Potential mechanism for bradykinin-activated and inositol tetrakisphosphate-dependent Ca2+ influx by Ras and GAP1 in fibroblast cells

Here we propose a molecular model for bradykinin receptor-operated and seco nd messenger (inositol-1,3,4,5-tetrakisphosphate)-evoked Ca2+ influx and it s potentiation by oncogenic Ras, which is not store-depletion-induced, so-c alled capacitative, Ca2+ influx. The principal idea for this hypothesis ste ms from observation that two bradykinin B-2 receptor-activated signal pathw ays, protein tyrosine phosphorylation and formation of inositol tetrakispho sphate, merge during the Ca2+ influx process and that GTPase activating-pro tein 1 (GAP 1) is inositol tetrakisphosphate binding protein. (C) 1999 Else vier Science B.V. All rights reserved.