α1-adrenergic receptors activate Ca²⁺-permeable cationic channels in prostate cancer epithelial cells
J. Clin. Invest. Stephanie Thebault, et al. 111:1691 doi:10.1172/JCI16293 [Go to this article.]

Figure 4
α1-AR–mediated [Ca²⁺]_i signaling in LNCaP cells is PLC- but not PKC-dependent. (a) Two superimposed representative [Ca²⁺]_i signals evoked by epinephrine (Epi) (1 μM) in the presence of the PLCβ inhibitor U73122 (10 μM, n = 12, no increase in [Ca²⁺]_i) and its inactive analogue U73343 (10 μM, n = 19). (b) Three superimposed representative [Ca²⁺]_i transients evoked by OAG (100 μM) in LNCaP cells pretreated for 30 minutes with one of the following PKC inhibitors: staurosporine (1 μM, n = 17), bis-indolylmaleimide I (500 nM, n = 33), or GÖ6976 (50 nM, n = 13), demonstrating the ineffectiveness of PKC inhibition. [Ca²⁺]_i signals were measured in Fura-2–loaded cells; all interventions on each panel are marked by horizontal bars.