG-I/MAVS signaling sensitizes tumor cells to CAR T-cell–mediated apoptosis. A–E, WT or Mavs − / − B16-EpCAM tumor cells were transfected with 3pRNA 24 hours prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. A and B, Tumor cells were sorted 24 hours after coculture for bulk RNA extraction. Relative expression of Puma and Bid ( A ) as well as Fas and Trailr2 ( B ) in B16-EpCAM cells. Data are normalized to unstim. B16 cells. C–E, Apoptosis induction ( C ), cleavage of caspase-3 ( D ), and viability ( E ) in B16-EpCAM cells by flow cytometry. All data are mean ± SEM of n = 3 to 6 replicates. F, B16-EpCAM cells were treated with 3pRNA as described above and were subsequently cocultured with either WT or Mavs − / − CAR T cells. Apoptosis induction in B16-EpCAM cells by flow cytometry is presented as mean ± SEM of n = 3 to 4 replicates. G, Different EGFR-expressing human tumor cell lines were transfected with 3pRNA for 24 hours prior to exposure to EGFR CAR or UTD T cells. Apoptosis induction in tumor cells by flow cytometry is presented as mean ± SEM of n = 3 replicates. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated.

    Article Snippet: For specific activation of RIG-I/MAVS, double-stranded in vitro -transcribed 3pRNA (sense, 5′- UCA AAC AGU CCU CGC AUG CCU AUA GUG AGU CG -3′) was synthesized using the 3pRNA synthesis MEGAshortscript T7 transcription kit (Thermo Fisher Scientific) as described previously ( ).

    Techniques: Transfection, Control, RNA Extraction, Expressing, Flow Cytometry

    Tumor-intrinsic MAVS signaling induces susceptibility to CAR T-cell killing via soluble factors and auto-/paracrine IFN signaling that can spread to bystander tumor cells. A, B16-EpCAM cells were pretreated with anti-IFNaR1 blocking antibody before 3pRNA transfection and subsequent coculture with anti-EpCAM CAR or UTD T cells. Apoptosis induction in tumor cells after 24 hours was determined by flow cytometry. Data are mean ± SEM of n = 3 replicates. B, WT or Mavs − / − B16-EpCAM cells were either directly transfected with 3pRNA or exposed to conditioned culture medium from 3pRNA-activated WT B16-EpCAM cells. Relative expression of Puma , Bid , and Ifnb1 in bystander B16-EpCAM cells was determined by RT-PCR. Data were normalized to unstimulated (unstim.) B16 cells and are mean ± SEM of n = 3 replicates. C, WT or Mavs − / − B16-EpCAM cells were exposed to anti-EpCAM CAR or UTD T cells in the presence of conditioned culture medium from 3pRNA-activated WT B16-EpCAM cells. Apoptosis induction by flow cytometry is presented as mean ± SEM of n = 6 replicates. All data are representative of or pooled from at least two independent experiments.

    Journal: Cancer Research

    Article Title: Targeting Intracellular Innate RNA-Sensing Systems Overcomes Resistance to CAR T-cell Therapy in Solid Tumors

    doi: 10.1158/0008-5472.CAN-24-3425

    Figure Lengend Snippet: Tumor-intrinsic MAVS signaling induces susceptibility to CAR T-cell killing via soluble factors and auto-/paracrine IFN signaling that can spread to bystander tumor cells. A, B16-EpCAM cells were pretreated with anti-IFNaR1 blocking antibody before 3pRNA transfection and subsequent coculture with anti-EpCAM CAR or UTD T cells. Apoptosis induction in tumor cells after 24 hours was determined by flow cytometry. Data are mean ± SEM of n = 3 replicates. B, WT or Mavs − / − B16-EpCAM cells were either directly transfected with 3pRNA or exposed to conditioned culture medium from 3pRNA-activated WT B16-EpCAM cells. Relative expression of Puma , Bid , and Ifnb1 in bystander B16-EpCAM cells was determined by RT-PCR. Data were normalized to unstimulated (unstim.) B16 cells and are mean ± SEM of n = 3 replicates. C, WT or Mavs − / − B16-EpCAM cells were exposed to anti-EpCAM CAR or UTD T cells in the presence of conditioned culture medium from 3pRNA-activated WT B16-EpCAM cells. Apoptosis induction by flow cytometry is presented as mean ± SEM of n = 6 replicates. All data are representative of or pooled from at least two independent experiments.

