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A complete separation of myo-inositol 1,4,5-4,5-(32)Ptrisphosphate prepared from human erythrocytes, and myo-2-3Hinositol 1,3,4-trisphosphate prepared from carbachol-stimulated rat parotid glands Irvine, Letcher, Lander by 15s it predominated over inositol 1,4,5-trisphosphate, and continued to rise so that after 15 min it was at 10-20 times the radiolabelling level of the 1,4,5-isomer. In contrast, after the initial rapid rise (maximal within 15s), inositol 1,4,5-trisphosphate levels declined to near control levels after 1 min and then rose again very gradually over the next 15 min. When a muscarinic blocker (atropine) was added after 15 min of carbachol stimulation, inositol 1,4,5-trisphosphate levels dropped to control levels within 2-3 min, whereas inositol 1,3,4-trisphosphate levels took at least 15 min to fall, consistent with the kinetics observed earlier for total parotid inositol trisphosphates [Downes in control tissues it must be less than 5% of the total PtdInsP2 radiolabelled by myo-[2-3Hinositol. These data indicate that, provided that inositol 1,4,5-trisphosphate is studied independently of inositol 1,3,4-trisphosphate, the former shows metabolic characteristics consistent with its proposed role as a second messenger for calcium mobilization. The metabolic profile of inositol 1,3,4-trisphosphate is entirely different, and its function and source remain unclear.
Irvine et al. (Mon,) studied this question.
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