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1
Properties of receptor-controlled inositol trisphosphate formation in parotid acinar cells.腮腺腺泡细胞中受体控制的肌醇三磷酸形成的特性。
Biochem J. 1985 Jan 1;225(1):263-6. doi: 10.1042/bj2250263.
2
Mobilization of intracellular calcium by methacholine and inositol 1,4,5-trisphosphate in rat parotid acinar cells.大鼠腮腺腺泡细胞中乙酰甲胆碱和肌醇1,4,5 -三磷酸对细胞内钙的动员作用。
J Dent Res. 1987 Feb;66(2):547-51. doi: 10.1177/00220345870660022701.
3
Activation of calcium entry by the tumor promoter thapsigargin in parotid acinar cells. Evidence that an intracellular calcium pool and not an inositol phosphate regulates calcium fluxes at the plasma membrane.肿瘤启动子毒胡萝卜素激活腮腺腺泡细胞中的钙内流。证据表明，调节质膜钙通量的是细胞内钙库而非肌醇磷酸。
J Biol Chem. 1989 Jul 25;264(21):12266-71.
4
Metabolism of inositol phosphates in parotid cells: implications for the pathway of the phosphoinositide effect and for the possible messenger role of inositol trisphosphate.腮腺细胞中肌醇磷酸的代谢：对磷酸肌醇效应途径及肌醇三磷酸可能的信使作用的影响。
Life Sci. 1984 Apr 2;34(14):1347-55. doi: 10.1016/0024-3205(84)90006-7.
5
Beta-adrenergic receptor stimulation induces inositol trisphosphate production and Ca2+ mobilization in rat parotid acinar cells.β-肾上腺素能受体刺激可诱导大鼠腮腺腺泡细胞产生肌醇三磷酸并动员钙离子。
J Biol Chem. 1988 Sep 5;263(25):12454-60.
6
Inositol 1,2-cyclic 4,5-trisphosphate is formed in the rat parotid gland on muscarinic stimulation.在毒蕈碱刺激下，大鼠腮腺中会形成肌醇1,2-环4,5-三磷酸。
Biochem Biophys Res Commun. 1987 Dec 31;149(3):1208-13. doi: 10.1016/0006-291x(87)90536-5.
7
Kinetics of inositol 1,4,5-trisphosphate and inositol cyclic 1:2,4,5-trisphosphate metabolism in intact rat parotid acinar cells. Relationship to calcium signalling.完整大鼠腮腺腺泡细胞中肌醇1,4,5-三磷酸和肌醇环1:2,4,5-三磷酸的代谢动力学。与钙信号传导的关系。
J Biol Chem. 1988 Jul 25;263(21):10314-9.
8
Homologous desensitization of substance-P-induced inositol polyphosphate formation in rat parotid acinar cells.大鼠腮腺腺泡细胞中P物质诱导的肌醇多磷酸形成的同源脱敏作用。
Biochem J. 1987 Jun 15;244(3):647-53. doi: 10.1042/bj2440647.
9
The effects of substance P and carbachol on inositol tris- and tetrakisphosphate formation and cytosolic free calcium in rat parotid acinar cells. A correlation between inositol phosphate levels and calcium entry.P物质和卡巴胆碱对大鼠腮腺腺泡细胞中肌醇三磷酸和肌醇四磷酸形成及胞质游离钙的影响。肌醇磷酸水平与钙内流之间的相关性。
J Biol Chem. 1987 Nov 5;262(31):14912-6.
10
The regulation of the phosphorylation of inositol 1,3,4-trisphosphate in cell-free preparations and its relevance to the formation of inositol 1,3,4,6-tetrakisphosphate in agonist-stimulated rat parotid acinar cells.无细胞制剂中肌醇1,3,4-三磷酸磷酸化的调节及其与激动剂刺激的大鼠腮腺腺泡细胞中肌醇1,3,4,6-四磷酸形成的相关性。
J Biol Chem. 1989 Nov 25;264(33):19871-8.

