mek 1 2 kinase inhibitor u0126  (Cell Signaling Technology Inc)

Journal: International journal of molecular sciences

Article Title: Cinnamaldehyde-Mediated Suppression of MMP-13, COX-2, and IL-6 Through MAPK and NF-κB Signaling Inhibition in Chondrocytes and Synoviocytes Under Inflammatory Conditions.

doi: 10.3390/ijms252312914

Figure Lengend Snippet: Figure 6. (A) Protein expression of MAPK pathways (pERK phosphorylation) in the presence of MEK1/2 inhibitor (U0126) in chondrocytes, followed by qualitative analysis. (B) Comparison of the downstream mediators of inflammation (COX-2, IL-6) in the presence of MEK 1/2 inhibitor and 50 µM of CA in synoviocytes, followed by qualitative analysis. (C) Protein expression pERK phosphorylation in the presence of MEK1/2 inhibitor (U0126) in synoviocytes, followed by qualitative analysis. (D) Comparison of the downstream mediators of inflammation (COX-2, IL-6) in the presence of MEK 1/2 inhibitor and 50 µM of CA in synoviocytes, followed by qualitative analysis. The figure represents the activity of CA and Inhibitor role in the ERK pathway inhibition. Data are presented as the mean ± standard deviation (n = 3). ns = non-significant, * p < 0.05, *** p < 0.001, and **** p < 0.0001 compared with the control group.

Article Snippet: Pre-treatment was carried out with either 10 μM of the NF-κB signaling inhibitor 5HPP-33 (Calbiochem, La Jolla, CA, USA) or 10 μM of the MEK 1/2 kinase inhibitor U0126 (Cell Signaling, Danvers, MA, USA) for 2 h. Subsequently, the cells were exposed to IL-1β (10 ng/mL) in the presence or absence of CA (0.5, 5, and 50 μM) for 24 h.

Techniques: Expressing, Phospho-proteomics, Comparison, Activity Assay, Inhibition, Standard Deviation, Control

Journal: bioRxiv

Article Title: Antibody targeting of surface PSGL-1 glycoprotein leads to lymphoma apoptosis and tumorigenesis inhibition

doi: 10.1101/2024.01.18.576249

Figure Lengend Snippet: A) Levels of phosphorylated ERK (p-ERK), ERK and α-tubulin in HUT-78, U2932, OCI-LY3 and Raji cell lines before and after 5 min of PL1 treatment. All cells were put under starvation conditions (only RPMI, no supplements) 2 h prior and during the experiment. B) Viability of HUT-78, U2932 and OCI-LY3 cell lines after 8 h of PL1 treatment in the presence or absence of 10 μM U0126 MEK1/2 inhibitor.

Article Snippet: MEK 1/2 inhibitor U0126 (cat. no. EI-282, Enzo Life Sciences) was used at 10 μM for the time-points described in the figures.

Techniques: