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torin1  (MedChemExpress)


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    MedChemExpress torin1
    (A and B) TE fold change analysis of common transcripts affected by sotorasib and CR-1-31B shows that mutant KRAS and EIF4A oppositely regulate the translation of these mRNAs. Most of the sotorasib TE down targets are TE upregulated following EIF4A inhibition with CR-1-31B. (C) TE fold change analysis of common translation factors between sotorasib and CR-1-31B reveals the upregulation of all the translation factors following CR-1-31B treatment, except for four proteins that are downregulated by CR-1-31B. (D and E) Relative luciferase activity driven by G-quadruplex (GQ) and GC-rich motifs in response to sotorasib, RMC-7977, or MRTX1133 treatment demonstrates that sotorasib induces GQ and GC-rich mRNA translation ( * p < 0.05 and *** p < 0.001). (F and G) Luciferase reporter assays using the full-length or mutated 5′UTR of EEF1A1 show altered luciferase activity upon CR-1-31B and <t>Torin1</t> treatment in MiaPaca-2 cells (* p < 0.05 and *** p < 0.001). (H) Combination treatment of CR-1-31B and Torin1 with mutant KRAS inhibitors in a panel of cancer cell lines harboring either G12C or G12D KRAS mutations leads to an additive enhancement of cell death, based on the zero interaction potency (ZIP) model. (I) Summary of our findings shows that the mutant KRAS-dependent mechanism of translational control uncouples the regulation of translation machinery from the regulation of the rest of the mRNA translation. Mutant KRAS-dependent mechanism is distinct from the mTOR and EIF4A-dependent mechanism that depends on longer and structured 5′UTR features and controls the translation of a distinct subset of mRNAs.
    Torin1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 177 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Mutant KRAS-driven selective mRNA translation reveals mechanisms and therapeutic vulnerabilities in cancer"

    Article Title: Mutant KRAS-driven selective mRNA translation reveals mechanisms and therapeutic vulnerabilities in cancer

    Journal: Cell reports

    doi: 10.1016/j.celrep.2026.117520

    (A and B) TE fold change analysis of common transcripts affected by sotorasib and CR-1-31B shows that mutant KRAS and EIF4A oppositely regulate the translation of these mRNAs. Most of the sotorasib TE down targets are TE upregulated following EIF4A inhibition with CR-1-31B. (C) TE fold change analysis of common translation factors between sotorasib and CR-1-31B reveals the upregulation of all the translation factors following CR-1-31B treatment, except for four proteins that are downregulated by CR-1-31B. (D and E) Relative luciferase activity driven by G-quadruplex (GQ) and GC-rich motifs in response to sotorasib, RMC-7977, or MRTX1133 treatment demonstrates that sotorasib induces GQ and GC-rich mRNA translation ( * p < 0.05 and *** p < 0.001). (F and G) Luciferase reporter assays using the full-length or mutated 5′UTR of EEF1A1 show altered luciferase activity upon CR-1-31B and Torin1 treatment in MiaPaca-2 cells (* p < 0.05 and *** p < 0.001). (H) Combination treatment of CR-1-31B and Torin1 with mutant KRAS inhibitors in a panel of cancer cell lines harboring either G12C or G12D KRAS mutations leads to an additive enhancement of cell death, based on the zero interaction potency (ZIP) model. (I) Summary of our findings shows that the mutant KRAS-dependent mechanism of translational control uncouples the regulation of translation machinery from the regulation of the rest of the mRNA translation. Mutant KRAS-dependent mechanism is distinct from the mTOR and EIF4A-dependent mechanism that depends on longer and structured 5′UTR features and controls the translation of a distinct subset of mRNAs.
    Figure Legend Snippet: (A and B) TE fold change analysis of common transcripts affected by sotorasib and CR-1-31B shows that mutant KRAS and EIF4A oppositely regulate the translation of these mRNAs. Most of the sotorasib TE down targets are TE upregulated following EIF4A inhibition with CR-1-31B. (C) TE fold change analysis of common translation factors between sotorasib and CR-1-31B reveals the upregulation of all the translation factors following CR-1-31B treatment, except for four proteins that are downregulated by CR-1-31B. (D and E) Relative luciferase activity driven by G-quadruplex (GQ) and GC-rich motifs in response to sotorasib, RMC-7977, or MRTX1133 treatment demonstrates that sotorasib induces GQ and GC-rich mRNA translation ( * p < 0.05 and *** p < 0.001). (F and G) Luciferase reporter assays using the full-length or mutated 5′UTR of EEF1A1 show altered luciferase activity upon CR-1-31B and Torin1 treatment in MiaPaca-2 cells (* p < 0.05 and *** p < 0.001). (H) Combination treatment of CR-1-31B and Torin1 with mutant KRAS inhibitors in a panel of cancer cell lines harboring either G12C or G12D KRAS mutations leads to an additive enhancement of cell death, based on the zero interaction potency (ZIP) model. (I) Summary of our findings shows that the mutant KRAS-dependent mechanism of translational control uncouples the regulation of translation machinery from the regulation of the rest of the mRNA translation. Mutant KRAS-dependent mechanism is distinct from the mTOR and EIF4A-dependent mechanism that depends on longer and structured 5′UTR features and controls the translation of a distinct subset of mRNAs.