引用本文的文献

1
Adrenergic regulation of formation of inositol phosphates in rat submandibular acini.大鼠下颌下腺腺泡中肌醇磷酸形成的肾上腺素能调节。
Biochem J. 1987 Feb 1;241(3):705-9. doi: 10.1042/bj2410705.
2
Regulation of calcium handling by rat parotid acinar cells.大鼠腮腺腺泡细胞钙处理的调节
Mol Cell Biochem. 1988 Jul-Aug;82(1-2):67-73. doi: 10.1007/BF00242518.
3
Ca2+ not cyclic AMP mediates the fluid secretory response to isoproterenol in the rat mandibular salivary gland: whole-cell patch-clamp studies.Ca2+而非环磷酸腺苷介导大鼠下颌唾液腺对异丙肾上腺素的液体分泌反应：全细胞膜片钳研究
Pflugers Arch. 1988 Nov;413(1):67-76. doi: 10.1007/BF00581230.
4
Effects of muscarinic, alpha-adrenergic, and substance P agonists and ionomycin on ion transport mechanisms in the rat parotid acinar cell. The dependence of ion transport on intracellular calcium.毒蕈碱、α-肾上腺素能、P物质激动剂和离子霉素对大鼠腮腺腺泡细胞离子转运机制的影响。离子转运对细胞内钙的依赖性。
J Gen Physiol. 1989 Feb;93(2):285-319. doi: 10.1085/jgp.93.2.285.
5
A Ca2+-linked increase in coupled cAMP synthesis and hydrolysis is an early event in cholinergic and beta-adrenergic stimulation of parotid secretion.在腮腺分泌的胆碱能和β-肾上腺素能刺激中，与Ca²⁺相关的偶联cAMP合成与水解的增加是早期事件。
Proc Natl Acad Sci U S A. 1988 Nov;85(21):7867-71. doi: 10.1073/pnas.85.21.7867.
6
Two modes of regulation of the phospholipase C-linked substance-P receptor in rat parotid acinar cells.大鼠腮腺腺泡细胞中磷脂酶C连接的P物质受体的两种调节模式。
Biochem J. 1988 Jul 15;253(2):459-66. doi: 10.1042/bj2530459.
7
Homologous desensitization of substance-P-induced inositol polyphosphate formation in rat parotid acinar cells.大鼠腮腺腺泡细胞中P物质诱导的肌醇多磷酸形成的同源脱敏作用。
Biochem J. 1987 Jun 15;244(3):647-53. doi: 10.1042/bj2440647.
8
Endothelium modulation of the effects of nitroglycerin on blood vessels from dogs with pacing-induced heart failure.内皮对硝酸甘油对起搏诱导的心力衰竭犬血管作用的调节
Br J Pharmacol. 1990 Sep;101(1):109-14. doi: 10.1111/j.1476-5381.1990.tb12098.x.
9
Release of endothelium-derived relaxing factor from pig cultured aortic endothelial cells, as assessed by changes in endothelial cell cyclic GMP content, is inhibited by a phorbol ester.通过内皮细胞环磷酸鸟苷含量的变化评估，佛波酯可抑制猪主动脉内皮细胞释放内皮源性舒张因子。
Br J Pharmacol. 1990 Mar;99(3):565-71. doi: 10.1111/j.1476-5381.1990.tb12969.x.
10
Effects of extracellular ATP on ion transport systems and [Ca2+]i in rat parotid acinar cells. Comparison with the muscarinic agonist carbachol.细胞外ATP对大鼠腮腺腺泡细胞离子转运系统及细胞内钙离子浓度的影响。与毒蕈碱激动剂卡巴胆碱的比较。
J Gen Physiol. 1990 Feb;95(2):319-46. doi: 10.1085/jgp.95.2.319.

