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 c...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展开更多
文摘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
