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mtor pathway activator mhy1485  (MedChemExpress)


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    MedChemExpress mtor pathway activator mhy1485
    Influence of GPT2 on mTOR signaling pathway activation and regulation of ADH1A expression. (A) Effects of inhibition of mTOR with AZD8055 on ADH1A expression in LC cells. (B) Effects of activation of mTOR with <t>MHY1485</t> on ADH1A expression in LC cells. (C) Effects of GPT2 on mTOR activation and ADH1A expression in LC cells. (D) Effects of AKT activation mediated by the activator SC79 on mTOR sensitization and ADH1A expression in LC cells. (E) Effects of GPT2 on the activation of AKT and mTOR in LC cells. (F) Effects of GPT2 on mTOR activation and ADH1A expression mediated by AKT activation in LC cells. (G) AKT–mTOR interaction, assessed with co-IP assays. (H) Effects of GPT2 on AKT–mTOR interaction, measured with co-IP assays in LC cells. ADH1A, alcohol dehydrogenase 1A; AKT, protein kinase B; co-IP, co-immunoprecipitation; GPT2, glutamic-pyruvic transaminase 2; LC, liver cancer; mTOR, mammalian target of rapamycin.
    Mtor Pathway Activator Mhy1485, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 340 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mtor+pathway/IRF1%2C+Human/pmc13326605-37-5-16
    Average 99 stars, based on 340 article reviews
    mtor pathway activator mhy1485 - by Bioz Stars, 2026-09
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    1) Product Images from "HBx-mediated GPT2 suppression promotes liver cancer development by downregulating ADH1A"

    Article Title: HBx-mediated GPT2 suppression promotes liver cancer development by downregulating ADH1A

    Journal: Cancer Biology & Medicine

    doi: 10.20892/j.issn.2095-3941.2025.0236

    Influence of GPT2 on mTOR signaling pathway activation and regulation of ADH1A expression. (A) Effects of inhibition of mTOR with AZD8055 on ADH1A expression in LC cells. (B) Effects of activation of mTOR with MHY1485 on ADH1A expression in LC cells. (C) Effects of GPT2 on mTOR activation and ADH1A expression in LC cells. (D) Effects of AKT activation mediated by the activator SC79 on mTOR sensitization and ADH1A expression in LC cells. (E) Effects of GPT2 on the activation of AKT and mTOR in LC cells. (F) Effects of GPT2 on mTOR activation and ADH1A expression mediated by AKT activation in LC cells. (G) AKT–mTOR interaction, assessed with co-IP assays. (H) Effects of GPT2 on AKT–mTOR interaction, measured with co-IP assays in LC cells. ADH1A, alcohol dehydrogenase 1A; AKT, protein kinase B; co-IP, co-immunoprecipitation; GPT2, glutamic-pyruvic transaminase 2; LC, liver cancer; mTOR, mammalian target of rapamycin.
    Figure Legend Snippet: Influence of GPT2 on mTOR signaling pathway activation and regulation of ADH1A expression. (A) Effects of inhibition of mTOR with AZD8055 on ADH1A expression in LC cells. (B) Effects of activation of mTOR with MHY1485 on ADH1A expression in LC cells. (C) Effects of GPT2 on mTOR activation and ADH1A expression in LC cells. (D) Effects of AKT activation mediated by the activator SC79 on mTOR sensitization and ADH1A expression in LC cells. (E) Effects of GPT2 on the activation of AKT and mTOR in LC cells. (F) Effects of GPT2 on mTOR activation and ADH1A expression mediated by AKT activation in LC cells. (G) AKT–mTOR interaction, assessed with co-IP assays. (H) Effects of GPT2 on AKT–mTOR interaction, measured with co-IP assays in LC cells. ADH1A, alcohol dehydrogenase 1A; AKT, protein kinase B; co-IP, co-immunoprecipitation; GPT2, glutamic-pyruvic transaminase 2; LC, liver cancer; mTOR, mammalian target of rapamycin.

    Techniques Used: Activation Assay, Expressing, Inhibition, Co-Immunoprecipitation Assay, Immunoprecipitation

    Related Articles

    Concentration Assay:

    Article Title: YTHDF3 Mediates the Occurrence and Development of Breast Cancer by Regulating Glycolysis Through the mTOR – HIF1α – LHDA Axis
    Article Snippet: Puromycin at a concentration of 10 mg/mL was obtained from MedChemExpress (Shanghai, China). .. The activator of the mTOR pathway, MHY1485, was obtained from MedChemExpress (Shanghai, China) at a concentration of 10 mM. .. Lentiviruses carrying short hairpin RNA (shRNA) against YTHDF3 were constructed by Genechem Company (Shanghai, China).



