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MedChemExpress renilla firefly luciferase dual assay kit
Renilla Firefly Luciferase Dual Assay Kit, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Selective activation of SBT777101 <t>Jurkat</t> reporter cells by citrullinated proteins. Representative dose–response curves showing fold-increase in luminescence ( y -axis) relative to baseline following incubation with increasing concentrations (log scale, x -axis) of citrullinated (red) or noncitrullinated (black) protein targets. Data points represent the mean ± SD of 3 replicates.
Nfat Luciferase Reporter Jurkat Cells, supplied by BPS Bioscience, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Addgene inc nfat luciferase reporter
(a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) <t>NFAT-luciferase</t> activation in FLAG-AT1R + TfR1 + <t>NFAT-Luc</t> + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.
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TransGen biotech co transdetect dualluciferase reporter assay kit
(a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) <t>NFAT-luciferase</t> activation in FLAG-AT1R + TfR1 + <t>NFAT-Luc</t> + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.
Transdetect Dualluciferase Reporter Assay Kit, supplied by TransGen biotech co, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Addgene inc pcdna3 luc
(a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) <t>NFAT-luciferase</t> activation in FLAG-AT1R + TfR1 + <t>NFAT-Luc</t> + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.
Pcdna3 Luc, 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
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MedChemExpress luciferin
(a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) <t>NFAT-luciferase</t> activation in FLAG-AT1R + TfR1 + <t>NFAT-Luc</t> + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.
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(a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) <t>NFAT-luciferase</t> activation in FLAG-AT1R + TfR1 + <t>NFAT-Luc</t> + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.
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(a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) <t>NFAT-luciferase</t> activation in FLAG-AT1R + TfR1 + <t>NFAT-Luc</t> + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.
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(a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) <t>NFAT-luciferase</t> activation in FLAG-AT1R + TfR1 + <t>NFAT-Luc</t> + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.
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Image Search Results


Selective activation of SBT777101 Jurkat reporter cells by citrullinated proteins. Representative dose–response curves showing fold-increase in luminescence ( y -axis) relative to baseline following incubation with increasing concentrations (log scale, x -axis) of citrullinated (red) or noncitrullinated (black) protein targets. Data points represent the mean ± SD of 3 replicates.

Journal: Toxicological Sciences

Article Title: Nonclinical safety assessment of SBT777101, a CAR-engineered regulatory T cell therapy for autoimmune diseases

doi: 10.1093/toxsci/kfag125

Figure Lengend Snippet: Selective activation of SBT777101 Jurkat reporter cells by citrullinated proteins. Representative dose–response curves showing fold-increase in luminescence ( y -axis) relative to baseline following incubation with increasing concentrations (log scale, x -axis) of citrullinated (red) or noncitrullinated (black) protein targets. Data points represent the mean ± SD of 3 replicates.

Article Snippet: NFAT-luciferase reporter Jurkat cells (BPS Bioscience) were stably transduced with the SBT777101 CAR.

Techniques: Activation Assay, Incubation

(a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) NFAT-luciferase activation in FLAG-AT1R + TfR1 + NFAT-Luc + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.

Journal: Nature

Article Title: GPCR antagonism via rewiring of receptor trafficking and degradation

doi: 10.1038/s41586-026-11088-0

Figure Lengend Snippet: (a) Schematic of native versus engineered GPCR trafficking (left). Native agonists typically induce GPCR internalization, followed by recycling or degradation. GTACs direct GPCRs for degradation by leveraging rapid, constitutive TfR1-mediated internalization. GTAC design (right): bifunctional antibody with GPCR-binding domain(s) and TfR1-binding domain(s) fused to an Fc. The control antibody lacks TfR1-binding domain(s). (b) Cell-surface GPCR levels (anti-FLAG flow cytometry) after treatment with GTACs or control antibodies. Cell-surface AT1R levels in FLAG-AT1R-GFP + TfR1 + Expi293 cells after 6 h treatment; cell-surface RXFP1 levels in FLAG-RXFP1 + TfR1 + Expi293 cells after 2 h treatment; cell-surface APJ levels in FLAG-APJ + TfR1 + HEK293T cells after 2 h treatment; and cell-surface A2AR levels in FLAG-A2AR + TfR1 + Expi293 cells after 6 h treatment. Data represent mean ± standard deviation (s.d.) from n = 3 replicates. (c) NFAT-luciferase activation in FLAG-AT1R + TfR1 + NFAT-Luc + Expi293 cells, after 2 h pre-treatment with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 4 h stimulation with varying concentration (left) or 9 nM (right) AngII. Data represent mean ± s.d. from n = 4 biological replicates. (d) β-arrestin recruitment in FLAG-AT1R-Tango + TfR1 + HTLA cells (luminescence) after pre-treatment for 2 h with 50 nM (left) or varying concentration (right) AT1R GTAC or Nb-Fc, followed by 14 h activation with varying concentrations (left) or 200 nM (right) AngII. Data represent mean ± s.d. from n = 3 biological replicates for both experiments. (e) RLN2-induced cAMP signaling in FLAG-RXFP1 + TfR1 + GloSensor + HEK293T cells (luminescence) after 2 h pre-treatment with 10 nM (left) or varying concentration (right) RXFP1 GTAC or control, followed by 30 min stimulation with RLN2 at varying concentrations (left) or 1 nM (right). Data represent mean ± s.d. from n = 3 biological replicates.

Article Snippet: NFAT luciferase reporter was a gift from Toren Finkel (Addgene plasmid #10959; http://n2t.net/addgene:10959 ; RRID:Addgene_10959).

Techniques: Binding Assay, Control, Flow Cytometry, Standard Deviation, Luciferase, Activation Assay, Concentration Assay