Skip to main content
. Author manuscript; available in PMC: 2016 Aug 19.
Published in final edited form as: ACS Chem Neurosci. 2015 Jun 12;6(8):1476–1485. doi: 10.1021/acschemneuro.5b00134

FIGURE 4. Pharmacological properties of CY chemical ligands in STAT3 transcriptional activation potential.

FIGURE 4

(a) Immunoblots of STAT3(P) (activated STAT3) from homogenates of STAT3 luciferase reporter HeLa stable cell line treated or untreated with oncostatin M (OncM). Levels of hnRNPA2B1 and Ranbp2 levels remain unchanged between OncM untreated and treated cells. (b) Luciferase activity induced by STAT3-transcriptional activation in the absence or presence of OncM and IL-6. (c) Dose-dependent responses of STAT3-transcriptional activity of STAT3 luciferase reporter HeLa stable cells treated with OncM in the absence and presence of small molecules (Cmp). (d) Levels of latent STAT3 and activated STAT3(P) remain unchanged in the absence or presence of small molecules with (e.g. Cmp 10) and without effect (e.g. Cmp 13) on OncM-stimulated STAT3 activity. (e) CsA suppresses the STAT3-transcriptional activity stimulated by OncM. Data shown represent the mean ± s.d., n =3 (b, c, d, e); n.s., non-significant. Legend: V, vehicle; Cmp, compound (small molecule).