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culture recombinant rat il 18  (R&D Systems)


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    R&D Systems culture recombinant rat il 18
    Culture Recombinant Rat Il 18, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/521/Recombinant+Rat+IL-18%2FIL-1F4+Protein/pm15890643-59-2-9
    Average 91 stars, based on 11 article reviews
    culture recombinant rat il 18 - by Bioz Stars, 2026-11
    91/100 stars

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    Related Articles

    Recombinant:

    Article Title: Wnt/β-catenin and Hedgehog pathways are involved in the inflammatory effect of Interleukin 18 on rat chondrocytes
    Article Snippet: .. Recombinant rat IL-18 and rat DKK-1 as Wnt/β-catenin inhibitor were purchased from R&D Systems, Abingdon, UK. .. Dulbecco's Modified Eagle's Medium (DMEM), penicillin and streptomycin, fetal bovine serum (FBS), 0.25% trypsin were obtained from Gibco RRL, Grand Island, NY, USA.

    Article Title: IL-18 Contributes to Bone Cancer Pain by Regulating Glia Cells and Neuron Interaction.
    Article Snippet: Glial cell hyperactivity has been proposed to be responsible for chronic pain, however, the mechanisms remain unclear.. Interleukin (IL)-18, released from glial cells, has been reported to be involved in neuropathic pain.. In this study, we investigated the role of IL-18 in bone cancer pain.

    Article Title: Type I IFNs and IL-18 regulate the antiviral response of primary human γδ T cells against dendritic cells infected with Dengue virus.
    Article Snippet: .. The reagents used and their final concentration in culture are as follows: 5 mg/ml B18R recombinant protein (eBioscience), 10 mg/ml anti–IL-18 (clone 125-2H; R&D Systems), 10 mg/ml anti–TNF-a (clone MAb1; eBioscience), 10 mg/ml IL-1R antagonist (R&D Systems), 10 mg/ml anti–IL-7 (clone BVD10-40F6; BioLegend), 10 mg/ml anti–IL-12 (clone C8.6; eBioscience), 10 mg/ml anti–IL-15 (clone MAB2471, R&D Systems), and 10 mg/ml mouse IgG1 isotype control (clone MOPC-21; eBioscience). .. 3-[[5-(2,3-Dichlorophenyl)-1H-tetrazol-1yl]methyl]pyridine hydrochloride (15D; Tocris) was used at a final concentration of 100 mM as a specific antagonist of the P2X7 receptor (24).

    Article Title: IL-18 binding protein suppresses IL-17-induced osteoclastogenesis and rectifies type 17 helper T cell / regulatory T cell imbalance in rheumatoid arthritis.
    Article Snippet: In brief, a 96-well plate (Eppendorf, Hamburg, Germany) was coated with monoclonal antibodies against IL-18, IL-18BP, IL-17A, and soluble RANKL (R&D Systems, Minneapolis, MN, USA) at a concentration of 4 μg/mL at 4 °C overnight. .. After blocking with phosphate-buffered saline/1% bovine serum albumin /0.05% Tween 20 for 2 h at room temperature (22–25 °C), the test samples and the standard recombinant IL-18, IL18BP, IL-17A, or soluble RANKL (R&D Systems) were added to the 96-well plate and incubated at room temperature for another 2 h. The plates were washed four times with phosphate-buffered saline/Tween 20, and then incubated with 500 ng/mL biotinylated mouse monoclonal antibodies against IL-18, IL-18BP, IL-17A, or soluble RANKL (R&D Systems) for 2 h at room temperature. .. After washing, the streptavidin–alkaline phosphate–horseradish peroxidase conjugate (Sigma, St Louis, MA, USA) was added to the wells for 2 h, followed by another wash, and incubation with 1 mg/mL p-nitrophenyl phosphate (Sigma) dissolved in diethanolamine (Sigma) to develop the colour reaction.

    Article Title: Rapamycin protects chondrocytes against IL-18-induced apoptosis and ameliorates rat osteoarthritis
    Article Snippet: .. Recombinant rat IL-18, rat 740Y-P as PI3K activator, rat SC79 as AKT activator, rat 3BDO as mTOR activator, and rat LY294002 as PI3K inhibitor were purchased from R&D Systems, Abingdon, UK. .. Dulbecco’s Modified Eagle’s Medium (DMEM), fetal bovine serum (FBS), penicillin and streptomycin, 0.25% trypsin were obtained from Gibco RRL, Grand Island, NY, USA.

