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4e1rcat  (MedChemExpress)


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    MedChemExpress 4e1rcat
    (A) Western blot analysis of A375 and MelJuso (NRAS-mutant) melanoma cells treated with increasing concentrations of the eIF4A inhibitor Rocaglamide A (RocA) for 20 h. Both cell lines exhibited dose-dependent increases in phosphorylated AMPK, accompanied by decreased levels of LKB1 and its cofactor MO25. (B) Western blot analysis of G361 (BRAF V600E -mutant, LKB1 -null) melanoma cells treated with increasing concentrations of RocA for 20 h. AMPK activation occurred in a dose-dependent manner despite the absence of functional LKB1, confirming LKB1-independent AMPK activation. (C) Western blot analysis of A375, MelJuso, and G361 cells treated with increasing concentrations of the eIF4E-eIF4G disruptor <t>4E1RCat</t> for 20 h. All three cell lines exhibited increased AMPK activity regardless of LKB1 status or driver mutation. (D) Western blot analysis of A375 and MelJuso cells transfected with two different LKB1-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. LKB1 knockdown did not prevent RocA-induced AMPK activation, confirming the LKB1-independent mechanism. Non-targeting control siRNA (si-NT) was used as a control. (D) Western blot analysis of A375, G361, and MelJuso cells transfected with CaMKKβ-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. CaMKKβ depletion did not impair RocA-induced AMPK activation, indicating that CaMKKβ is not required for AMPK activation by eIF4F inhibition. Non-targeting control siRNAs (si-NT) were used as a control. (E) Western blot analysis of A375 and MelJuso cells transfected with MLK3-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. MLK3 protein levels decreased following both RocA treatment and siRNA-mediated knockdown, but MLK3 depletion did not prevent RocA-induced AMPK activation. Non-targeting siRNAs (si-NT) were used as a control. Vinculin, GAPDH, or total AMPK levels served as loading controls. The control samples (CTRL) were treated with an equivalent volume of the vehicle (DMSO). The upper index letters refer to the corresponding loading control detected on the same membrane.
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    1) Product Images from "Translational control of AMPK activity in melanoma"

    Article Title: Translational control of AMPK activity in melanoma

    Journal: bioRxiv

    doi: 10.64898/2025.12.30.697000

    (A) Western blot analysis of A375 and MelJuso (NRAS-mutant) melanoma cells treated with increasing concentrations of the eIF4A inhibitor Rocaglamide A (RocA) for 20 h. Both cell lines exhibited dose-dependent increases in phosphorylated AMPK, accompanied by decreased levels of LKB1 and its cofactor MO25. (B) Western blot analysis of G361 (BRAF V600E -mutant, LKB1 -null) melanoma cells treated with increasing concentrations of RocA for 20 h. AMPK activation occurred in a dose-dependent manner despite the absence of functional LKB1, confirming LKB1-independent AMPK activation. (C) Western blot analysis of A375, MelJuso, and G361 cells treated with increasing concentrations of the eIF4E-eIF4G disruptor 4E1RCat for 20 h. All three cell lines exhibited increased AMPK activity regardless of LKB1 status or driver mutation. (D) Western blot analysis of A375 and MelJuso cells transfected with two different LKB1-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. LKB1 knockdown did not prevent RocA-induced AMPK activation, confirming the LKB1-independent mechanism. Non-targeting control siRNA (si-NT) was used as a control. (D) Western blot analysis of A375, G361, and MelJuso cells transfected with CaMKKβ-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. CaMKKβ depletion did not impair RocA-induced AMPK activation, indicating that CaMKKβ is not required for AMPK activation by eIF4F inhibition. Non-targeting control siRNAs (si-NT) were used as a control. (E) Western blot analysis of A375 and MelJuso cells transfected with MLK3-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. MLK3 protein levels decreased following both RocA treatment and siRNA-mediated knockdown, but MLK3 depletion did not prevent RocA-induced AMPK activation. Non-targeting siRNAs (si-NT) were used as a control. Vinculin, GAPDH, or total AMPK levels served as loading controls. The control samples (CTRL) were treated with an equivalent volume of the vehicle (DMSO). The upper index letters refer to the corresponding loading control detected on the same membrane.
    Figure Legend Snippet: (A) Western blot analysis of A375 and MelJuso (NRAS-mutant) melanoma cells treated with increasing concentrations of the eIF4A inhibitor Rocaglamide A (RocA) for 20 h. Both cell lines exhibited dose-dependent increases in phosphorylated AMPK, accompanied by decreased levels of LKB1 and its cofactor MO25. (B) Western blot analysis of G361 (BRAF V600E -mutant, LKB1 -null) melanoma cells treated with increasing concentrations of RocA for 20 h. AMPK activation occurred in a dose-dependent manner despite the absence of functional LKB1, confirming LKB1-independent AMPK activation. (C) Western blot analysis of A375, MelJuso, and G361 cells treated with increasing concentrations of the eIF4E-eIF4G disruptor 4E1RCat for 20 h. All three cell lines exhibited increased AMPK activity regardless of LKB1 status or driver mutation. (D) Western blot analysis of A375 and MelJuso cells transfected with two different LKB1-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. LKB1 knockdown did not prevent RocA-induced AMPK activation, confirming the LKB1-independent mechanism. Non-targeting control siRNA (si-NT) was used as a control. (D) Western blot analysis of A375, G361, and MelJuso cells transfected with CaMKKβ-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. CaMKKβ depletion did not impair RocA-induced AMPK activation, indicating that CaMKKβ is not required for AMPK activation by eIF4F inhibition. Non-targeting control siRNAs (si-NT) were used as a control. (E) Western blot analysis of A375 and MelJuso cells transfected with MLK3-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. MLK3 protein levels decreased following both RocA treatment and siRNA-mediated knockdown, but MLK3 depletion did not prevent RocA-induced AMPK activation. Non-targeting siRNAs (si-NT) were used as a control. Vinculin, GAPDH, or total AMPK levels served as loading controls. The control samples (CTRL) were treated with an equivalent volume of the vehicle (DMSO). The upper index letters refer to the corresponding loading control detected on the same membrane.