    Techniques Used: Mutagenesis, Inhibition, Luciferase, Activity Assay, Control

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    Article Snippet: KO-947 (Cat. No. HY-112181), MK-8353 (Cat. No. HY-111407), EN6 (Cat. No. 1808714-73-9), and Torin-1 (Cat. No. HY-13003) were obtained from MedChemExpress (Monmouth, NJ, USA).

    Article Title: Cleavage of TOM1 by the SARS-CoV-2 main protease NSP5 prevents autophagic degradation of viral envelope.
    Article Snippet: Z-VAD-FMK (HY-16658B), rapamycin (AY-22989), torin 1 (HY-13003), and Mpro inhibitor N3 hemihydrate (HY-136149A) were purchased from MedChemexpress.

    Article Title: Isoginkgetin protects against degeneration of ALS motor neurons via regulating the GSK-3β–TFEB signaling axis
    Article Snippet: The reagents used in this study were as follows: Isoginkgetin (HY-N2117; MCE; Dissolved in DMSO), Torin 1 (HY-13003; MCE), BI-D1870 (HY-10510; MCE), XAV-939 (HY-15147; MCE), LY294002 (HY-10108; MCE), Go6976 (HY-10183; MCE), ATP (HY-B2176; MCE), N2 (17502–048; Gibco), B27 (17504–044; Gibco), L -ascorbic acid (4055–50–81–7; Tocris Bioscience), CHIR-99021 (252917–06–9; Tocris Bioscience), DMH-1 (4126; Tocris Bioscience), SB431542 (1614; Tocris Bioscience), retinoic acid (04–0021; Stemgent), Purmorphamine (04–0009; Stemgent), valproic acid (VPA)(04–0007; Stemgent), compound E (6476; Tocris Bioscience), insulin-like growth factor (IGF) (HY-P7018; MCE), brain-derived neurotrophic factor (BDNF) (HY-P7116A; MCE), ciliary neurotrophic factor (CNTF) (HY-P7146; MCE), Y-27632 (S1049; SELLECKCHEM), and MG-132 (HY-13259; MCE).

    Concentration Assay:

    Article Title: Oncogenic RAS-driven α2 integrin induction under nutrient stress promotes cancer cell motility
    Article Snippet: .. DMEM, high glucose, pyruvate; DMEM/F-12, glutamax; dialyzed foetal bovine serum (FBS), horse serum (HS) were from Gibco; DMEM, no amino acids from US Biological life sciences; FBS, Hydrocortisone and Insulin solution human from Sigma-Aldrich; Penicillin/ Streptomycin (Pen/strep) from Life technologies; Rat tail high concentration Collagen type I from Corning; Growth factor-reduced Matrigel from SLS; Hoechst 33342 from Invitrogen; NHS-Fluorescein, Phalloidin Alexa Fluor 555, Paraformaldehyde and pHrodo TM iFL Red STP ester from ThermoFisher; Vectashield mounting reagent with DAPI from VECTOR laboratories; 4-15% Mini PROTEAN TGX stain Free Protein gels from BioRad Laboratories; Protein ladder “Color Prestained Protein Standard” from New England Biolabs; High-Capacity cDNA Reverse Transcription kit from Applied biosystems; qPCRBIO SyGreen Blue Mix Lo-ROX from PCR BIOSYSTEMS; FITC-Anti Human CD49b (ITGA2) Antibody from Biolegend (#359306); Mouse anti-human CD49b (ITGA2) antibody from BD biosciences (#611017); P44/42 MAPK (ERK1/2) antibody (#9102) and Phospho-p44/42 MAPK (ERK1/2) antibody (#9101) from Cell signalling; GAPDH antibody from Santa Cruz Biotechnology (#sc-47724); α-Tubulin was from Cell signalling (#3873); IR Dye 680LT anti-Rabbit antibody and IR Dye 800LT anti-Mouse antibody from LICOR Biosciences; E64d (Aloxistatin) from AdooQ Bioscience; BTT-3033 and Torin-1 from Tocris Biosciences; MRTX1133, GCN2iB and RMC-6236 from MedChemExpress; Selumetinib from Selleck Chemicals. ..

    Staining:

    Article Title: Oncogenic RAS-driven α2 integrin induction under nutrient stress promotes cancer cell motility
    Article Snippet: .. DMEM, high glucose, pyruvate; DMEM/F-12, glutamax; dialyzed foetal bovine serum (FBS), horse serum (HS) were from Gibco; DMEM, no amino acids from US Biological life sciences; FBS, Hydrocortisone and Insulin solution human from Sigma-Aldrich; Penicillin/ Streptomycin (Pen/strep) from Life technologies; Rat tail high concentration Collagen type I from Corning; Growth factor-reduced Matrigel from SLS; Hoechst 33342 from Invitrogen; NHS-Fluorescein, Phalloidin Alexa Fluor 555, Paraformaldehyde and pHrodo TM iFL Red STP ester from ThermoFisher; Vectashield mounting reagent with DAPI from VECTOR laboratories; 4-15% Mini PROTEAN TGX stain Free Protein gels from BioRad Laboratories; Protein ladder “Color Prestained Protein Standard” from New England Biolabs; High-Capacity cDNA Reverse Transcription kit from Applied biosystems; qPCRBIO SyGreen Blue Mix Lo-ROX from PCR BIOSYSTEMS; FITC-Anti Human CD49b (ITGA2) Antibody from Biolegend (#359306); Mouse anti-human CD49b (ITGA2) antibody from BD biosciences (#611017); P44/42 MAPK (ERK1/2) antibody (#9102) and Phospho-p44/42 MAPK (ERK1/2) antibody (#9101) from Cell signalling; GAPDH antibody from Santa Cruz Biotechnology (#sc-47724); α-Tubulin was from Cell signalling (#3873); IR Dye 680LT anti-Rabbit antibody and IR Dye 800LT anti-Mouse antibody from LICOR Biosciences; E64d (Aloxistatin) from AdooQ Bioscience; BTT-3033 and Torin-1 from Tocris Biosciences; MRTX1133, GCN2iB and RMC-6236 from MedChemExpress; Selumetinib from Selleck Chemicals. ..

    Reverse Transcription:

    Article Title: Oncogenic RAS-driven α2 integrin induction under nutrient stress promotes cancer cell motility
    Article Snippet: .. DMEM, high glucose, pyruvate; DMEM/F-12, glutamax; dialyzed foetal bovine serum (FBS), horse serum (HS) were from Gibco; DMEM, no amino acids from US Biological life sciences; FBS, Hydrocortisone and Insulin solution human from Sigma-Aldrich; Penicillin/ Streptomycin (Pen/strep) from Life technologies; Rat tail high concentration Collagen type I from Corning; Growth factor-reduced Matrigel from SLS; Hoechst 33342 from Invitrogen; NHS-Fluorescein, Phalloidin Alexa Fluor 555, Paraformaldehyde and pHrodo TM iFL Red STP ester from ThermoFisher; Vectashield mounting reagent with DAPI from VECTOR laboratories; 4-15% Mini PROTEAN TGX stain Free Protein gels from BioRad Laboratories; Protein ladder “Color Prestained Protein Standard” from New England Biolabs; High-Capacity cDNA Reverse Transcription kit from Applied biosystems; qPCRBIO SyGreen Blue Mix Lo-ROX from PCR BIOSYSTEMS; FITC-Anti Human CD49b (ITGA2) Antibody from Biolegend (#359306); Mouse anti-human CD49b (ITGA2) antibody from BD biosciences (#611017); P44/42 MAPK (ERK1/2) antibody (#9102) and Phospho-p44/42 MAPK (ERK1/2) antibody (#9101) from Cell signalling; GAPDH antibody from Santa Cruz Biotechnology (#sc-47724); α-Tubulin was from Cell signalling (#3873); IR Dye 680LT anti-Rabbit antibody and IR Dye 800LT anti-Mouse antibody from LICOR Biosciences; E64d (Aloxistatin) from AdooQ Bioscience; BTT-3033 and Torin-1 from Tocris Biosciences; MRTX1133, GCN2iB and RMC-6236 from MedChemExpress; Selumetinib from Selleck Chemicals. ..



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    Image Search Results


    (A and B) TE fold change analysis of common transcripts affected by sotorasib and CR-1-31B shows that mutant KRAS and EIF4A oppositely regulate the translation of these mRNAs. Most of the sotorasib TE down targets are TE upregulated following EIF4A inhibition with CR-1-31B. (C) TE fold change analysis of common translation factors between sotorasib and CR-1-31B reveals the upregulation of all the translation factors following CR-1-31B treatment, except for four proteins that are downregulated by CR-1-31B. (D and E) Relative luciferase activity driven by G-quadruplex (GQ) and GC-rich motifs in response to sotorasib, RMC-7977, or MRTX1133 treatment demonstrates that sotorasib induces GQ and GC-rich mRNA translation ( * p < 0.05 and *** p < 0.001). (F and G) Luciferase reporter assays using the full-length or mutated 5′UTR of EEF1A1 show altered luciferase activity upon CR-1-31B and Torin1 treatment in MiaPaca-2 cells (* p < 0.05 and *** p < 0.001). (H) Combination treatment of CR-1-31B and Torin1 with mutant KRAS inhibitors in a panel of cancer cell lines harboring either G12C or G12D KRAS mutations leads to an additive enhancement of cell death, based on the zero interaction potency (ZIP) model. (I) Summary of our findings shows that the mutant KRAS-dependent mechanism of translational control uncouples the regulation of translation machinery from the regulation of the rest of the mRNA translation. Mutant KRAS-dependent mechanism is distinct from the mTOR and EIF4A-dependent mechanism that depends on longer and structured 5′UTR features and controls the translation of a distinct subset of mRNAs.

    Journal: Cell reports

    Article Title: Mutant KRAS-driven selective mRNA translation reveals mechanisms and therapeutic vulnerabilities in cancer

    doi: 10.1016/j.celrep.2026.117520

    Figure Lengend Snippet: (A and B) TE fold change analysis of common transcripts affected by sotorasib and CR-1-31B shows that mutant KRAS and EIF4A oppositely regulate the translation of these mRNAs. Most of the sotorasib TE down targets are TE upregulated following EIF4A inhibition with CR-1-31B. (C) TE fold change analysis of common translation factors between sotorasib and CR-1-31B reveals the upregulation of all the translation factors following CR-1-31B treatment, except for four proteins that are downregulated by CR-1-31B. (D and E) Relative luciferase activity driven by G-quadruplex (GQ) and GC-rich motifs in response to sotorasib, RMC-7977, or MRTX1133 treatment demonstrates that sotorasib induces GQ and GC-rich mRNA translation ( * p < 0.05 and *** p < 0.001). (F and G) Luciferase reporter assays using the full-length or mutated 5′UTR of EEF1A1 show altered luciferase activity upon CR-1-31B and Torin1 treatment in MiaPaca-2 cells (* p < 0.05 and *** p < 0.001). (H) Combination treatment of CR-1-31B and Torin1 with mutant KRAS inhibitors in a panel of cancer cell lines harboring either G12C or G12D KRAS mutations leads to an additive enhancement of cell death, based on the zero interaction potency (ZIP) model. (I) Summary of our findings shows that the mutant KRAS-dependent mechanism of translational control uncouples the regulation of translation machinery from the regulation of the rest of the mRNA translation. Mutant KRAS-dependent mechanism is distinct from the mTOR and EIF4A-dependent mechanism that depends on longer and structured 5′UTR features and controls the translation of a distinct subset of mRNAs.