    Article Title: Exploring the application of sildenafil for high-fat diet-induced erectile dysfunction based on interleukin-18-mediated NLRP3/Caspase-1 signaling pathway.
    Article Snippet: In the Sil group, the ED rats received Sil (20 mg/kg/d; Solarbio). .. In IL-18 group, recombinant IL-18 protein (200 ng/kg/d; R&D Systems) was intraperitoneally injected into the ED rats. ..

    Article Title: Delayed Activation of Spinal Microglia Contributes to the Maintenance of Bone Cancer Pain in Female Wistar Rats via P2X7 Receptor and IL-18
    Article Snippet: .. The inhibitor of microglial activation minocycline (Sigma-Aldrich), astrocyte metabolic inhibitor fluorocitrate (Sigma-Aldrich), P2X7 antagonist brilliant blue G (BBG; Sigma-Aldrich), recombinant human IL-18 binding protein [IL-18BP (an inhibitor of IL-18 activity); R&D Systems], and recombinant rat IL-18 (R&D Systems) were dissolved and diluted in sterile PBS. .. The specific p38 inhibitor SB239063 (Tocris Bioscience) was dissolved in 10% DMSO.

    Binding Assay:

    Article Title: IL-18 Contributes to Bone Cancer Pain by Regulating Glia Cells and Neuron Interaction.
    Article Snippet: Glial cell hyperactivity has been proposed to be responsible for chronic pain, however, the mechanisms remain unclear.. Interleukin (IL)-18, released from glial cells, has been reported to be involved in neuropathic pain.. In this study, we investigated the role of IL-18 in bone cancer pain.

    Article Title: Delayed Activation of Spinal Microglia Contributes to the Maintenance of Bone Cancer Pain in Female Wistar Rats via P2X7 Receptor and IL-18
    Article Snippet: .. The inhibitor of microglial activation minocycline (Sigma-Aldrich), astrocyte metabolic inhibitor fluorocitrate (Sigma-Aldrich), P2X7 antagonist brilliant blue G (BBG; Sigma-Aldrich), recombinant human IL-18 binding protein [IL-18BP (an inhibitor of IL-18 activity); R&D Systems], and recombinant rat IL-18 (R&D Systems) were dissolved and diluted in sterile PBS. .. The specific p38 inhibitor SB239063 (Tocris Bioscience) was dissolved in 10% DMSO.

    Concentration Assay:

    Article Title: Type I IFNs and IL-18 regulate the antiviral response of primary human γδ T cells against dendritic cells infected with Dengue virus.
    Article Snippet: .. The reagents used and their final concentration in culture are as follows: 5 mg/ml B18R recombinant protein (eBioscience), 10 mg/ml anti–IL-18 (clone 125-2H; R&D Systems), 10 mg/ml anti–TNF-a (clone MAb1; eBioscience), 10 mg/ml IL-1R antagonist (R&D Systems), 10 mg/ml anti–IL-7 (clone BVD10-40F6; BioLegend), 10 mg/ml anti–IL-12 (clone C8.6; eBioscience), 10 mg/ml anti–IL-15 (clone MAB2471, R&D Systems), and 10 mg/ml mouse IgG1 isotype control (clone MOPC-21; eBioscience). .. 3-[[5-(2,3-Dichlorophenyl)-1H-tetrazol-1yl]methyl]pyridine hydrochloride (15D; Tocris) was used at a final concentration of 100 mM as a specific antagonist of the P2X7 receptor (24).