    Techniques Used: Western Blot, Mutagenesis, Activation Assay, Functional Assay, Activity Assay, Transfection, Knockdown, Control, Inhibition, Membrane



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    (A) Western blot analysis of A375 and MelJuso (NRAS-mutant) melanoma cells treated with increasing concentrations of the eIF4A inhibitor Rocaglamide A (RocA) for 20 h. Both cell lines exhibited dose-dependent increases in phosphorylated AMPK, accompanied by decreased levels of LKB1 and its cofactor MO25. (B) Western blot analysis of G361 (BRAF V600E -mutant, LKB1 -null) melanoma cells treated with increasing concentrations of RocA for 20 h. AMPK activation occurred in a dose-dependent manner despite the absence of functional LKB1, confirming LKB1-independent AMPK activation. (C) Western blot analysis of A375, MelJuso, and G361 cells treated with increasing concentrations of the eIF4E-eIF4G disruptor <t>4E1RCat</t> for 20 h. All three cell lines exhibited increased AMPK activity regardless of LKB1 status or driver mutation. (D) Western blot analysis of A375 and MelJuso cells transfected with two different LKB1-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. LKB1 knockdown did not prevent RocA-induced AMPK activation, confirming the LKB1-independent mechanism. Non-targeting control siRNA (si-NT) was used as a control. (D) Western blot analysis of A375, G361, and MelJuso cells transfected with CaMKKβ-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. CaMKKβ depletion did not impair RocA-induced AMPK activation, indicating that CaMKKβ is not required for AMPK activation by eIF4F inhibition. Non-targeting control siRNAs (si-NT) were used as a control. (E) Western blot analysis of A375 and MelJuso cells transfected with MLK3-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. MLK3 protein levels decreased following both RocA treatment and siRNA-mediated knockdown, but MLK3 depletion did not prevent RocA-induced AMPK activation. Non-targeting siRNAs (si-NT) were used as a control. Vinculin, GAPDH, or total AMPK levels served as loading controls. The control samples (CTRL) were treated with an equivalent volume of the vehicle (DMSO). The upper index letters refer to the corresponding loading control detected on the same membrane.
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    (A) Western blot analysis of A375 and MelJuso (NRAS-mutant) melanoma cells treated with increasing concentrations of the eIF4A inhibitor Rocaglamide A (RocA) for 20 h. Both cell lines exhibited dose-dependent increases in phosphorylated AMPK, accompanied by decreased levels of LKB1 and its cofactor MO25. (B) Western blot analysis of G361 (BRAF V600E -mutant, LKB1 -null) melanoma cells treated with increasing concentrations of RocA for 20 h. AMPK activation occurred in a dose-dependent manner despite the absence of functional LKB1, confirming LKB1-independent AMPK activation. (C) Western blot analysis of A375, MelJuso, and G361 cells treated with increasing concentrations of the eIF4E-eIF4G disruptor <t>4E1RCat</t> for 20 h. All three cell lines exhibited increased AMPK activity regardless of LKB1 status or driver mutation. (D) Western blot analysis of A375 and MelJuso cells transfected with two different LKB1-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. LKB1 knockdown did not prevent RocA-induced AMPK activation, confirming the LKB1-independent mechanism. Non-targeting control siRNA (si-NT) was used as a control. (D) Western blot analysis of A375, G361, and MelJuso cells transfected with CaMKKβ-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. CaMKKβ depletion did not impair RocA-induced AMPK activation, indicating that CaMKKβ is not required for AMPK activation by eIF4F inhibition. Non-targeting control siRNAs (si-NT) were used as a control. (E) Western blot analysis of A375 and MelJuso cells transfected with MLK3-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. MLK3 protein levels decreased following both RocA treatment and siRNA-mediated knockdown, but MLK3 depletion did not prevent RocA-induced AMPK activation. Non-targeting siRNAs (si-NT) were used as a control. Vinculin, GAPDH, or total AMPK levels served as loading controls. The control samples (CTRL) were treated with an equivalent volume of the vehicle (DMSO). The upper index letters refer to the corresponding loading control detected on the same membrane.
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    (A) Western blot analysis of A375 and MelJuso (NRAS-mutant) melanoma cells treated with increasing concentrations of the eIF4A inhibitor Rocaglamide A (RocA) for 20 h. Both cell lines exhibited dose-dependent increases in phosphorylated AMPK, accompanied by decreased levels of LKB1 and its cofactor MO25. (B) Western blot analysis of G361 (BRAF V600E -mutant, LKB1 -null) melanoma cells treated with increasing concentrations of RocA for 20 h. AMPK activation occurred in a dose-dependent manner despite the absence of functional LKB1, confirming LKB1-independent AMPK activation. (C) Western blot analysis of A375, MelJuso, and G361 cells treated with increasing concentrations of the eIF4E-eIF4G disruptor 4E1RCat for 20 h. All three cell lines exhibited increased AMPK activity regardless of LKB1 status or driver mutation. (D) Western blot analysis of A375 and MelJuso cells transfected with two different LKB1-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. LKB1 knockdown did not prevent RocA-induced AMPK activation, confirming the LKB1-independent mechanism. Non-targeting control siRNA (si-NT) was used as a control. (D) Western blot analysis of A375, G361, and MelJuso cells transfected with CaMKKβ-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. CaMKKβ depletion did not impair RocA-induced AMPK activation, indicating that CaMKKβ is not required for AMPK activation by eIF4F inhibition. Non-targeting control siRNAs (si-NT) were used as a control. (E) Western blot analysis of A375 and MelJuso cells transfected with MLK3-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. MLK3 protein levels decreased following both RocA treatment and siRNA-mediated knockdown, but MLK3 depletion did not prevent RocA-induced AMPK activation. Non-targeting siRNAs (si-NT) were used as a control. Vinculin, GAPDH, or total AMPK levels served as loading controls. The control samples (CTRL) were treated with an equivalent volume of the vehicle (DMSO). The upper index letters refer to the corresponding loading control detected on the same membrane.