本文引用的文献

1
Lithium amplifies agonist-dependent phosphatidylinositol responses in brain and salivary glands.锂可增强大脑和唾液腺中激动剂依赖性磷脂酰肌醇反应。
Biochem J. 1982 Sep 15;206(3):587-95. doi: 10.1042/bj2060587.
2
Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate.1,4,5-三磷酸肌醇促使胰腺腺泡细胞非线粒体胞内钙库释放钙离子。
Nature. 1983;306(5938):67-9. doi: 10.1038/306067a0.
3
The second messenger linking receptor activation to internal Ca release in liver.将受体激活与肝脏内部钙释放相联系的第二信使。
Nature. 1984;309(5963):63-6. doi: 10.1038/309063a0.
4
Metabolism of inositol phosphates in parotid cells: implications for the pathway of the phosphoinositide effect and for the possible messenger role of inositol trisphosphate.腮腺细胞中肌醇磷酸的代谢：对磷酸肌醇效应途径及肌醇三磷酸可能的信使作用的影响。
Life Sci. 1984 Apr 2;34(14):1347-55. doi: 10.1016/0024-3205(84)90006-7.
5
Breakdown of polyphosphoinositides and not phosphatidylinositol accounts for muscarinic agonist-stimulated inositol phospholipid metabolism in rat parotid glands.多磷酸肌醇而非磷脂酰肌醇的分解代谢是毒蕈碱激动剂刺激大鼠腮腺中肌醇磷脂代谢的原因。
Biochem J. 1983 Dec 15;216(3):633-40. doi: 10.1042/bj2160633.
6
Rapid accumulation of inositol trisphosphate reveals that agonists hydrolyse polyphosphoinositides instead of phosphatidylinositol.肌醇三磷酸的快速积累表明，激动剂水解多磷酸肌醇而非磷脂酰肌醇。
Biochem J. 1983 Jun 15;212(3):849-58. doi: 10.1042/bj2120849.
7
Changes in the levels of inositol phosphates after agonist-dependent hydrolysis of membrane phosphoinositides.膜磷酸肌醇在激动剂依赖性水解后肌醇磷酸水平的变化。
Biochem J. 1983 May 15;212(2):473-82. doi: 10.1042/bj2120473.
8
Role of phosphatidylinositol turnover in alpha 1 and of adenylate cyclase inhibition in alpha 2 effects of catecholamines.磷脂酰肌醇代谢在儿茶酚胺α1效应中的作用以及腺苷酸环化酶抑制在儿茶酚胺α2效应中的作用。
Life Sci. 1980 Apr 14;26(15):1183-94. doi: 10.1016/0024-3205(80)90062-4.
9
The relationship between muscarinic receptor binding and ion movements in rat parotid cells.大鼠腮腺细胞中毒蕈碱受体结合与离子运动之间的关系。
J Physiol. 1980 Feb;299:521-31. doi: 10.1113/jphysiol.1980.sp013140.
10
Nature of the receptor-regulated calcium pool in the rat parotid gland.大鼠腮腺中受体调节性钙池的性质
J Physiol. 1982 Oct;331:557-65. doi: 10.1113/jphysiol.1982.sp014391.

腮腺腺泡细胞中受体控制的肌醇三磷酸形成的特性。

Properties of receptor-controlled inositol trisphosphate formation in parotid acinar cells.

作者信息

Aub D L, Putney J W

出版信息

Biochem J. 1985 Jan 1;225(1):263-6. doi: 10.1042/bj2250263.

DOI:10.1042/bj2250263
PMID:3883986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1144579/
Abstract

Activation of muscarinic receptors in rat parotid cells results in breakdown of polyphosphoinositides liberating inositol phosphates, including inositol trisphosphate. Formation of inositol trisphosphate appears independent of agonist-induced Ca2+ mobilization, since neither formation nor degradation of inositol trisphosphate are appreciably altered in low-calcium media, and elevation of cytosolic Ca2+ with a calcium ionophore does not cause an increase in cellular inositol trisphosphate. Further, activation of substance P receptors and alpha 1-adrenoreceptors, but not beta-adrenoreceptors, increases inositol trisphosphate formation. The dose-response curve for methacholine activation of inositol trisphosphate formation more closely approximates the curve for receptor occupancy than for Ca2+-activated K+ release. These results are all consistent with the suggestion that inositol trisphosphate could function as a second messenger linking receptor occupation to cellular Ca2+ mobilization.

摘要

毒蕈碱受体在大鼠腮腺细胞中的激活导致多磷酸肌醇分解，释放出肌醇磷酸，包括肌醇三磷酸。肌醇三磷酸的形成似乎与激动剂诱导的Ca2+动员无关，因为在低钙培养基中，肌醇三磷酸的形成和降解均未明显改变，并且用钙离子载体提高胞质Ca2+水平不会导致细胞内肌醇三磷酸增加。此外，P物质受体和α1-肾上腺素能受体而非β-肾上腺素能受体的激活会增加肌醇三磷酸的形成。与Ca2+激活的K+释放曲线相比，乙酰甲胆碱激活肌醇三磷酸形成的剂量反应曲线更接近受体占据曲线。这些结果均与肌醇三磷酸可作为将受体占据与细胞Ca2+动员联系起来的第二信使这一观点一致。