erk inhibition  (MedChemExpress)

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: Kaempferol inhibits hepatitis B virus replication via ERK/FOXO1 pathway-mediated suppression of the viral core promoter

doi: 10.3389/fcimb.2026.1780484

Figure Lengend Snippet: KP inhibits the HBV core promoter (Cp) activity via the ERK/FOXO1 axis. (A) Schematic diagram of the HBV promoter regions. (B) Dual-luciferase reporter assays show that KP (25 μM) specifically suppresses the activity of the Cp, with minimal effects on SpI, SpII, or Xp in Huh7 cells. (C, D) Western blot analysis reveals that KP treatment in HepG2.2.15 cells increases phosphorylation of FOXO1 (p-FOXO1) (C) and ERK (p-ERK) (D) , while decreases FOXO1 (C) in a dose-dependent manner. (E) Consistent effects are observed in mouse liver tissues, with KP upregulating p-ERK and p-FOXO1, while downregulating FOXO1. (F) The ERK inhibitor U0126 blocks KP-induced phosphorylation of ERK and FOXO1 in HepG2.2.15 cells. (G) U0126 (5 μM) reverses the KP-mediated suppression of Cp activity in Huh7 cells. ** P < 0.01.

Article Snippet: The ERK inhibitor U0126 was obtained from MedChemExpress.

Techniques: Activity Assay, Luciferase, Western Blot, Phospho-proteomics

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: Kaempferol inhibits hepatitis B virus replication via ERK/FOXO1 pathway-mediated suppression of the viral core promoter

doi: 10.3389/fcimb.2026.1780484

Figure Lengend Snippet: The ERK inhibitor U0126 rescues the anti-HBV effects of KP. HepG2.2.15 cells were treated with KP (0, 1, 5, 25 μM), the ERK inhibitor U0126 (5 μM), the polymerase inhibitor ETV (0.03 nM), or their combinations. (A, B) Levels of secreted HBsAg (A) and HBeAg (B) . (C, D) Levels of intracellular (C) and extracellular (D) HBV DNA. (E, F) Levels of viral pgRNA (E) and total HBV RNA (F) . U0126 co-treatment significantly attenuates the suppression of all viral markers by KP, confirming the dependency of KP’s action on ERK signaling. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The ERK inhibitor U0126 was obtained from MedChemExpress.

Techniques:

Journal: bioRxiv

Article Title: An APP-centered molecular gateway integrates innate immunity and retinoic acid signaling to drive irreversible metamorphic commitment

doi: 10.64898/2026.01.22.700939

Figure Lengend Snippet: (A) Settlement rate of inhibitor-treated larvae. The box plots with superimposed jitter plots display the larval settlement rate under various inhibitor treatments. The biofilm stimulus condition is used as the positive control. The concentration of each inhibitor is indicated on the horizontal axis. The data represent the settlement rate of larvae remaining attached out of 10 larvae across six independent biological replicates (total n = 60). Statistical significance among treatment groups was assessed using one-way ANOVA followed by Tukey’s HSD post hoc test, with grouping letters indicating significant differences ( p < 0.05); treatments sharing a letter are not significantly different. (B) Quantitative assessment of the functional hierarchy. The box plots with superimposed jitter plots show the Metamorphic Progression Scores (MPS) for larvae treated with various pharmacological inhibitors with or without all-trans retinoic acid (RA). The MPS was calculated based on the metamorphic stage reached by the larvae in the identical assays used for the settlement rate analysis in (A). The concentration of each inhibitor is indicated on the horizontal axis. The MPS represents the average metamorphic stage reached (0 = brachiolaria; 1 = early; 2 = middle; 3 = late; 4 = pre-juvenile; 5 = juvenile). Statistical significance among the treatment groups was assessed using one-way ANOVA followed by Tukey’s HSD post hoc test ( *p < 0.05; n.s., not significant). A significant RA-dependent rescue condition (a statistically significant increase in MPS compared with the inhibitor-alone condition) is highlighted in grey, establishing the functional hierarchy of the pathways relative to the RA commitment signal. (C) Representative image illustrating pathway functional hierarchy. Images show representative larval morphology under the control, inhibitor-only, and inhibitor + RA conditions. These images specifically represent the high-concentration inhibitor treatments (MyD88 inhibitor: 50 µM; MAPK inhibitors: 10 µM; IKKβ and HSP90AA1 inhibitors: 1 µM). MyD88 inhibition completely blocks the behavioral decision of settlement. JNK and p38 inhibition caused a distinct early-stage arrest (low MPS), and the effects of their inhibition were significantly rescued by RA co-treatment. In contrast, ERK inhibition arrested metamorphosis at the middle stage, and this block was not rescued by exogenous RA. Similarly, IKKβ and HSP90AA1 inhibition arrested metamorphosis at later stages, and this block was not rescued by exogenous RA, functionally placing all three pathways (ERK, IKKβ, and HSP90AA1) downstream of the RA commitment signal. Scale bar: 200 µm. Inhibitors used: T6167923 (MyD88 inhibitor), IKK-16 (IKKβ inhibitor), U0126 (ERK inhibitor), SP600125 (JNK inhibitor), SB202190 (p38 inhibitor), and Luminespib (HSP90AA1 inhibitor).

Article Snippet: The inhibitors were dissolved in DMSO and applied at the indicated concentrations: the MyD88 inhibitor T6167923 (5 or 50 μM; MedChemExpress), the IKKβ inhibitor IKK-16 (0.1 or 1 μM; MedChemExpress), and MAPK inhibitors SP600125 (JNK), SB202190 (p38), and U0126 (ERK) (1 or 10 μM; MedChemExpress or FUJIFILM Wako Pure Chemical Corporation), and the HSP90AA1 inhibitors luminespib (0.1 or 1 μM; Chemscene).

Techniques: Positive Control, Concentration Assay, Functional Assay, Control, Inhibition, Blocking Assay