Voltage dependent potassium channels like Kv1.1 tend to open when a cell depolarizes. It is no surprise, therefore, that Kv1.1 channels exert an influence on the action potential. If faulty N-glycosylation of Kv1.1 was to delay its opening, what would be the likely response?
Question 5 options:
The depolarization phase of the action potential would be slower
The repolarization phase of the action potential would be faster
The repolarization phase of the action potential would be slower