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Agonist-activated Ca~(2+) entry is important in many biological responses such as secretion and cell growth. In nonexcitable cells which have no voltage-operated Ca~(2+) channels (VOCC), agonist-receptor interaction can trigger Ca~(2+) entry across the plasmalemma via several entry pathways (Fig 1): (A) channels which are intrinsic structures of the receptor (receptor-operated channels),(B) channels which are coupled to receptors via a G-protein (G-protein-operated channels), (C) channels which are activated by some second messengers (second-messenger-operated channels), and(D) channels which open upon intraeellular nonmitochondrial Ca~(2+) store depletion (Ca~(2+) release-activated channels) resulting from inositol 1, 4, 5-trisphosphate-induced Ca~(2+) release or inhibition of Ca~(2+) re-uptake (see next section). Ca~(2+) entry via
Agonist-activated Ca~(2+) entry is important in many biological responses such as secretion and cell growth. In nonexcitable cells which have no voltage-operated Ca~(2+) channels (VOCC), agonist-receptor interaction can trigger Ca ((2)) entry across the plasmalemma via several entry pathways (Fig 1): (A) channels which are intrinsic structures of the receptor (receptor-operated channels), (B) channels which are coupled to receptors via a G-protein (G-protein-operated channels), (C) channels which are activated by some second messengers (second-messenger-operated channels), and (D) channels which open upon intraeellular nonmitochondrial Ca 2+ store depletion (Ca~ (2+) release-activated channels) resulting from inositol 1, 4, 5-trisphosphate-induced Ca~(2+) release or inhibition of Ca~(2+) re-uptake (see next section). Ca~(2) +) entry via