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ampk inhibitor  (MedChemExpress)


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    MedChemExpress ampk inhibitor
    Ampk Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 47 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ampk+in+3/AMPK-IN-3/pm42056521-782-26-32
    Average 95 stars, based on 47 article reviews
    ampk inhibitor - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Stable Transfection:

    Article Title: BNIP3-mediated mitophagy boosts the competitive dominant growth of lenvatinib resistant cells via reprogramming energy metabolism in HCC
    Article Snippet: .. To analyse the molecular mechanism of cell competition, Huh7R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5ug/ml puromycin; Huh7R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R was constructed by pre-treating with 2μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Article Title: BNIP3-mediated mitophagy boosts the competitive growth of Lenvatinib-resistant cells via energy metabolism reprogramming in HCC
    Article Snippet: .. To analyze the molecular mechanism of cell competition, Huh7R/PLC-PRF-5R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5 ug/ml puromycin; Huh7R/PLC-PRF-5R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5 ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R/PLC-PRF-5R was constructed by pre-treating with 2 μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Expressing:

    Article Title: BNIP3-mediated mitophagy boosts the competitive dominant growth of lenvatinib resistant cells via reprogramming energy metabolism in HCC
    Article Snippet: .. To analyse the molecular mechanism of cell competition, Huh7R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5ug/ml puromycin; Huh7R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R was constructed by pre-treating with 2μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Article Title: BNIP3-mediated mitophagy boosts the competitive growth of Lenvatinib-resistant cells via energy metabolism reprogramming in HCC
    Article Snippet: .. To analyze the molecular mechanism of cell competition, Huh7R/PLC-PRF-5R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5 ug/ml puromycin; Huh7R/PLC-PRF-5R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5 ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R/PLC-PRF-5R was constructed by pre-treating with 2 μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    shRNA:

    Article Title: BNIP3-mediated mitophagy boosts the competitive dominant growth of lenvatinib resistant cells via reprogramming energy metabolism in HCC
    Article Snippet: .. To analyse the molecular mechanism of cell competition, Huh7R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5ug/ml puromycin; Huh7R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R was constructed by pre-treating with 2μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Article Title: BNIP3-mediated mitophagy boosts the competitive growth of Lenvatinib-resistant cells via energy metabolism reprogramming in HCC
    Article Snippet: .. To analyze the molecular mechanism of cell competition, Huh7R/PLC-PRF-5R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5 ug/ml puromycin; Huh7R/PLC-PRF-5R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5 ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R/PLC-PRF-5R was constructed by pre-treating with 2 μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Construct:

    Article Title: BNIP3-mediated mitophagy boosts the competitive dominant growth of lenvatinib resistant cells via reprogramming energy metabolism in HCC
    Article Snippet: .. To analyse the molecular mechanism of cell competition, Huh7R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5ug/ml puromycin; Huh7R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R was constructed by pre-treating with 2μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Article Title: BNIP3-mediated mitophagy boosts the competitive growth of Lenvatinib-resistant cells via energy metabolism reprogramming in HCC
    Article Snippet: .. To analyze the molecular mechanism of cell competition, Huh7R/PLC-PRF-5R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5 ug/ml puromycin; Huh7R/PLC-PRF-5R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5 ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R/PLC-PRF-5R was constructed by pre-treating with 2 μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Selection:

    Article Title: BNIP3-mediated mitophagy boosts the competitive dominant growth of lenvatinib resistant cells via reprogramming energy metabolism in HCC
    Article Snippet: .. To analyse the molecular mechanism of cell competition, Huh7R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5ug/ml puromycin; Huh7R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R was constructed by pre-treating with 2μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Article Title: BNIP3-mediated mitophagy boosts the competitive growth of Lenvatinib-resistant cells via energy metabolism reprogramming in HCC
    Article Snippet: .. To analyze the molecular mechanism of cell competition, Huh7R/PLC-PRF-5R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5 ug/ml puromycin; Huh7R/PLC-PRF-5R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5 ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R/PLC-PRF-5R was constructed by pre-treating with 2 μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Plasmid Preparation:

