Table 1 Midpoint voltage of activation and steady-state inactivation with a standard Boltzmann distribution fit

From: Cardiac sodium channel palmitoylation regulates channel availability and myocyte excitability with implications for arrhythmia generation

 

Activation

Inactivation

 

V1/2 (mV)

K (mV)

V1/2 (mV)

K (mV)

Nav1.5 stable

−33.4±0.3

7.8±0.2

−90.4±0.6

7.1±0.5

Nav1.5 stable 2BP

−34.1±0.4

8.9±0.4*

−103±0.5*

8.1±0.4*

Nav1.5 stable PA

−29.9±0.4

7.7±0.4

−83.4±0.4*

6.3±0.4

Nav1.5 transient

−46.3±0.4

6.9±0.3

−90.8±0.5

7.3±0.4

Nav1.5 transient 2BP

−50.8±0.6

7.8±0.5

−108.4±0.7*

9.7±0.6

Nav1.5-AAAA

−48.2±0.4

8.1±0.4

−103.4±0.7†

9.0±0.6

Nav1.5-AAAA 2BP

−50.4±0.5

7.7±0.4

−106.0±0.5

8.4±0.5

Nav1.5 C981F

−50.2±0.5

8.1±0.4

−100.2±0.5†

6.9±0.4

Nav1.5 C981F 2BP

−52.6±0.4

7.3±0.4

−100.7±0.7

8.3±0.6

Nav1.5 C981A

−47.8±0.7

6.7±0.6

−100.5±0.6†

7.9±0.5

Nav1.5 C981A 2BP

−43.2±0.7

8.5±0.6

−104.8±0.9

10.3±0.8

Nav1.5 cardiomyocytes

−37.3±0.3

7.1±0.3

−76.6±0.5

8.2±0.4

Nav1.5 cardiomyocytes 2BP

−42.2±0.6

8.5±0.5*

−99.4±0.6*

10.1±0.5*

Nav1.5 cardiomyocytes Palmitic acid

−36.1±0.5

6.7±0.5

−71.0±0.5*

7.3±0.5

  1. *indicates P<0.05 compared with the corresponding non-treatment group. The two-tailed, Student’s t-test was used to study the statistical significance.
  2. †indicates P<0.05 compared with wild-type group.
  3. All data are shown as mean±s.e.m.