Citations Search

Notes: This study investigates the role of the ERK1/ERK2 (MAPK) pathway in growth regulation of venous ulcer fibroblasts. Human normal (n-fb) and venous ulcer (w-fb) fibroblasts were isolated and grown in culture in the presence or absence of the MEK-1 inhibitor PD 98059. AntiACTIVE^® MAPK pAb was used in immunoblots to determine the expression of phosphorylated ERK1/ERK2 in n-fb and w-fb. In separate experiments, human neonatal foreskin fibroblasts were obtained and cultured in the presence of wound fluid from venous ulcers plus or minus PD 98059 to determine whether or not wound fluid had an inhibitory effect on expression of MAPK ERK1/2. Immunoblot analysis using AntiACTIVE^® MAPK pAb indicated that wound fluid decreased phosphorylated ERK1/ERK2 expression; addition of PD 98059 did not further decrease expression of phosphorylated ERK1/ERK2 in these cells. (3537)

Notes: This study investigated the signaling mechanisms involved in 17β-estradiol- (E2) and tamoxifen-induced release of neurotrophic factors from rat cortical astrocyte cultures. The TGFβ1, TGFβ2, BDNF and GDNF E_max^® ImmunoAssay Systems were used to measure the release of these neurotrophic factors from astrocyte cultures treated with E2 or tamoxifen. Both E2 and tamoxifen induced the release of TGFβ1 and TGFβ2, but did not stimulate release of BDNF or GDNF. The PI3K inhibitors LY294002 and wortmanin, and the Akt inhibitor blocked TGFβ release, suggesting the involvement of the PI3K/Akt signaling pathway. The MAPK kinase inhibitors PD98059 and U0126 had no effect. E2 was found to induce transient Akt ^Ser473 phosphorylation, and this effect was blocked by LY294002 pretreatment, demonstrating a role for PI3K in the observed E2-mediated Akt phosphorylation. (3479)

Notes: The MEK Inhibitor U0126 was shown to inhibit MAPK phosphorylation completely and to a greater extent than PD98059. The inactivation had very little effect on neurite outgrowth. MAPK phosphorylation was determined with the Anti-ACTIVE^® MAPK pAb by Western blotting. (0297)

Notes: HEK 293 cells stably expressing the mu-opioid receptor respond to agonists by MAPK phosphorylation. Activation of the MAPK was totally inhibited by the MEK Inhibitor U0126 at 100nM as judged by immunocytochemistry. The PD98059 required 20µM for the same inhibition. (0411)

Notes: Pretreatment of REF52 cells for 15minutes with 50µM U0126 MEK Inhibitor prior to stimulation with EGF blocked all ERK phosphorylation. The same experiment with the PD98059 inhibitor did not block ERK phosphorylation. (0377)

Notes: The effect of the U0126, MEK Inhibitor is reported and compared to that of the inhibitor PD98059. PD98059 inhibited an Erk-dependent glycerol-phosphate dehydrogenase activity by 60% at 10µM. The same inhibition was seen with U0126 at 0.5µM. Also, 10µM PD98059 produced 50% inhibition of LIF-stimulated C/EBP gene expression whereas 10µM U0126 completely prevented the expression (no other concentrations of U0126 reported). (1484)