HY-136427 Search Results


93
MedChemExpress dnmt inhibitor rg108
Role of DNA methylation in the lonafarnib affected activity, total expression, membrane expression, and phosphorylation of a7nAChR. (A) Levels of a7nAChR total proteins in the hippocampus of control and lonafarnib-treated mice treated with vehicle, DNMT inhibitor <t>RG108</t> or anisomycin. ** P < 0.01 vs. control mice, ## P < 0.01 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (B) Evoked I ACh by ACh (3 mM) in the slices of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin, ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (C) Levels of biotinylated a7nAChR (membrane surface) protein in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. Surface a7nAChR was normalized by surface GluR2 protein, which was again normalized by vehicle-treated control group. ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (D) Levels of phospho-a7nAChR in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. The expression of protein and the amplitude of evoked I ACh were normalized by the values of control group with vehicle.
Dnmt Inhibitor Rg108, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
dnmt inhibitor rg108 - by Bioz Stars, 2026-02
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91
MedChemExpress synthetic fkbp ligand gpi1485
Role of DNA methylation in the lonafarnib affected activity, total expression, membrane expression, and phosphorylation of a7nAChR. (A) Levels of a7nAChR total proteins in the hippocampus of control and lonafarnib-treated mice treated with vehicle, DNMT inhibitor <t>RG108</t> or anisomycin. ** P < 0.01 vs. control mice, ## P < 0.01 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (B) Evoked I ACh by ACh (3 mM) in the slices of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin, ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (C) Levels of biotinylated a7nAChR (membrane surface) protein in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. Surface a7nAChR was normalized by surface GluR2 protein, which was again normalized by vehicle-treated control group. ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (D) Levels of phospho-a7nAChR in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. The expression of protein and the amplitude of evoked I ACh were normalized by the values of control group with vehicle.
Synthetic Fkbp Ligand Gpi1485, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/synthetic fkbp ligand gpi1485/product/MedChemExpress
Average 91 stars, based on 1 article reviews
synthetic fkbp ligand gpi1485 - by Bioz Stars, 2026-02
91/100 stars
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Image Search Results


Role of DNA methylation in the lonafarnib affected activity, total expression, membrane expression, and phosphorylation of a7nAChR. (A) Levels of a7nAChR total proteins in the hippocampus of control and lonafarnib-treated mice treated with vehicle, DNMT inhibitor RG108 or anisomycin. ** P < 0.01 vs. control mice, ## P < 0.01 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (B) Evoked I ACh by ACh (3 mM) in the slices of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin, ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (C) Levels of biotinylated a7nAChR (membrane surface) protein in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. Surface a7nAChR was normalized by surface GluR2 protein, which was again normalized by vehicle-treated control group. ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (D) Levels of phospho-a7nAChR in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. The expression of protein and the amplitude of evoked I ACh were normalized by the values of control group with vehicle.

Journal: Frontiers in Pharmacology

Article Title: Farnesyl Transferase Inhibitor Lonafarnib Enhances α7nAChR Expression Through Inhibiting DNA Methylation of CHRNA7 and Increases α7nAChR Membrane Trafficking

doi: 10.3389/fphar.2020.589780

Figure Lengend Snippet: Role of DNA methylation in the lonafarnib affected activity, total expression, membrane expression, and phosphorylation of a7nAChR. (A) Levels of a7nAChR total proteins in the hippocampus of control and lonafarnib-treated mice treated with vehicle, DNMT inhibitor RG108 or anisomycin. ** P < 0.01 vs. control mice, ## P < 0.01 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (B) Evoked I ACh by ACh (3 mM) in the slices of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin, ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (C) Levels of biotinylated a7nAChR (membrane surface) protein in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. Surface a7nAChR was normalized by surface GluR2 protein, which was again normalized by vehicle-treated control group. ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (D) Levels of phospho-a7nAChR in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. The expression of protein and the amplitude of evoked I ACh were normalized by the values of control group with vehicle.

Article Snippet: CaMKII inhibitor KN93 and DNMT inhibitor RG108 were purchased from MCE.

Techniques: DNA Methylation Assay, Activity Assay, Expressing, Membrane, Control, Comparison

Lonafarnib administration affects CaMKII signaling pathways, partially modulating the membrane expression of a7nAChR. (A and B) Levels of phospho-PKC and phospho-PKA in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. (C) Levels of phospho-CaMKII in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. ** P < 0.01 vs. control mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (D) Levels of biotinylated a7nAChR (membrane) protein in the hippocampus of control and lonafarnib-treated mice treated with vehicle or CaMKII pathway blocker KN93. Surface a7nAChR was normalized by surface GluR2 protein, which was again normalized by vehicle-treated control group. ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (E) Levels of a7nAChR total proteins in the hippocampus of control and lonafarnib-treated mice treated with vehicle and KN93, and total a7nAChR was normalized by GAPDH, which was again normalized by vehicle-treated group. ** P < 0.01 vs. control mice (two-way ANOVA, followed by Tukey’s multiple comparison test). The expression of protein was normalized by the values of control group with vehicle.

Journal: Frontiers in Pharmacology

Article Title: Farnesyl Transferase Inhibitor Lonafarnib Enhances α7nAChR Expression Through Inhibiting DNA Methylation of CHRNA7 and Increases α7nAChR Membrane Trafficking

doi: 10.3389/fphar.2020.589780

Figure Lengend Snippet: Lonafarnib administration affects CaMKII signaling pathways, partially modulating the membrane expression of a7nAChR. (A and B) Levels of phospho-PKC and phospho-PKA in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. (C) Levels of phospho-CaMKII in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. ** P < 0.01 vs. control mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (D) Levels of biotinylated a7nAChR (membrane) protein in the hippocampus of control and lonafarnib-treated mice treated with vehicle or CaMKII pathway blocker KN93. Surface a7nAChR was normalized by surface GluR2 protein, which was again normalized by vehicle-treated control group. ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (E) Levels of a7nAChR total proteins in the hippocampus of control and lonafarnib-treated mice treated with vehicle and KN93, and total a7nAChR was normalized by GAPDH, which was again normalized by vehicle-treated group. ** P < 0.01 vs. control mice (two-way ANOVA, followed by Tukey’s multiple comparison test). The expression of protein was normalized by the values of control group with vehicle.

Article Snippet: CaMKII inhibitor KN93 and DNMT inhibitor RG108 were purchased from MCE.

Techniques: Membrane, Expressing, Control, Comparison