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. Author manuscript; available in PMC: 2016 Nov 1.
Published in final edited form as: Bioessays. 2015 Sep 10;37(11):1243–1252. doi: 10.1002/bies.201500081

Figure 6.

Figure 6

Mechanism of decay of Rh*. A: Schematic drawing indicating phosphorylation of Rh* by rhodopsin kinase (RK or GRK1), followed by binding of arrestin to phosphorylated rhodopsin. B: Comparison of mean responses from 41 WT rods (black), 22 RKBark7 rods (blue) having one-seventh the normal expression level of rhodopsin kinase [7], and 19 RKS561L rods (red) having 12-times the normal expression level of rhodopsin kinase [66]. Single-photon responses were calculated from the squared mean and variance (for example [66]). Currents have been normalized to the circulating current in darkness, giving the faction of channels closed as a function of time. The fraction of channels closed is thus the same as the normalized current defined in the legends to Figs. 2–4.