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. 2011 Mar 16;31(11):4074–4086. doi: 10.1523/JNEUROSCI.5707-10.2011

Figure 8.

Figure 8.

Characterization of a minimal TRIP8b domain that inhibits HCN1 gating using TRIP8b-HCN1 fusion proteins. Shift in ΔV1/2 produced when wild-type or mutant TRIP8b(1a-4) was fused to the N terminus of HCN1. ΔV1/2 values obtained relative to V1/2 of GFP-HCN1 fusion construct. All constructs expressed using cRNA injections in Xenopus oocytes (HCN1 fusions, 0.5 μg/μl; HCN1ΔCX fusions, 0.2 μg/μl). Population data show the difference between the V1/2 obtained when HCN1 was fused to GFP and the V1/2 when HCN1 was fused to indicated TRIP8b construct. All data points were matched by batch of oocytes, as above. Mean ΔV1/2 values ± SEM (n) are as follows: TRIP8b-HCN1, 13.8 ± 0.9 mV (n = 14, GFP-HCN1; n = 14, 1a4-HCN1); TRIP8bmini-HCN1, 14.7 ± 0.7 mV (n=14, GFP-HCN1; n = 14, mini-HCN1); TRIP8bΔint-HCN1, 4.5 ± 0.6 mV (n = 12, GFP-HCN1; n = 12, Δint-HCN1); TRIP8bmini-HCN1ΔCX, 12.6 ± 0.4 mV (n = 14, GFP-HCN1ΔCX; n = 14, mini-HCN1ΔCX); TRIP8bΔint-HCN1ΔCX, 2.1 ± 0.5 mV (n = 14, GFP-HCN1ΔCX; n = 14, Δint-HCN1ΔCX).