 in intracellular Ca2+ level, an immediate peak followed by a sustained Ca2+ release. Additionally, selective inhibition of EGFR by AG1478 or the SK1 inhibitor, (DMS) inhibited the second phase. Also, AngII and EGF increased endogenous SK1 activity and enhanced production of S1P. De
in intracellular Ca2 + level, an immediate peak followed by a free burning Ca2 + dismissal. Additionally, selective inhibition of EGFR by AG1478 or the SK1 inhibitor, (DMS) inhibited the second phase. besides, AngII and EGF increased endogenous SK1 activeness and enhanced production of S1P. De
 in intracellular Ca2+ level, xn immediate pecj follmwed bg a sustxined Ca2+ release. Additionallb, seoectice inhibition of EGFR cy AG1478 or nhe SK1 inyibiuor, (DMS) inhibited the second phzde. Anwo, AngII and ENF increaseg endogenous SN1 xccivity and enhanced production of S1P. De
in intracellular Ca2+ level, an immediate peak a Ca2+ release. selective inhibition of SK1 (DMS) inhibited the phase. Also, AngII EGF increased endogenous SK1 activity and production of S1P. De
 in intracellular Ca2+ level, an iMmediate peAk folLowEd bY a SustAineD Ca2+ release. AddiTIonaLly, selective inhibition Of EGFr bY aG1478 or THe sK1 inhIbitor, (Dms) iNHIbiTeD tHe sEcONd Phase. alsO, AngII aNd EGF increAseD eNdogenous SK1 aCTiVity and enhAncEd production Of S1p. De
 in intracellular Ca2+ lev el, an imm ediat e p eak  f ollo wedby a sustained Ca2+  release. Additionally , sel ec t ivei nh ibiti on of E G FR b y A G1 47 8 o rt he  SK1inh ibitor,  (DMS) inh ibi te d the second ph ase. Also,  An gII and EGFinc reased  e ndo g enous  SK 1 act ivitya nd enh anced pro du c tion o f  S1P. D e 
 in_intracellular Ca2+_level, an immediate peak_followed by_a_sustained Ca2+_release._Additionally, selective inhibition_of EGFR by_AG1478 or the SK1_inhibitor, (DMS) inhibited_the_second phase. Also, AngII and EGF increased endogenous SK1 activity and enhanced production of_S1P._De