FIGURE

Fig. 1

ID
ZDB-FIG-210526-52
Publication
Hu et al., 2021 - An Arrhythmic Mutation E7K Facilitates TRPM4 Channel Activation via Enhanced PIP2 Interaction
Other Figures
All Figure Page
Back to All Figure Page
Fig. 1

E7K mutant presented a higher PI(4,5)P28-PI(4,5)P2 (5 μM) restored TRPM4 channel activity over its initial magnitude. Vertical deflections reflect ramp- or step pulse-induced currents. (B) Representative data from two inside-out patch membranes (WT and E7K) demonstrating the dose-dependent reactivation of TRPM4 channels in response to various concentrations of diC8-PI(4,5)P2. (C) The degree of reactivation by diC8-PI(4,5)P2 (relative current) is defined as (I[x] − I[post-desens])/(I[20μM diC8-PIP2] − I[post-desens]), where I[x] and I respectively denote the amplitudes of TRPM4 currents reactivated by given (‘X’ μM) and maximal (20 μM) concentrations of diC8-PI(4,5)P2, and I[post-desens] is that of the basal TRPM4 current after desensitization to 300 μM Ca2+ [13]. Averaged concentration-response curves for the TRPM4 channel reactivation by diC8-PI(4,5)P2 are fitted by the Hill-type equation: 1/(1 + (EC50/[diC8PIP2])n. It gives EC50 values of 2.40 ± 0.23 μM and 1.44 ± 0.20 μM; Hill coefficient (n) values of 1.5 and 1.2 for WT and E7K, respectively. * p < 0.05 with ANOVA followed by Tukey’s post hoc tests (n = 5).

Expression Data

Expression Detail
Antibody Labeling
Phenotype Data

Phenotype Detail
Acknowledgments
This image is the copyrighted work of the attributed author or publisher, and ZFIN has permission only to display this image to its users. Additional permissions should be obtained from the applicable author or publisher of the image. Full text @ Cells