    Article Title: BNIP3-mediated mitophagy boosts the competitive dominant growth of lenvatinib resistant cells via reprogramming energy metabolism in HCC
    Article Snippet: .. To analyse the molecular mechanism of cell competition, Huh7R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5ug/ml puromycin; Huh7R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R was constructed by pre-treating with 2μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Article Title: BNIP3-mediated mitophagy boosts the competitive growth of Lenvatinib-resistant cells via energy metabolism reprogramming in HCC
    Article Snippet: .. To analyze the molecular mechanism of cell competition, Huh7R/PLC-PRF-5R stably expressing BNIP3 / ENO2 -short hairpin RNA (sh BNIP3 / ENO2 ) was constructed via transfecting cells with sh BNIP3 / ENO2 lentivirus obtained from the Liver Cancer Institute and following the selection of DMEM containing 5 ug/ml puromycin; Huh7R/PLC-PRF-5R transitorily overexpressing BNIP3 (oe BNIP3 ) was constructed via transfecting Lipofectamine 3000 reagent (Thermo Fisher, USA) with BNIP3 plasmid (Sangon, China) and following the selection of DMEM containing 5 ug/ml neomyein sulfate (Solarbio, China); AMPK-activated/inhibited Huh7R/PLC-PRF-5R was constructed by pre-treating with 2 μm AMPK-activator-2 (MCE, USA)/15μm AMPK-IN-3 (MCE, USA). ..

    Extraction:

    Article Title: Lian Qiao Wen Dan Decoction attenuates gastric carcinogenesis by alleviating oxidative phosphorylation dysfunction.
    Article Snippet: Measurement of adenosine triphosphate (ATP) levels and NAD+/NADH ratio ATP levels were detected using the firefly luciferase-based ATP assay kit (S0026, Beyotime, Beijing, China) according to the manufacturer’s instructions. .. For the cell experiments, GC cells were treated with different concentrations of quercetin (HY-18,085, PubChem CID: 5280,343), kaempferol (HY-14,590, PubChem CID: 5280,863) and AMPK-IN-3 (HY-151,361, PubChem CID: 162,664,520) (MCE, Edison, USA) for 48 h. Gastric tissues or cells were lysed in extraction buffer on ice and centrifuged at 4 ◦C for 10 min at 12,000 rpm. ..

    other:

    Article Title: α-KG alleviates mitochondrial dysfunction and attenuates HPDLSCs senescence in periodontitis through LKB1-AMPK activation.
    Article Snippet: Periodontitis is a chronic inflammatory disease characterized by persistent inflammation that induces senescence and functional impairment of human periodontal ligament stem cells (HPDLSCs), thereby hindering periodontal regeneration.. Mitochondrial dysfunction is a key driver of inflammation-induced stem cell senescence.. However, the signaling mechanisms remain unclear.



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    <t>AMPK</t> mediated the SOX9–STAT3 axis in VSMCs stimulated with PDGF-BB. (A) KEGG pathway enrichment map of SOX9-bound genes in PDGF-BB-treated VSMCs. (B–C) Western blot analysis (B) showed the protein levels of p-STAT3, STAT3, SOX9, p-AMPK, AMPK, α-SMA, and SM22α in the VSMCs induced by PDGF-BB (C) . n = 6; **p < 0.01; NS indicates not significant. (D–H) Western blot analysis (D) showed the protein levels of STAT3 (E) , SOX9 (F) , α-SMA (G) , and SM22α (H) in the VSMCs treated with DMSO, AMPK inhibitor, PDGF-BB, and PDGF-BB + AMPK inhibitor, respectively. n = 4; *p < 0.05; **p < 0.01. (I–M) : Western blot analysis (I) showed the protein levels of p-STAT3 (J) , STAT3 (K) , α-SMA (L) , and SM22α (M) in the VSMCs treated with si-NC, si-NC + PDGF-BB, si-SOX9, and si-SOX9 +PDGF-BB, respectively. n = 4; *p < 0.05; **p < 0.01.
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    Image Search Results


