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hek dualtm htlr3 reporter cells  (InvivoGen)


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    InvivoGen hek dualtm htlr3 reporter cells
    (A) Schematic representation depicting the role of TBK1 in regulation of TNFR1- and IFN-induced signalling and cell death. (B) IRF pathway activation was assessed using a secreted Lucia luciferase reporter assay in HEK-Dual TM <t>hTLR3</t> cells. Cells were preincubated with 1 µM CCT412020 (12 h) prior to stimulation with poly (I:C) (1 µg/ml) for 6 h. IRF-dependent signalling was quantified by measuring secreted Lucia luciferase activity in the culture supernatant using a luminometer. (C) NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with poly(I:C) (1 µg/mL) for 6 h. NF-κB-dependent SEAP activity was quantified by measuring absorbance at 595 nm. (D) TNF induced NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with TNF (10 ng/mL) for 6 h. NF-κB–dependent SEAP activity was quantified by measuring absorbance at 595 nm. (E) Cell viability was assessed using a CellTiter-Glo (CTG) assay in the breast cancer cell lines MCF7. Cells were pre-treated with CCT412020 (1 µM) and IFNβ (1 ng/ml) for 24 h, after which TNF (10 ng/ml) was added either as a single agents or in combination for additional 44 h. Viability was quantified following treatment to evaluate the impact of TBK1 degradation alone or in combination with pro-inflammatory cytokine signalling. (F) Dose-response analysis of CCT412020 in MCF7 cells in the presence or absence of IFNβ (1 ng/ml) for 48h. Cell viability was assessed using a CellTiter-Glo assay, and DC₅₀ values were determined from a representative experiment. (G) Cell viability in HCC38 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (H) Cell viability in BT549 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (I) Cell viability was assessed using a CellTiter-Glo (CTG) assay in MC38 and MC38 hCRBN cells. Cells were treated with CCT412020 for 18 h in the presence or absence of TNF. Viability was quantified following treatment to evaluate the impact of TBK1 degradation and the contribution of human CRBN expression to TNF-mediated cytotoxic responses. (J) Long-term clonogenic survival (7 days) was assessed in MC38 and MC38 hCRBN cells following treatment with CCT412020 in the presence or absence of TNFα. Cells were treated as indicated and allowed to grow for colony formation. Representative images of stained colonies in culture wells are shown, and clonogenic survival was quantified (K) from scanned plates and plotted as indicated.
    Hek Dualtm Htlr3 Reporter Cells, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hek dualtm htlr3 reporter cells/product/InvivoGen
    Average 94 stars, based on 16 article reviews
    hek dualtm htlr3 reporter cells - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Developing potent and selective TBK1 molecular glue degraders for cancer immunotherapy"

    Article Title: Developing potent and selective TBK1 molecular glue degraders for cancer immunotherapy

