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Results: 3

1.
Fig. 2

Fig. 2. From: Functional analysis of a novel potassium channel (KCNA1) mutation in hereditary myokymia.

Sequence chromatograms demonstrating c.676C>A resulting in T226K substitution in KCNA1. A DNA sequence from an affected patient (I-2) heterozygous for the mutation (top) and from a normal control (bottom) are presented

Haijun Chen, et al. Neurogenetics. 2007 April;8(2):131-135.
2.
Fig. 1

Fig. 1. From: Functional analysis of a novel potassium channel (KCNA1) mutation in hereditary myokymia.

Family pedigree. Squares indicate males, circles indicate females. Blackened symbols denote individuals with myokymia. Alleles at codon 226 are indicated (Thr = wild-type, Lys = mutation)

Haijun Chen, et al. Neurogenetics. 2007 April;8(2):131-135.
3.
Fig. 3

Fig. 3. From: Functional analysis of a novel potassium channel (KCNA1) mutation in hereditary myokymia.

Missense mutation T226K induces loss of function of human Kv1.1 channels expressed in Xenopus oocytes. ac Representative family of whole-oocyte currents recorded from oocytes expressing human Kv1.1-WT (a), Kv1.1-T226K (b), and both Kv1.1 WT and T226K (c). Currents were evoked by a series of 350-ms test pulses from −80 to +60 mV in 10-mV increments from a hold potential of −90 mV. Tail currents were recoded at −40 mV. Scale bar, 100 ms and 1 μA. d I–V curves for three experimental conditions in ac. Data were collected for 10–15 oocytes in each group. The peak currents in a and c are significantly different at test voltages between 0 and +60 mV (P < 0.05)

Haijun Chen, et al. Neurogenetics. 2007 April;8(2):131-135.

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