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. Author manuscript; available in PMC: 2012 May 14.
Published in final edited form as: Nature. 2011 Feb 23;471(7339):499–503. doi: 10.1038/nature09884

Figure 3. Duplications and triplications of 7q36.3 result in increased VIPR2 transcription and cyclic-AMP signaling.

Figure 3

(a) Quantitative PCR results of VIPR2 mRNA from lymphoblastoid cell lines. Two to four subjects were tested for each of four genotypes (subtelomeric duplication, VIPR2 duplication, exon 3/4 triplication, and normal diploid copy number as control). Results are expressed as the mean fold-change of CNV carriers relative to the mean of control samples. (b-c) Cyclic AMP accumulation was measured in the same cell lines in response to VIP (100nM) and the VPAC2 agonist BAY 55-9837 (100nM). Results are expressed as fold-change over forskolin/IBMX alone. (d) No significant differences were observed in cAMP response to another GPCR agonist, Prostaglandin E2 (PGE2, 1 μM), demonstrating that the effects are specific to VPAC2. For subjects, error bars represent standard error of the mean computed across replicates. Differences between the groups of 9 duplication carriers and 4 controls were tested using unpaired two sample t-tests.