    Journal: bioRxiv

    doi: 10.64898/2026.01.30.702304

    (A) Schematic representation depicting the role of TBK1 in regulation of TNFR1- and IFN-induced signalling and cell death. (B) IRF pathway activation was assessed using a secreted Lucia luciferase reporter assay in HEK-Dual TM hTLR3 cells. Cells were preincubated with 1 µM CCT412020 (12 h) prior to stimulation with poly (I:C) (1 µg/ml) for 6 h. IRF-dependent signalling was quantified by measuring secreted Lucia luciferase activity in the culture supernatant using a luminometer. (C) NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with poly(I:C) (1 µg/mL) for 6 h. NF-κB-dependent SEAP activity was quantified by measuring absorbance at 595 nm. (D) TNF induced NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with TNF (10 ng/mL) for 6 h. NF-κB–dependent SEAP activity was quantified by measuring absorbance at 595 nm. (E) Cell viability was assessed using a CellTiter-Glo (CTG) assay in the breast cancer cell lines MCF7. Cells were pre-treated with CCT412020 (1 µM) and IFNβ (1 ng/ml) for 24 h, after which TNF (10 ng/ml) was added either as a single agents or in combination for additional 44 h. Viability was quantified following treatment to evaluate the impact of TBK1 degradation alone or in combination with pro-inflammatory cytokine signalling. (F) Dose-response analysis of CCT412020 in MCF7 cells in the presence or absence of IFNβ (1 ng/ml) for 48h. Cell viability was assessed using a CellTiter-Glo assay, and DC₅₀ values were determined from a representative experiment. (G) Cell viability in HCC38 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (H) Cell viability in BT549 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (I) Cell viability was assessed using a CellTiter-Glo (CTG) assay in MC38 and MC38 hCRBN cells. Cells were treated with CCT412020 for 18 h in the presence or absence of TNF. Viability was quantified following treatment to evaluate the impact of TBK1 degradation and the contribution of human CRBN expression to TNF-mediated cytotoxic responses. (J) Long-term clonogenic survival (7 days) was assessed in MC38 and MC38 hCRBN cells following treatment with CCT412020 in the presence or absence of TNFα. Cells were treated as indicated and allowed to grow for colony formation. Representative images of stained colonies in culture wells are shown, and clonogenic survival was quantified (K) from scanned plates and plotted as indicated.
    Figure Legend Snippet: (A) Schematic representation depicting the role of TBK1 in regulation of TNFR1- and IFN-induced signalling and cell death. (B) IRF pathway activation was assessed using a secreted Lucia luciferase reporter assay in HEK-Dual TM hTLR3 cells. Cells were preincubated with 1 µM CCT412020 (12 h) prior to stimulation with poly (I:C) (1 µg/ml) for 6 h. IRF-dependent signalling was quantified by measuring secreted Lucia luciferase activity in the culture supernatant using a luminometer. (C) NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with poly(I:C) (1 µg/mL) for 6 h. NF-κB-dependent SEAP activity was quantified by measuring absorbance at 595 nm. (D) TNF induced NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with TNF (10 ng/mL) for 6 h. NF-κB–dependent SEAP activity was quantified by measuring absorbance at 595 nm. (E) Cell viability was assessed using a CellTiter-Glo (CTG) assay in the breast cancer cell lines MCF7. Cells were pre-treated with CCT412020 (1 µM) and IFNβ (1 ng/ml) for 24 h, after which TNF (10 ng/ml) was added either as a single agents or in combination for additional 44 h. Viability was quantified following treatment to evaluate the impact of TBK1 degradation alone or in combination with pro-inflammatory cytokine signalling. (F) Dose-response analysis of CCT412020 in MCF7 cells in the presence or absence of IFNβ (1 ng/ml) for 48h. Cell viability was assessed using a CellTiter-Glo assay, and DC₅₀ values were determined from a representative experiment. (G) Cell viability in HCC38 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (H) Cell viability in BT549 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (I) Cell viability was assessed using a CellTiter-Glo (CTG) assay in MC38 and MC38 hCRBN cells. Cells were treated with CCT412020 for 18 h in the presence or absence of TNF. Viability was quantified following treatment to evaluate the impact of TBK1 degradation and the contribution of human CRBN expression to TNF-mediated cytotoxic responses. (J) Long-term clonogenic survival (7 days) was assessed in MC38 and MC38 hCRBN cells following treatment with CCT412020 in the presence or absence of TNFα. Cells were treated as indicated and allowed to grow for colony formation. Representative images of stained colonies in culture wells are shown, and clonogenic survival was quantified (K) from scanned plates and plotted as indicated.