    Control:

    Article Title: Type I IFNs and IL-18 regulate the antiviral response of primary human γδ T cells against dendritic cells infected with Dengue virus.
    Article Snippet: .. The reagents used and their final concentration in culture are as follows: 5 mg/ml B18R recombinant protein (eBioscience), 10 mg/ml anti–IL-18 (clone 125-2H; R&D Systems), 10 mg/ml anti–TNF-a (clone MAb1; eBioscience), 10 mg/ml IL-1R antagonist (R&D Systems), 10 mg/ml anti–IL-7 (clone BVD10-40F6; BioLegend), 10 mg/ml anti–IL-12 (clone C8.6; eBioscience), 10 mg/ml anti–IL-15 (clone MAB2471, R&D Systems), and 10 mg/ml mouse IgG1 isotype control (clone MOPC-21; eBioscience). .. 3-[[5-(2,3-Dichlorophenyl)-1H-tetrazol-1yl]methyl]pyridine hydrochloride (15D; Tocris) was used at a final concentration of 100 mM as a specific antagonist of the P2X7 receptor (24).

    Blocking Assay:

    Article Title: IL-18 binding protein suppresses IL-17-induced osteoclastogenesis and rectifies type 17 helper T cell / regulatory T cell imbalance in rheumatoid arthritis.
    Article Snippet: In brief, a 96-well plate (Eppendorf, Hamburg, Germany) was coated with monoclonal antibodies against IL-18, IL-18BP, IL-17A, and soluble RANKL (R&D Systems, Minneapolis, MN, USA) at a concentration of 4 μg/mL at 4 °C overnight. .. After blocking with phosphate-buffered saline/1% bovine serum albumin /0.05% Tween 20 for 2 h at room temperature (22–25 °C), the test samples and the standard recombinant IL-18, IL18BP, IL-17A, or soluble RANKL (R&D Systems) were added to the 96-well plate and incubated at room temperature for another 2 h. The plates were washed four times with phosphate-buffered saline/Tween 20, and then incubated with 500 ng/mL biotinylated mouse monoclonal antibodies against IL-18, IL-18BP, IL-17A, or soluble RANKL (R&D Systems) for 2 h at room temperature. .. After washing, the streptavidin–alkaline phosphate–horseradish peroxidase conjugate (Sigma, St Louis, MA, USA) was added to the wells for 2 h, followed by another wash, and incubation with 1 mg/mL p-nitrophenyl phosphate (Sigma) dissolved in diethanolamine (Sigma) to develop the colour reaction.

    Saline:

    Article Title: IL-18 binding protein suppresses IL-17-induced osteoclastogenesis and rectifies type 17 helper T cell / regulatory T cell imbalance in rheumatoid arthritis.
    Article Snippet: In brief, a 96-well plate (Eppendorf, Hamburg, Germany) was coated with monoclonal antibodies against IL-18, IL-18BP, IL-17A, and soluble RANKL (R&D Systems, Minneapolis, MN, USA) at a concentration of 4 μg/mL at 4 °C overnight. .. After blocking with phosphate-buffered saline/1% bovine serum albumin /0.05% Tween 20 for 2 h at room temperature (22–25 °C), the test samples and the standard recombinant IL-18, IL18BP, IL-17A, or soluble RANKL (R&D Systems) were added to the 96-well plate and incubated at room temperature for another 2 h. The plates were washed four times with phosphate-buffered saline/Tween 20, and then incubated with 500 ng/mL biotinylated mouse monoclonal antibodies against IL-18, IL-18BP, IL-17A, or soluble RANKL (R&D Systems) for 2 h at room temperature. .. After washing, the streptavidin–alkaline phosphate–horseradish peroxidase conjugate (Sigma, St Louis, MA, USA) was added to the wells for 2 h, followed by another wash, and incubation with 1 mg/mL p-nitrophenyl phosphate (Sigma) dissolved in diethanolamine (Sigma) to develop the colour reaction.

    Incubation:

    Article Title: IL-18 binding protein suppresses IL-17-induced osteoclastogenesis and rectifies type 17 helper T cell / regulatory T cell imbalance in rheumatoid arthritis.
    Article Snippet: In brief, a 96-well plate (Eppendorf, Hamburg, Germany) was coated with monoclonal antibodies against IL-18, IL-18BP, IL-17A, and soluble RANKL (R&D Systems, Minneapolis, MN, USA) at a concentration of 4 μg/mL at 4 °C overnight. .. After blocking with phosphate-buffered saline/1% bovine serum albumin /0.05% Tween 20 for 2 h at room temperature (22–25 °C), the test samples and the standard recombinant IL-18, IL18BP, IL-17A, or soluble RANKL (R&D Systems) were added to the 96-well plate and incubated at room temperature for another 2 h. The plates were washed four times with phosphate-buffered saline/Tween 20, and then incubated with 500 ng/mL biotinylated mouse monoclonal antibodies against IL-18, IL-18BP, IL-17A, or soluble RANKL (R&D Systems) for 2 h at room temperature. .. After washing, the streptavidin–alkaline phosphate–horseradish peroxidase conjugate (Sigma, St Louis, MA, USA) was added to the wells for 2 h, followed by another wash, and incubation with 1 mg/mL p-nitrophenyl phosphate (Sigma) dissolved in diethanolamine (Sigma) to develop the colour reaction.