    Article Snippet: Torin1 , MedChemExpress , Cat# HY-13003.

    Techniques: Mutagenesis, Inhibition, Luciferase, Activity Assay, Control

    (A, B, C, D) HFF cells were kept in basal conditions (t = 0) or starved (t = 4) in the absence (CTRL) or presence of either (A) 0.3 μM SAR405, (B) 50 nM bafilomycin A (BAF), (C) 20 μM chloroquine (CQ), or (D) cells were not starved but instead treated with 200 nM Torin-1 (depicting results only at t = 4). The expression of miR-21-5p and miR-4488 was quantified by RT–qPCR. Relative quantity (RQ) was calculated by normalizing the relative expression of the miRNA in starved cells to its expression in control cells (t = 0). For statistical analysis procedures, see legend to .

    Journal: Life Science Alliance

    Article Title: A microRNA generated via lysosomal processing of ribosomal RNA suppresses proinflammatory responses

    doi: 10.26508/lsa.202503536

    Figure Lengend Snippet: (A, B, C, D) HFF cells were kept in basal conditions (t = 0) or starved (t = 4) in the absence (CTRL) or presence of either (A) 0.3 μM SAR405, (B) 50 nM bafilomycin A (BAF), (C) 20 μM chloroquine (CQ), or (D) cells were not starved but instead treated with 200 nM Torin-1 (depicting results only at t = 4). The expression of miR-21-5p and miR-4488 was quantified by RT–qPCR. Relative quantity (RQ) was calculated by normalizing the relative expression of the miRNA in starved cells to its expression in control cells (t = 0). For statistical analysis procedures, see legend to .

    Article Snippet: Chloroquine (C6628; Sigma-Aldrich), bafilomycin A1 (BML-CM110-0100; Enzo), SAR405 (533063; Sigma-Aldrich), and Torin-1 (inh-tor1; InvivoGen) were added to the fresh medium at the onset of the treatment.

    Techniques: Expressing, Quantitative RT-PCR, Control

    (A) Schematic representation of the pre-miR-4488 sequence, highlighting in blue circles the first 18 nucleotides of the mature miRNA and in red circles the sequence of the primer detecting the pre-miR-4488. (B) Control HFFs or HFFs treated with 200 nM Torin-1 for 4 h were harvested and processed for subcellular fractionation as described in the Materials and Methods section. Cytosolic and lysosome-containing fractions were subjected to RNA extraction, and the relative amounts of pre-miR-4488 were determined by RT–qPCR, using the pre-miR-4488–derived primer.

    Journal: Life Science Alliance

    Article Title: A microRNA generated via lysosomal processing of ribosomal RNA suppresses proinflammatory responses

    doi: 10.26508/lsa.202503536

    Figure Lengend Snippet: (A) Schematic representation of the pre-miR-4488 sequence, highlighting in blue circles the first 18 nucleotides of the mature miRNA and in red circles the sequence of the primer detecting the pre-miR-4488. (B) Control HFFs or HFFs treated with 200 nM Torin-1 for 4 h were harvested and processed for subcellular fractionation as described in the Materials and Methods section. Cytosolic and lysosome-containing fractions were subjected to RNA extraction, and the relative amounts of pre-miR-4488 were determined by RT–qPCR, using the pre-miR-4488–derived primer.

    Article Snippet: Chloroquine (C6628; Sigma-Aldrich), bafilomycin A1 (BML-CM110-0100; Enzo), SAR405 (533063; Sigma-Aldrich), and Torin-1 (inh-tor1; InvivoGen) were added to the fresh medium at the onset of the treatment.

    Techniques: Sequencing, Control, Fractionation, RNA Extraction, Quantitative RT-PCR, Derivative Assay