Why is A23187 treatment ineffective in mice with a mutation

Why is A23187 treatment ineffective in mice with a mutation in PMCA4 but not Slo3?

Solution

Ans:- The mouse in slo3 gene enodes a K+ channel that is regulated by changes in cytosolic pH.Slo3 is the principal potassium channel responsible for capacitation induced hyperpolarization.Now when exposed to A2317 an ionophore which directly permits calcium entry and so the treatment is effective. But this becomes inefective when A23187 treatment in mice takes place with a mutation in PMCA4.