Abstract: Objective To understand the role of KCNE2 in functional regulation of Kv4.3,the major α subunit of transient outward current(Ito)in human heart.Methods The cDNAs of Kv4.3 or Kv4.3 plus KCNE2 were transfected into COS-7 cells and 24-36 h after the transfection,the channel proteins were expressed in the surface membrane of the cells and the channel currents were recorded with patch-clamp technique in whole-cell mode.Results KCNE2 played an important role in modulating the channel function.The recorded current density was decreased in cells co-expressing KCNE2 and Kv4.3 to 152.96±33.71 pA/pF(n=16)as compared with Kv4.3-expressing cells with a mean current density of 375.13±112.87 pA/pF(n=11).At the recording voltage of 60 mV,KCNE2 increased the time to peak(TTP)of the current.TTP in only Kv4.3-expressing cells was 4.82±0.32 ms(n=11),significantly shorter than the TTP of 20.41±2.13 ms(n=16)in cells co-expressing Kv4.3 and KCNE2(P<0.05).In the presence of KCNE2,the voltage-dependent inactivation of Kv4.3 showed a positive shift.The voltage of half maximum inactivation(V0.5)was decreased significantly from-53.62±1.24 mV(n=8)in Kv4.3 group to-46.58±1.6 mV(n=10)in KCNE2 co-expression group(P<0.05).KCNE2 accelerated the recovery of the channel from inactivation,reducing the recovery time constant(τ)from 193.43±17.98 ms to 137.71±18.29 ms.Conclusion KCNE2 might serve as an important β subunit and play a role in the regulation of Ito function in human heart.