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. Author manuscript; available in PMC: 2012 May 1.
Published in final edited form as: Gastroenterology. 2011 Jan 26;140(5):1586–96.e6. doi: 10.1053/j.gastro.2011.01.039

Figure 7.

Figure 7

Activation of CRF2 suppresses phosphorylation of pERK in PC-LMMPn and cAMP production in HEK-293 cells. (A-B) Western blot analysis of pERK1/2 in response to CRF, Ucn 1 or Ucn 2 (A). Blockade of the CRF-induced pERK by Ucn 2 or by a selective CRF1 antagonist, NBI-3965 and enhancement of the response by selective CRF2 antagonist astressin2-B (B). Bar, mean±SEM, n=3/group, * p<0.05 vs no-treatment and the respective10 nM dose in A, †p<0.05 vs all other groups in A, #p<0.05 vs the no-treatment and the respective CRF or Ucn 1 alone dose in A. (C): Dose-dependent increases in intracellular cAMP production in CRF1α, CRF2β and CRF1α+CRF2β transfected HEK-293 cells stimulated with CRF for 30 min. Note the 10-fold decrease in potency of CRF in CRF1 and CRF2 coexpressing cells vs. in CRF1 only expressing cells.