    Journal: bioRxiv

    Article Title: Translational control of AMPK activity in melanoma

    doi: 10.64898/2025.12.30.697000

    Figure Lengend Snippet: (A) Western blot analysis of A375 and MelJuso (NRAS-mutant) melanoma cells treated with increasing concentrations of the eIF4A inhibitor Rocaglamide A (RocA) for 20 h. Both cell lines exhibited dose-dependent increases in phosphorylated AMPK, accompanied by decreased levels of LKB1 and its cofactor MO25. (B) Western blot analysis of G361 (BRAF V600E -mutant, LKB1 -null) melanoma cells treated with increasing concentrations of RocA for 20 h. AMPK activation occurred in a dose-dependent manner despite the absence of functional LKB1, confirming LKB1-independent AMPK activation. (C) Western blot analysis of A375, MelJuso, and G361 cells treated with increasing concentrations of the eIF4E-eIF4G disruptor 4E1RCat for 20 h. All three cell lines exhibited increased AMPK activity regardless of LKB1 status or driver mutation. (D) Western blot analysis of A375 and MelJuso cells transfected with two different LKB1-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. LKB1 knockdown did not prevent RocA-induced AMPK activation, confirming the LKB1-independent mechanism. Non-targeting control siRNA (si-NT) was used as a control. (D) Western blot analysis of A375, G361, and MelJuso cells transfected with CaMKKβ-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. CaMKKβ depletion did not impair RocA-induced AMPK activation, indicating that CaMKKβ is not required for AMPK activation by eIF4F inhibition. Non-targeting control siRNAs (si-NT) were used as a control. (E) Western blot analysis of A375 and MelJuso cells transfected with MLK3-targeting siRNAs for 48 h, combined with 100 nM RocA treatment for the last 20 h. MLK3 protein levels decreased following both RocA treatment and siRNA-mediated knockdown, but MLK3 depletion did not prevent RocA-induced AMPK activation. Non-targeting siRNAs (si-NT) were used as a control. Vinculin, GAPDH, or total AMPK levels served as loading controls. The control samples (CTRL) were treated with an equivalent volume of the vehicle (DMSO). The upper index letters refer to the corresponding loading control detected on the same membrane.

    Article Snippet: Small-molecule inhibitor stocks of Rocaglamide A, 4E1RCat, CR-1-31-B, Rotenone (MedChemExpress), PD184352, YM201636 (Selleckchem) and Okadaic acid (Merck) were prepared in dimethylsulfoxide (DMSO, Merck).

    Techniques: Western Blot, Mutagenesis, Activation Assay, Functional Assay, Activity Assay, Transfection, Knockdown, Control, Inhibition, Membrane