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    Influence of GPT2 on mTOR signaling pathway activation and regulation of ADH1A expression. (A) Effects of inhibition of mTOR with AZD8055 on ADH1A expression in LC cells. (B) Effects of activation of mTOR with <t>MHY1485</t> on ADH1A expression in LC cells. (C) Effects of GPT2 on mTOR activation and ADH1A expression in LC cells. (D) Effects of AKT activation mediated by the activator SC79 on mTOR sensitization and ADH1A expression in LC cells. (E) Effects of GPT2 on the activation of AKT and mTOR in LC cells. (F) Effects of GPT2 on mTOR activation and ADH1A expression mediated by AKT activation in LC cells. (G) AKT–mTOR interaction, assessed with co-IP assays. (H) Effects of GPT2 on AKT–mTOR interaction, measured with co-IP assays in LC cells. ADH1A, alcohol dehydrogenase 1A; AKT, protein kinase B; co-IP, co-immunoprecipitation; GPT2, glutamic-pyruvic transaminase 2; LC, liver cancer; mTOR, mammalian target of rapamycin.
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    Influence of GPT2 on mTOR signaling pathway activation and regulation of ADH1A expression. (A) Effects of inhibition of mTOR with AZD8055 on ADH1A expression in LC cells. (B) Effects of activation of mTOR with MHY1485 on ADH1A expression in LC cells. (C) Effects of GPT2 on mTOR activation and ADH1A expression in LC cells. (D) Effects of AKT activation mediated by the activator SC79 on mTOR sensitization and ADH1A expression in LC cells. (E) Effects of GPT2 on the activation of AKT and mTOR in LC cells. (F) Effects of GPT2 on mTOR activation and ADH1A expression mediated by AKT activation in LC cells. (G) AKT–mTOR interaction, assessed with co-IP assays. (H) Effects of GPT2 on AKT–mTOR interaction, measured with co-IP assays in LC cells. ADH1A, alcohol dehydrogenase 1A; AKT, protein kinase B; co-IP, co-immunoprecipitation; GPT2, glutamic-pyruvic transaminase 2; LC, liver cancer; mTOR, mammalian target of rapamycin.

    Journal: Cancer Biology & Medicine

    Article Title: HBx-mediated GPT2 suppression promotes liver cancer development by downregulating ADH1A

    doi: 10.20892/j.issn.2095-3941.2025.0236

    Figure Lengend Snippet: Influence of GPT2 on mTOR signaling pathway activation and regulation of ADH1A expression. (A) Effects of inhibition of mTOR with AZD8055 on ADH1A expression in LC cells. (B) Effects of activation of mTOR with MHY1485 on ADH1A expression in LC cells. (C) Effects of GPT2 on mTOR activation and ADH1A expression in LC cells. (D) Effects of AKT activation mediated by the activator SC79 on mTOR sensitization and ADH1A expression in LC cells. (E) Effects of GPT2 on the activation of AKT and mTOR in LC cells. (F) Effects of GPT2 on mTOR activation and ADH1A expression mediated by AKT activation in LC cells. (G) AKT–mTOR interaction, assessed with co-IP assays. (H) Effects of GPT2 on AKT–mTOR interaction, measured with co-IP assays in LC cells. ADH1A, alcohol dehydrogenase 1A; AKT, protein kinase B; co-IP, co-immunoprecipitation; GPT2, glutamic-pyruvic transaminase 2; LC, liver cancer; mTOR, mammalian target of rapamycin.

    Article Snippet: The AKT activator SC79, the mTOR pathway activator MHY1485, and its inhibitor AZD8055 were obtained from MedChemExpress (Shanghai, China).

