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. Author manuscript; available in PMC: 2012 Aug 22.
Published in final edited form as: J Neurosci. 2012 Feb 22;32(8):2683–2695. doi: 10.1523/JNEUROSCI.4125-11.2011

Figure 3.

Figure 3

Neurabin attenuates A1R-mediated G protein signaling in cells. A, Neurabin expression attenuates A1R-mediated inhibition of cAMP production. Cells expressing HA-A1R alone or in combination with either neurabin or spinophilin were treated with 10 μM forskolin alone or forskolin plus 1 μM R-PIA. Surface receptor density in each experimental group was comparable, as verified by intact cell ELISA using an anti-HA antibody. n=11 for cells expressing the A1R alone; n=8 for cells expressing the A1R and neurabin; n=5 for cells expressing the A1R and spinophilin. Data are expressed as fold change in cAMP production over forskolin alone control (defined as 1.0 fold). *, p<0.05, R-PIA stimulated vs. control. B, R-PIA induces similar levels of receptor internalization from the cell surface in cells either with or without exogenous expression of neurabin or spinophilin. Surface receptor density in cells described in (A) was examined by intact cell ELISA using an anti-HA antibody. *, p<0.05 when comparing cell surface A1R in R-PIA treated cells vs. nontreated controls.