Tcs jnk 6o

NF-κB inhibitor Bay 11–7082 (30 μM; Sigma-Aldrich), p38 MAPK inhibitor SB202190 (1 μM; Tocris bio-techne), ERK inhibitor FR 180204 (30 nM - 10 μM; Tocris bio-techne), JNK inhibitor TCS JNK 6o (30 nM - 10 μM; Tocris bio-techne), AP-1 Inhibitor SR 11302 (10μM - 100μM; Tocris bio-techne), and MEK inhibitor U0126 (100 μM; Promega). Actinomycin D (Sigma-Aldrich) was used at a concentration of 10 μg/mL.

Tumor Necrosis Factor alpha (TNF-α), Transforming Growth Factor beta 1 (TGFβ1), Transforming Growth Factor beta 2 (TGFβ2) and Interleukin 6 (IL-6) were purchased from PeproTech (Rocky Hill, NJ, USA). Recombinant human VEGF 165 protein was purchased from R&D Systems (Minneapolis, MN, USA). Aflibercept (Eylea) was purchased from Regeneron Pharmaceuticals (Tarrytown, NY, USA). _D-glucose, mannitol, _L-glucose and RUNX1 inhibitor Ro5–3335 were purchased from Millipore-Sigma (Burlington, MA, USA). Small molecule inhibitors and activators purchased from commercial sources included TNF-α-TNFR1 binding inhibitor CAY10500 and JNK activator anisomycin, (Santa Cruz Biotechnology, Dallas, TX, USA); NF-κB inhibitors Caffeic acid phenethyl ester (CAPE) and Honokiol; dual NF-κB and JNK inhibitor Withaferin A, JNK inhibitors SP600125 and TCS JNK 6o; p38/MAPK inhibitors SB259063 and SB202190 (Tocris Bioscience, Bristol, UK); and AP-1 inhibitor, SR11302 (R&D Systems). The CBFβ-RUNX1 protein-protein interaction inhibitor, AI-14–91, and an inactive control compound of similar chemical structure, AI-4–88, were synthesized as described previously [36 (link)].