mitogen activated protein kinase mapk pathway inhibitors  (TargetMol)

Journal: bioRxiv

Article Title: Rescuing functional defects in a zebrafish model of CDKL5 deficiency disorder: Contribution to the identification of new therapeutic compounds

doi: 10.64898/2026.03.12.711124

Figure Lengend Snippet: Total distance traveled by 5 dpf cdkl5 -/- zebrafish larvae following treatment with 149 compounds from the MAPK Inhibitor Library (10 μM). Each dot represents the mean ± SEM distance traveled by 48 cdkl5 -/- larvae per compound, normalized to DMSO-treated WT controls. The green and grey horizontal lines indicate the mean ± SEM distance traveled by DMSO-treated WT and DMSO-treated cdkl5 -/- larvae, respectively. Statistical analysis was performed using one-way ANOVA followed by Dunnett’s post hoc test. Compounds classified as great candidates (green dots) significantly increased ( p <0.05) the distance traveled by cdkl5 ⁻/⁻ larvae to levels not significantly different from those of DMSO-treated WT controls ( p >0.05). Compounds classified as good candidates (blue dots) significantly increased ( p <0.05) the distance traveled by cdkl5 ⁻/⁻ larvae but remained significantly lower than that of DMSO-treated WT controls ( p <0.05). The compound classified as overabundant candidate (red dot) resulted in a significantly greater distance traveled by cdkl5 ⁻/⁻ larvae compared to both DMSO-treated cdkl5 ⁻/⁻ and WT control larvae ( p <0.05).

Article Snippet: Two compound libraries were used in this study: the MAPK Inhibitor Library (258 compounds, catalog no. L3400) and the Histone Modification Library (347 compounds, catalog no. L4900), both purchased from Selleckchem (Houston, USA).

Techniques: Control

Journal: Advanced Science

Article Title: Enhancing Tendon Regeneration: Investigating the Impact of Topography on the Secretome of Adipose‐Derived Stem Cells

doi: 10.1002/advs.202417447

Figure Lengend Snippet: ACM improves cell proliferation and tendon differentiation of TSPCs by activating MAPK and Integrin pathways. A) Western blot of p‐MEK and MEK in TSPCs after treatment of RCM, RCM+U0126, ACM, or ACM+U0126 for 18 h. B) Western blot of p‐ERK, ERK in TSPCs after treatment of RCM, RCM+U0126, ACM, or ACM+U0126 treatment for 18 h. C) Gene expression of PCNA in different groups at day 3. D) Proliferation of TSPCs measured by CCK‐8 at 1, 3, and 5 days, n = 5 technically independent samples for each group, ** p < 0.01 **** p < 0.0001. E) Gene expression of SCX, TNMD, and MKX in different groups at day 3. Levels at the RCM group were set as 1. Data were shown as Mean ± SD, n = 3 technically independent samples for each group, * p < 0.05, ** p < 0.01. F) Gene expression of PCNA in different groups at day 3, *** p < 0.001. G) Proliferation of TSPCs measured by CCK‐8 at 1, 3, and 5 days, n = 5 technically independent samples for each group, **** p < 0.0001. H) Gene expression of SCX, TNMD, and MKX in different groups at day 3. Levels at the RCM group were set as 1. Data were shown as Mean ± SD, n = 3 technically independent samples for each group, * p < 0.05.

Article Snippet: When TSPCs reached to 90% confluence, the cells were treated with CMs or CMs combined with 20 μ m U0126 (Selleck, S1102) to inhibit MAPK signaling pathway, or CMs combined with 40 μ m RGD peptides (Selleck, S8008) to inhibit integrin signaling pathway.

Techniques: Western Blot, Gene Expression, CCK-8 Assay