We characterized the alpha(1B)-adrenoreceptor (alpha(1B)-AR)-mediated intracellular Ca2+ signaling involving G(alphah) (transglutaminase 11, TGII) and phospholipase C (PLC)-delta1 using DDTI-MF2 cell. Expression of wild-type TGII and a TGII mutant lacking transglutaminase activity resulted in significant increases in a rapid peak and a sustained level of intracellular Ca2+ concentration ([Ca2+],) in response to activation of the alpha(1B)-AR. Expression of a TGII mutant lacking the interaction with the receptor or PLC-delta1 substantially reduced both the peak and sustained levels of [Ca2+](i). Expression of TGII mutants lacking the interaction with PLC-delta1 resulted in a reduced capacitative Ca2+ entry. Reduced expression of PLC-delta1 displayed a transient elevation of [Ca2+], and a reduction in capacitative Ca2+ entry. Expression of the C2-domain of PLC-51, which contains the TGII interaction site, resulted in reduction of the alpha(1B)-AR-evoked peak increase in [Ca2+](i), while the sustained elevation in [Ca2+], and capacitative Ca2+ entry remained unchanged. These findings demonstrate that stimulation of PLC-delta1 via coupling of the alpha(1B)-AR with TGII evokes both Ca2+ release and capacitative Ca 2, entry and that capacitative Ca2+ entry is mediated by the interaction of TGII with PLC-delta1. (C) 2002 Elsevier Science (USA). All rights reserved.