    AMPK mediated the SOX9–STAT3 axis in VSMCs stimulated with PDGF-BB. (A) KEGG pathway enrichment map of SOX9-bound genes in PDGF-BB-treated VSMCs. (B–C) Western blot analysis (B) showed the protein levels of p-STAT3, STAT3, SOX9, p-AMPK, AMPK, α-SMA, and SM22α in the VSMCs induced by PDGF-BB (C) . n = 6; **p < 0.01; NS indicates not significant. (D–H) Western blot analysis (D) showed the protein levels of STAT3 (E) , SOX9 (F) , α-SMA (G) , and SM22α (H) in the VSMCs treated with DMSO, AMPK inhibitor, PDGF-BB, and PDGF-BB + AMPK inhibitor, respectively. n = 4; *p < 0.05; **p < 0.01. (I–M) : Western blot analysis (I) showed the protein levels of p-STAT3 (J) , STAT3 (K) , α-SMA (L) , and SM22α (M) in the VSMCs treated with si-NC, si-NC + PDGF-BB, si-SOX9, and si-SOX9 +PDGF-BB, respectively. n = 4; *p < 0.05; **p < 0.01.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: SOX9 mediates the phenotypic transformation of vascular smooth muscle cells in restenosis after carotid artery injury

    doi: 10.3389/fcell.2025.1592594

    Figure Lengend Snippet: AMPK mediated the SOX9–STAT3 axis in VSMCs stimulated with PDGF-BB. (A) KEGG pathway enrichment map of SOX9-bound genes in PDGF-BB-treated VSMCs. (B–C) Western blot analysis (B) showed the protein levels of p-STAT3, STAT3, SOX9, p-AMPK, AMPK, α-SMA, and SM22α in the VSMCs induced by PDGF-BB (C) . n = 6; **p < 0.01; NS indicates not significant. (D–H) Western blot analysis (D) showed the protein levels of STAT3 (E) , SOX9 (F) , α-SMA (G) , and SM22α (H) in the VSMCs treated with DMSO, AMPK inhibitor, PDGF-BB, and PDGF-BB + AMPK inhibitor, respectively. n = 4; *p < 0.05; **p < 0.01. (I–M) : Western blot analysis (I) showed the protein levels of p-STAT3 (J) , STAT3 (K) , α-SMA (L) , and SM22α (M) in the VSMCs treated with si-NC, si-NC + PDGF-BB, si-SOX9, and si-SOX9 +PDGF-BB, respectively. n = 4; *p < 0.05; **p < 0.01.

    Article Snippet: Recombinant murine PDGF-BB and AMPK inhibitors ( HY-151361 , MCE) were purchased from PeproTech (Rocky Hill, NJ, United States) and MCE (Shanghai, China), respectively.

    Techniques: Western Blot

    Schematic illustration of the role of the SOX9–STAT3 axis in VSMC transformation, proliferation, and migration and its contribution to neointimal hyperplasia following carotid balloon injury. PDGF-BB stimulates the phosphorylation of AMPK in VSMCs, which subsequently upregulates the expression of SOX9. Then, SOX9 translocates into the nucleus, where it directly binds to the promoter region of STAT3, leading to its activation. This signaling cascade drives VSMC transformation, proliferation, and migration, ultimately contributing to the pathological development of neointimal hyperplasia following carotid balloon injury.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: SOX9 mediates the phenotypic transformation of vascular smooth muscle cells in restenosis after carotid artery injury

    doi: 10.3389/fcell.2025.1592594

    Figure Lengend Snippet: Schematic illustration of the role of the SOX9–STAT3 axis in VSMC transformation, proliferation, and migration and its contribution to neointimal hyperplasia following carotid balloon injury. PDGF-BB stimulates the phosphorylation of AMPK in VSMCs, which subsequently upregulates the expression of SOX9. Then, SOX9 translocates into the nucleus, where it directly binds to the promoter region of STAT3, leading to its activation. This signaling cascade drives VSMC transformation, proliferation, and migration, ultimately contributing to the pathological development of neointimal hyperplasia following carotid balloon injury.

    Article Snippet: Recombinant murine PDGF-BB and AMPK inhibitors ( HY-151361 , MCE) were purchased from PeproTech (Rocky Hill, NJ, United States) and MCE (Shanghai, China), respectively.

    Techniques: Transformation Assay, Migration, Phospho-proteomics, Expressing, Activation Assay