| Research Abstract |
Cellular stimulation from the surrounding extracellular environment via mechanisms including plasma membrane receptors induces activation of Ca^<2+>-permeable cation channels that form essential signaling pathways in controlling biological responses. An imp ortant clue to understand the molecular mechanisms underlying these cation channels (termed as receptor-activated cation channels (RACC)) was only provided through studies of the transient receptor potential (trp) protein (TRP), which controls light-induced cationic currents in Drosophila photoreceptor cells. By using the genetic information and recombinant expression technique, numerous mammalian TRP homologues have been discovered. This further lead to identification of novel RACC_s. In the session, I would like to introduce our contribution to the recent dramatic progress in investigating mammalian RACC_s, revealing 1) critical involvement of TRP1 in both nyinduced Ca^<2+> release and store-operated Ca2+ entry, 2) identification of TRP6 as α_1-adrenergic receptor-activated cation channels in smooth muscle cells, and 3) essential interaction between redoxsy stem and TRP-related channel activation. Thus, TRP-related channels are revealed to be a powerful tool in understanding important physiological responses and for the invention of novel pharmaceutical targets.
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