    Bioprocessing:

    Article Title: IL-18 binding protein suppresses IL-17-induced osteoclastogenesis and rectifies type 17 helper T cell / regulatory T cell imbalance in rheumatoid arthritis.
    Article Snippet: In brief, a 96-well plate (Eppendorf, Hamburg, Germany) was coated with monoclonal antibodies against IL-18, IL-18BP, IL-17A, and soluble RANKL (R&D Systems, Minneapolis, MN, USA) at a concentration of 4 μg/mL at 4 °C overnight. .. After blocking with phosphate-buffered saline/1% bovine serum albumin /0.05% Tween 20 for 2 h at room temperature (22–25 °C), the test samples and the standard recombinant IL-18, IL18BP, IL-17A, or soluble RANKL (R&D Systems) were added to the 96-well plate and incubated at room temperature for another 2 h. The plates were washed four times with phosphate-buffered saline/Tween 20, and then incubated with 500 ng/mL biotinylated mouse monoclonal antibodies against IL-18, IL-18BP, IL-17A, or soluble RANKL (R&D Systems) for 2 h at room temperature. .. After washing, the streptavidin–alkaline phosphate–horseradish peroxidase conjugate (Sigma, St Louis, MA, USA) was added to the wells for 2 h, followed by another wash, and incubation with 1 mg/mL p-nitrophenyl phosphate (Sigma) dissolved in diethanolamine (Sigma) to develop the colour reaction.

    Injection:

    Article Title: Exploring the application of sildenafil for high-fat diet-induced erectile dysfunction based on interleukin-18-mediated NLRP3/Caspase-1 signaling pathway.
    Article Snippet: In the Sil group, the ED rats received Sil (20 mg/kg/d; Solarbio). .. In IL-18 group, recombinant IL-18 protein (200 ng/kg/d; R&D Systems) was intraperitoneally injected into the ED rats. ..

    Activation Assay:

    Article Title: Delayed Activation of Spinal Microglia Contributes to the Maintenance of Bone Cancer Pain in Female Wistar Rats via P2X7 Receptor and IL-18
    Article Snippet: .. The inhibitor of microglial activation minocycline (Sigma-Aldrich), astrocyte metabolic inhibitor fluorocitrate (Sigma-Aldrich), P2X7 antagonist brilliant blue G (BBG; Sigma-Aldrich), recombinant human IL-18 binding protein [IL-18BP (an inhibitor of IL-18 activity); R&D Systems], and recombinant rat IL-18 (R&D Systems) were dissolved and diluted in sterile PBS. .. The specific p38 inhibitor SB239063 (Tocris Bioscience) was dissolved in 10% DMSO.

    Activity Assay:

    Article Title: Delayed Activation of Spinal Microglia Contributes to the Maintenance of Bone Cancer Pain in Female Wistar Rats via P2X7 Receptor and IL-18
    Article Snippet: .. The inhibitor of microglial activation minocycline (Sigma-Aldrich), astrocyte metabolic inhibitor fluorocitrate (Sigma-Aldrich), P2X7 antagonist brilliant blue G (BBG; Sigma-Aldrich), recombinant human IL-18 binding protein [IL-18BP (an inhibitor of IL-18 activity); R&D Systems], and recombinant rat IL-18 (R&D Systems) were dissolved and diluted in sterile PBS. .. The specific p38 inhibitor SB239063 (Tocris Bioscience) was dissolved in 10% DMSO.