    Techniques Used: Activation Assay, Luciferase, Reporter Assay, Activity Assay, Incubation, CTG Assay, Glo Assay, Expressing, Staining



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    hek dualtm htlr3 reporter cells  (InvivoGen)
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    InvivoGen hek dualtm htlr3 reporter cells
    (A) Schematic representation depicting the role of TBK1 in regulation of TNFR1- and IFN-induced signalling and cell death. (B) IRF pathway activation was assessed using a secreted Lucia luciferase reporter assay in HEK-Dual TM <t>hTLR3</t> cells. Cells were preincubated with 1 µM CCT412020 (12 h) prior to stimulation with poly (I:C) (1 µg/ml) for 6 h. IRF-dependent signalling was quantified by measuring secreted Lucia luciferase activity in the culture supernatant using a luminometer. (C) NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with poly(I:C) (1 µg/mL) for 6 h. NF-κB-dependent SEAP activity was quantified by measuring absorbance at 595 nm. (D) TNF induced NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with TNF (10 ng/mL) for 6 h. NF-κB–dependent SEAP activity was quantified by measuring absorbance at 595 nm. (E) Cell viability was assessed using a CellTiter-Glo (CTG) assay in the breast cancer cell lines MCF7. Cells were pre-treated with CCT412020 (1 µM) and IFNβ (1 ng/ml) for 24 h, after which TNF (10 ng/ml) was added either as a single agents or in combination for additional 44 h. Viability was quantified following treatment to evaluate the impact of TBK1 degradation alone or in combination with pro-inflammatory cytokine signalling. (F) Dose-response analysis of CCT412020 in MCF7 cells in the presence or absence of IFNβ (1 ng/ml) for 48h. Cell viability was assessed using a CellTiter-Glo assay, and DC₅₀ values were determined from a representative experiment. (G) Cell viability in HCC38 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (H) Cell viability in BT549 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (I) Cell viability was assessed using a CellTiter-Glo (CTG) assay in MC38 and MC38 hCRBN cells. Cells were treated with CCT412020 for 18 h in the presence or absence of TNF. Viability was quantified following treatment to evaluate the impact of TBK1 degradation and the contribution of human CRBN expression to TNF-mediated cytotoxic responses. (J) Long-term clonogenic survival (7 days) was assessed in MC38 and MC38 hCRBN cells following treatment with CCT412020 in the presence or absence of TNFα. Cells were treated as indicated and allowed to grow for colony formation. Representative images of stained colonies in culture wells are shown, and clonogenic survival was quantified (K) from scanned plates and plotted as indicated.
    Hek Dualtm Htlr3 Reporter Cells, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hek dualtm htlr3 reporter cells/product/InvivoGen
    Average 94 stars, based on 1 article reviews
    hek dualtm htlr3 reporter cells - by Bioz Stars, 2026-02
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    (A) Schematic representation depicting the role of TBK1 in regulation of TNFR1- and IFN-induced signalling and cell death. (B) IRF pathway activation was assessed using a secreted Lucia luciferase reporter assay in HEK-Dual TM hTLR3 cells. Cells were preincubated with 1 µM CCT412020 (12 h) prior to stimulation with poly (I:C) (1 µg/ml) for 6 h. IRF-dependent signalling was quantified by measuring secreted Lucia luciferase activity in the culture supernatant using a luminometer. (C) NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with poly(I:C) (1 µg/mL) for 6 h. NF-κB-dependent SEAP activity was quantified by measuring absorbance at 595 nm. (D) TNF induced NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with TNF (10 ng/mL) for 6 h. NF-κB–dependent SEAP activity was quantified by measuring absorbance at 595 nm. (E) Cell viability was assessed using a CellTiter-Glo (CTG) assay in the breast cancer cell lines MCF7. Cells were pre-treated with CCT412020 (1 µM) and IFNβ (1 ng/ml) for 24 h, after which TNF (10 ng/ml) was added either as a single agents or in combination for additional 44 h. Viability was quantified following treatment to evaluate the impact of TBK1 degradation alone or in combination with pro-inflammatory cytokine signalling. (F) Dose-response analysis of CCT412020 in MCF7 cells in the presence or absence of IFNβ (1 ng/ml) for 48h. Cell viability was assessed using a CellTiter-Glo assay, and DC₅₀ values were determined from a representative experiment. (G) Cell viability in HCC38 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (H) Cell viability in BT549 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (I) Cell viability was assessed using a CellTiter-Glo (CTG) assay in MC38 and MC38 hCRBN cells. Cells were treated with CCT412020 for 18 h in the presence or absence of TNF. Viability was quantified following treatment to evaluate the impact of TBK1 degradation and the contribution of human CRBN expression to TNF-mediated cytotoxic responses. (J) Long-term clonogenic survival (7 days) was assessed in MC38 and MC38 hCRBN cells following treatment with CCT412020 in the presence or absence of TNFα. Cells were treated as indicated and allowed to grow for colony formation. Representative images of stained colonies in culture wells are shown, and clonogenic survival was quantified (K) from scanned plates and plotted as indicated.