    Article Snippet: For specific activation of RIG-I/MAVS, double-stranded in vitro -transcribed 3pRNA (sense, 5′- UCA AAC AGU CCU CGC AUG CCU AUA GUG AGU CG -3′) was synthesized using the 3pRNA synthesis MEGAshortscript T7 transcription kit (Thermo Fisher Scientific) as described previously ( ).

    Techniques: Blocking Assay, Transfection, Flow Cytometry, Expressing, Reverse Transcription Polymerase Chain Reaction

    Therapeutically activated tumor-intrinsic RIG-I/MAVS signaling imprints a cytolytic phenotype on CAR T cells. A and B, B16-EpCAM tumor cells were transfected with 3pRNA prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. Expression of CD69, IFNγ, and granzyme B ( A ) and Fas ligand (FasL; B ) on T cells was measured by flow cytometry 24 hours after coculture. Data are mean ± SEM of n = 6 replicates. C, Anti-EpCAM CAR or UTD T cells were cocultured with 3pRNA-treated WT or Mavs − / − B16-EpCAM for 24 hours before rechallenge with steady-state WT B16-EpCAM cells. Apoptosis induction in initial and rechallenge B16 cells was determined by flow cytometry. All data are mean ± SEM of n = 6 replicates. D, Anti-EpCAM CAR T cells were exposed to conditioned culture medium from RIG-I–treated B16-EpCAM cells. Expression of CD25, PD-1, CD69, and granzyme B on CAR T cells is presented as mean ± SEM of n = 3 replicates. E, Apoptosis induction in 3pRNA-treated B16-EpCAM cells 24 hours after coculture with WT or Ifnar1 − / − anti-EpCAM CAR or UTD T cells. Data are mean ± SEM of n = 4 replicates. F, Heatmap showing the relative release of cytokines and chemokines from B16-EpCAM, Panc02-EpCAM, and MG846-MSLN cells in response to RIG-I activation. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated. C, Created in BioRender. Soliman, N. (2025) https://BioRender.com/l0n2a28 .

    Journal: Cancer Research

    Article Title: Targeting Intracellular Innate RNA-Sensing Systems Overcomes Resistance to CAR T-cell Therapy in Solid Tumors

    doi: 10.1158/0008-5472.CAN-24-3425

    Figure Lengend Snippet: Therapeutically activated tumor-intrinsic RIG-I/MAVS signaling imprints a cytolytic phenotype on CAR T cells. A and B, B16-EpCAM tumor cells were transfected with 3pRNA prior to exposure to anti-EpCAM CAR T cells or UTD control T cells. Expression of CD69, IFNγ, and granzyme B ( A ) and Fas ligand (FasL; B ) on T cells was measured by flow cytometry 24 hours after coculture. Data are mean ± SEM of n = 6 replicates. C, Anti-EpCAM CAR or UTD T cells were cocultured with 3pRNA-treated WT or Mavs − / − B16-EpCAM for 24 hours before rechallenge with steady-state WT B16-EpCAM cells. Apoptosis induction in initial and rechallenge B16 cells was determined by flow cytometry. All data are mean ± SEM of n = 6 replicates. D, Anti-EpCAM CAR T cells were exposed to conditioned culture medium from RIG-I–treated B16-EpCAM cells. Expression of CD25, PD-1, CD69, and granzyme B on CAR T cells is presented as mean ± SEM of n = 3 replicates. E, Apoptosis induction in 3pRNA-treated B16-EpCAM cells 24 hours after coculture with WT or Ifnar1 − / − anti-EpCAM CAR or UTD T cells. Data are mean ± SEM of n = 4 replicates. F, Heatmap showing the relative release of cytokines and chemokines from B16-EpCAM, Panc02-EpCAM, and MG846-MSLN cells in response to RIG-I activation. All data are representative of or pooled from at least two independent experiments. Unstim., unstimulated. C, Created in BioRender. Soliman, N. (2025) https://BioRender.com/l0n2a28 .

    Article Snippet: For specific activation of RIG-I/MAVS, double-stranded in vitro -transcribed 3pRNA (sense, 5′- UCA AAC AGU CCU CGC AUG CCU AUA GUG AGU CG -3′) was synthesized using the 3pRNA synthesis MEGAshortscript T7 transcription kit (Thermo Fisher Scientific) as described previously ( ).

    Techniques: Transfection, Control, Expressing, Flow Cytometry, Activation Assay