    Sterility:

    Article Title: Delayed Activation of Spinal Microglia Contributes to the Maintenance of Bone Cancer Pain in Female Wistar Rats via P2X7 Receptor and IL-18
    Article Snippet: .. The inhibitor of microglial activation minocycline (Sigma-Aldrich), astrocyte metabolic inhibitor fluorocitrate (Sigma-Aldrich), P2X7 antagonist brilliant blue G (BBG; Sigma-Aldrich), recombinant human IL-18 binding protein [IL-18BP (an inhibitor of IL-18 activity); R&D Systems], and recombinant rat IL-18 (R&D Systems) were dissolved and diluted in sterile PBS. .. The specific p38 inhibitor SB239063 (Tocris Bioscience) was dissolved in 10% DMSO.



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    97
    MedChemExpress cgas inhibitor
    ( A ) Heatmaps of cell viability and excess over Bliss (EOB) in the indicated NRAS-mutated cancer cell lines left untreated or treated with increasing (semi-log) doses of the pan-RAS(ON) inhibitor (RASi-ON) RMC-7977 (10 −10.5 –10 −7 M) with or without the FTI tipifarnib (HRASi; 10 −10 –10 −6.5 M) for 72 hours under 3D culture conditions. Data are the average (heatmaps) or individual values and mean ± S.D. (SUM EOB) from N = 3 independent experiments, each with n = 3 technical replicates. Significance was assessed by one sample t and Wilcoxon test, * P < 0.05, ** P < 0.01 compared to Bliss Independence (additive drug effect, EOB = 0); and by ANOVA with Tukey’s correction for multiple comparisons, ^ P < 0.05, ^^ P < 0.01 compared to <t>G12D-mutated</t> <t>TALL-1</t> and KE-37 cells. ( B ) Unifying schematic model depicting the contribution of WT RAS proteins to mutant NRAS signaling depending on the specific codon mutation. In cells harboring “cycling” G12X mutants, WT RAS augments RTK-stimulated mutant RAS signaling to enhance transformation. In cells harboring “GTP-locked” Q61X mutants, RTK-stimulated WT RAS signaling serves as an obligate partner to promote downstream effector signaling and transforming potential. The differential requirements for WT RAS revealed from genetic depletion and DepMap analysis suggest non-overlapping therapeutic strategies: inhibiting proximal RTK pathway (SOS1i) synergizes with inhibitors of cycling G12X mutants, whereas inhibiting WT HRAS using tipifarnib creates a synthetic vulnerability when combined with a pan-RAS(ON) inhibitor in GTP-locked Q61X-mutated cells.
    Cgas Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Antagonism of cGAS or STING in the ACC reversed the hyperalgesia caused by CCI. (A) Experimental flow chart. (B) Verification of the ACC catheterization with methylene blue. (C) RU.521 and C-176 (Selleck) significantly increased MT as compared with DMSO (n = 7, ANOVA, *** P < 0.001; ### P < 0.001). (D) RU.521 and C-176 significantly decreased ATS compared with DMSO (n = 7, ANOVA, *** P < 0.001; ### P < 0.001). Data are presented as mean ± standard error of the mean. CCI: chronic constriction injury, MT: mechanical threshold, DMSO: dimethyl sulfoxide, ATS: acetone test score, cGAS: GMP–AMP synthase, STING: stimulator of interferon genes, ACC: anterior cingulate cortex, ANOVA: analysis of variance.

    Journal: The Korean Journal of Pain

    Article Title: cGAS–STING signaling in the anterior cingulate cortex modulates electroacupuncture analgesia in a rat neuropathic pain model

    doi: 10.3344/kjp.26061

    Figure Lengend Snippet: Antagonism of cGAS or STING in the ACC reversed the hyperalgesia caused by CCI. (A) Experimental flow chart. (B) Verification of the ACC catheterization with methylene blue. (C) RU.521 and C-176 (Selleck) significantly increased MT as compared with DMSO (n = 7, ANOVA, *** P < 0.001; ### P < 0.001). (D) RU.521 and C-176 significantly decreased ATS compared with DMSO (n = 7, ANOVA, *** P < 0.001; ### P < 0.001). Data are presented as mean ± standard error of the mean. CCI: chronic constriction injury, MT: mechanical threshold, DMSO: dimethyl sulfoxide, ATS: acetone test score, cGAS: GMP–AMP synthase, STING: stimulator of interferon genes, ACC: anterior cingulate cortex, ANOVA: analysis of variance.