    Journal: bioRxiv

    Article Title: Developing potent and selective TBK1 molecular glue degraders for cancer immunotherapy

    doi: 10.64898/2026.01.30.702304

    Figure Lengend Snippet: (A) Schematic representation depicting the role of TBK1 in regulation of TNFR1- and IFN-induced signalling and cell death. (B) IRF pathway activation was assessed using a secreted Lucia luciferase reporter assay in HEK-Dual TM hTLR3 cells. Cells were preincubated with 1 µM CCT412020 (12 h) prior to stimulation with poly (I:C) (1 µg/ml) for 6 h. IRF-dependent signalling was quantified by measuring secreted Lucia luciferase activity in the culture supernatant using a luminometer. (C) NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with poly(I:C) (1 µg/mL) for 6 h. NF-κB-dependent SEAP activity was quantified by measuring absorbance at 595 nm. (D) TNF induced NF-κB pathway activity was measured using a SEAP reporter assay in HEK-Dual™ hTLR3 cells. Cells were pre-incubated with the 1 µM CCT412020 for 12 h prior to stimulation with TNF (10 ng/mL) for 6 h. NF-κB–dependent SEAP activity was quantified by measuring absorbance at 595 nm. (E) Cell viability was assessed using a CellTiter-Glo (CTG) assay in the breast cancer cell lines MCF7. Cells were pre-treated with CCT412020 (1 µM) and IFNβ (1 ng/ml) for 24 h, after which TNF (10 ng/ml) was added either as a single agents or in combination for additional 44 h. Viability was quantified following treatment to evaluate the impact of TBK1 degradation alone or in combination with pro-inflammatory cytokine signalling. (F) Dose-response analysis of CCT412020 in MCF7 cells in the presence or absence of IFNβ (1 ng/ml) for 48h. Cell viability was assessed using a CellTiter-Glo assay, and DC₅₀ values were determined from a representative experiment. (G) Cell viability in HCC38 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (H) Cell viability in BT549 cells was assessed using a CellTiter-Glo (CTG) as in (E) . (I) Cell viability was assessed using a CellTiter-Glo (CTG) assay in MC38 and MC38 hCRBN cells. Cells were treated with CCT412020 for 18 h in the presence or absence of TNF. Viability was quantified following treatment to evaluate the impact of TBK1 degradation and the contribution of human CRBN expression to TNF-mediated cytotoxic responses. (J) Long-term clonogenic survival (7 days) was assessed in MC38 and MC38 hCRBN cells following treatment with CCT412020 in the presence or absence of TNFα. Cells were treated as indicated and allowed to grow for colony formation. Representative images of stained colonies in culture wells are shown, and clonogenic survival was quantified (K) from scanned plates and plotted as indicated.

    Article Snippet: HEK-DualTM hTLR3 reporter cells (InvivoGen; Cat. #hkd-htlr3) were seeded in 96-well plates at a density of 1.0 × 104 cells per well and allowed to adhere overnight.

    Techniques: Activation Assay, Luciferase, Reporter Assay, Activity Assay, Incubation, CTG Assay, Glo Assay, Expressing, Staining