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. 2017 Feb;149(2):277–293. doi: 10.1085/jgp.201611721

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© 2017 Yan et al.

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Figure 5. — ApoCaM regulates persistent Na⁺ current in neuronal Na_V channels. (A and B) Exemplar traces for Na_V1.2^TTX-R (WT) and the Na_V1.2 mutant R1918H showing increased persistent Na⁺ current for the R1918H mutant (but not for WT) and rescue by CaM overexpression for the R1918H mutant. (C) Summary data showing rescue by CaM for the Na_V1.2 mutants H1853R and R1918H. (D) Summary data showing increased τ of inactivation and rescue by CaM for the Na_V1.2 mutants H1853R and R1918H. (E) Exemplar traces for Na_V1.6^TTX-R (WT) expressed in HEK293T cells showing reduced persistent Na⁺ current by CaM overexpression. (F) Exemplar traces for Na_V1.6^TTX-R expressed in cultured cerebellar Purkinje neurons and reduced persistent Na⁺ current by CaM overexpression. (G) Exemplar traces of total Na_V Na⁺ current in cultured cerebellar Purkinje neuron showing reduction in persistent Na⁺ current after CaM overexpression. The inset shows GFP-expressing cultured cerebellar Purkinje neuron. Bar, 20 µm. (H) Summary data for Na_V1.6 expressed in HEK293T cells or in cultured cerebellar Purkinje neurons or total Na_V Na⁺ current in cultured cerebellar Purkinje neurons. Data are presented as mean ± SEM. *, P < 0.05; **, P < 0.01.