    Article Snippet: The cGAS inhibitor RU.521 (Selleck) and the STING inhibitor C-176 (Selleck) were dissolved in 10% dimethyl sulfoxide (DMSO) at a concentration of 20 μg/μL, based on previous reports and the authors’ pilot experiments [ , , ].

    Techniques: Analysis

    ( A ) Heatmaps of cell viability and excess over Bliss (EOB) in the indicated NRAS-mutated cancer cell lines left untreated or treated with increasing (semi-log) doses of the pan-RAS(ON) inhibitor (RASi-ON) RMC-7977 (10 −10.5 –10 −7 M) with or without the FTI tipifarnib (HRASi; 10 −10 –10 −6.5 M) for 72 hours under 3D culture conditions. Data are the average (heatmaps) or individual values and mean ± S.D. (SUM EOB) from N = 3 independent experiments, each with n = 3 technical replicates. Significance was assessed by one sample t and Wilcoxon test, * P < 0.05, ** P < 0.01 compared to Bliss Independence (additive drug effect, EOB = 0); and by ANOVA with Tukey’s correction for multiple comparisons, ^ P < 0.05, ^^ P < 0.01 compared to G12D-mutated TALL-1 and KE-37 cells. ( B ) Unifying schematic model depicting the contribution of WT RAS proteins to mutant NRAS signaling depending on the specific codon mutation. In cells harboring “cycling” G12X mutants, WT RAS augments RTK-stimulated mutant RAS signaling to enhance transformation. In cells harboring “GTP-locked” Q61X mutants, RTK-stimulated WT RAS signaling serves as an obligate partner to promote downstream effector signaling and transforming potential. The differential requirements for WT RAS revealed from genetic depletion and DepMap analysis suggest non-overlapping therapeutic strategies: inhibiting proximal RTK pathway (SOS1i) synergizes with inhibitors of cycling G12X mutants, whereas inhibiting WT HRAS using tipifarnib creates a synthetic vulnerability when combined with a pan-RAS(ON) inhibitor in GTP-locked Q61X-mutated cells.

    Journal: Science signaling

    Article Title: HRAS promotes mutant NRAS-driven transformation with codon and allele specificity

    doi: 10.1126/scisignal.aej6209

    Figure Lengend Snippet: ( A ) Heatmaps of cell viability and excess over Bliss (EOB) in the indicated NRAS-mutated cancer cell lines left untreated or treated with increasing (semi-log) doses of the pan-RAS(ON) inhibitor (RASi-ON) RMC-7977 (10 −10.5 –10 −7 M) with or without the FTI tipifarnib (HRASi; 10 −10 –10 −6.5 M) for 72 hours under 3D culture conditions. Data are the average (heatmaps) or individual values and mean ± S.D. (SUM EOB) from N = 3 independent experiments, each with n = 3 technical replicates. Significance was assessed by one sample t and Wilcoxon test, * P < 0.05, ** P < 0.01 compared to Bliss Independence (additive drug effect, EOB = 0); and by ANOVA with Tukey’s correction for multiple comparisons, ^ P < 0.05, ^^ P < 0.01 compared to G12D-mutated TALL-1 and KE-37 cells. ( B ) Unifying schematic model depicting the contribution of WT RAS proteins to mutant NRAS signaling depending on the specific codon mutation. In cells harboring “cycling” G12X mutants, WT RAS augments RTK-stimulated mutant RAS signaling to enhance transformation. In cells harboring “GTP-locked” Q61X mutants, RTK-stimulated WT RAS signaling serves as an obligate partner to promote downstream effector signaling and transforming potential. The differential requirements for WT RAS revealed from genetic depletion and DepMap analysis suggest non-overlapping therapeutic strategies: inhibiting proximal RTK pathway (SOS1i) synergizes with inhibitors of cycling G12X mutants, whereas inhibiting WT HRAS using tipifarnib creates a synthetic vulnerability when combined with a pan-RAS(ON) inhibitor in GTP-locked Q61X-mutated cells.

    Article Snippet: TALL-1 and KE-37 were purchased from DSMZ.

    Techniques: Mutagenesis, Transformation Assay, Analysis