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. 2016 Oct 18;157(12):4865–4874. doi: 10.1210/en.2016-1448

Figure 5.

Figure 5.

The novel CRFR1j splice variant is unable to activate the intracellular cAMP signaling pathway. A, Activation of a cAMP-response element luciferase reporter in HEK293T cells transfected with CRFR1α (full length, functional isoform) or CRFR1j, after treatment with the CRFR1 agonist, sauvagine (0–30 nM). Cells transfected with CRFR1α showed increasing activity with increasing sauvagine concentration. In contrast, cells transfected with 10 times the amount of CRFR1j showed no activity at the highest dose of sauvagine. B, Activation of a cAMP-response element luciferase reporter by sauvagine (0–10 nM) in HEK293T cells transfected with varying amounts of the novel CRFR1j splice variant (1–100 ng), indicating a complete lack of activation at all concentrations. Experiments were performed in triplicate. Data represent means and SEs. Statistics compare sauvagine treatment with the no-treatment group for each transfection. *, P < .05, **, P < .01, ***, P < .001 (ns, P > .05).