    Techniques: Activation Assay, Expressing, Inhibition, Co-Immunoprecipitation Assay, Immunoprecipitation

    YTHDF3 regulates the glycolysis level of breast cancer through the mTOR–HIF1α–LDHA axis. (A) Relative mRNA expression of HIF1α in shNC and shYTHDF3 groups in MDA‐MB‐231 and MCF‐7 cells; (B) the correlation between YTHDF3 and HIF1α was predicted using the GEPIA website; (C) expression of key proteins in the mTOR–HIF1α–LDHA axis in shNC and shYTHDF3 groups in MDA‐MB‐231 and MCF‐7 cells; (D) after adding activator MHY1445, the growth ability of cancer cells in shNC and shYTHDF3 groups was detected by CCK‐8 assay; (E) the lactate level of cancer cells in shNC and shYTHDF3 groups treated with activator MHY1485; and (F) expression of proteins of cancer cells in shNC and shYTHDF3 groups treated with activator MHY1485.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: YTHDF3 Mediates the Occurrence and Development of Breast Cancer by Regulating Glycolysis Through the mTOR – HIF1α – LHDA Axis

    doi: 10.1111/jcmm.71105

    Figure Lengend Snippet: YTHDF3 regulates the glycolysis level of breast cancer through the mTOR–HIF1α–LDHA axis. (A) Relative mRNA expression of HIF1α in shNC and shYTHDF3 groups in MDA‐MB‐231 and MCF‐7 cells; (B) the correlation between YTHDF3 and HIF1α was predicted using the GEPIA website; (C) expression of key proteins in the mTOR–HIF1α–LDHA axis in shNC and shYTHDF3 groups in MDA‐MB‐231 and MCF‐7 cells; (D) after adding activator MHY1445, the growth ability of cancer cells in shNC and shYTHDF3 groups was detected by CCK‐8 assay; (E) the lactate level of cancer cells in shNC and shYTHDF3 groups treated with activator MHY1485; and (F) expression of proteins of cancer cells in shNC and shYTHDF3 groups treated with activator MHY1485.

    Article Snippet: The activator of the mTOR pathway, MHY1485, was obtained from MedChemExpress (Shanghai, China) at a concentration of 10 mM.

    Techniques: Expressing, CCK-8 Assay

    Effects of Gln and RAPA on the mTOR/Notch1 axis and MUC2 expression in HT-29 cells. (A) The expression of mTOR, p-mTOR, Notch1, and GAPDH. (B) Immunofluorescence analysis of MUC2 in HT-29 cells (800×). Data are presented as mean ± SD (n = 3). One-way ANOVA was carried out followed by Tukey’s test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

    Journal: Frontiers in Oncology

    Article Title: Glutamine alleviates radiation-induced intestinal injury in rats via the mTOR/Notch1 axis

    doi: 10.3389/fonc.2026.1735401

    Figure Lengend Snippet: Effects of Gln and RAPA on the mTOR/Notch1 axis and MUC2 expression in HT-29 cells. (A) The expression of mTOR, p-mTOR, Notch1, and GAPDH. (B) Immunofluorescence analysis of MUC2 in HT-29 cells (800×). Data are presented as mean ± SD (n = 3). One-way ANOVA was carried out followed by Tukey’s test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

    Article Snippet: To investigate the role of mTOR/notch1 pathway on Gln radio-resistance effects in colon, HT-29 cells were treated with the 10 μmol/L Jagged-1 (MCE, USA) , which activates the Notch1 receptor.

    Techniques: Expressing, Immunofluorescence

    Effects of Gln and Jagged-1 on the mTOR/Notch1 axis and MUC2 expression in HT-29 cells. (A) The expression of mTOR, p-mTOR, Notch1, and GAPDH. (B) Immunofluorescence analysis of MUC2 in HT-29 cells (800×). Data are presented as mean ± SD (n = 3). One-way ANOVA was carried out followed by Tukey’s test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

    Journal: Frontiers in Oncology

    Article Title: Glutamine alleviates radiation-induced intestinal injury in rats via the mTOR/Notch1 axis

    doi: 10.3389/fonc.2026.1735401

    Figure Lengend Snippet: Effects of Gln and Jagged-1 on the mTOR/Notch1 axis and MUC2 expression in HT-29 cells. (A) The expression of mTOR, p-mTOR, Notch1, and GAPDH. (B) Immunofluorescence analysis of MUC2 in HT-29 cells (800×). Data are presented as mean ± SD (n = 3). One-way ANOVA was carried out followed by Tukey’s test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

    Article Snippet: To investigate the role of mTOR/notch1 pathway on Gln radio-resistance effects in colon, HT-29 cells were treated with the 10 μmol/L Jagged-1 (MCE, USA) , which activates the Notch1 receptor.

    Techniques: Expressing, Immunofluorescence