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点突变的p21ras将毒蕈碱受体与钙通道及多磷酸肌醇水解偶联起来。

Point-mutated p21ras couples a muscarinic receptor to calcium channels and polyphosphoinositide hydrolysis.

作者信息

Chiarugi V P, Pasquali F, Vannucchi S, Ruggiero M

出版信息

Biochem Biophys Res Commun. 1986 Dec 15;141(2):591-9. doi: 10.1016/s0006-291x(86)80214-5.

DOI:10.1016/s0006-291x(86)80214-5
PMID:2432894
Abstract

A high-affinity muscarinic receptor is detectable both in normal 3T3 mouse fibroblasts and in their transformed counterpart obtained by transfection with the oncogene EJ/T24-H-ras. However, only the transformed cell line is responsive to muscarinic agonist carbamylcholine in terms of Ca2+ influx and polyphosphoinositide hydrolysis, whereas the normal cell line is unresponsive. Using a point-mutated p21ras protein and monoclonal antibodies anti-p21ras, we provide evidences that p21ras couples to receptor-operating calcium channels and to polyphosphoinositide hydrolysis a muscarinic receptor which is uncoupled in normal mouse fibroblasts.

摘要

在正常的3T3小鼠成纤维细胞及其通过癌基因EJ/T24-H-ras转染获得的转化细胞中均能检测到高亲和力的毒蕈碱受体。然而,就Ca2+内流和多磷酸肌醇水解而言,只有转化细胞系对毒蕈碱激动剂氨甲酰胆碱有反应,而正常细胞系无反应。利用点突变的p21ras蛋白和抗p21ras单克隆抗体,我们提供证据表明p21ras与受体操纵的钙通道以及与正常小鼠成纤维细胞中未偶联的毒蕈碱受体的多磷酸肌醇水解偶联。

相似文献

1
Point-mutated p21ras couples a muscarinic receptor to calcium channels and polyphosphoinositide hydrolysis.点突变的p21ras将毒蕈碱受体与钙通道及多磷酸肌醇水解偶联起来。
Biochem Biophys Res Commun. 1986 Dec 15;141(2):591-9. doi: 10.1016/s0006-291x(86)80214-5.
2
Transformation of BALB/3T3 cells with EJ/T24/H-ras oncogene inhibits adenylate cyclase response to beta-adrenergic agonist while increases muscarinic receptor dependent hydrolysis of inositol lipids.
Biochem Biophys Res Commun. 1985 Nov 15;132(3):900-7. doi: 10.1016/0006-291x(85)91892-3.
3
Agonist-induced desensitization of muscarinic receptor-mediated calcium efflux without concomitant desensitization of phosphoinositide hydrolysis.激动剂诱导的毒蕈碱受体介导的钙外流脱敏,而磷酸肌醇水解无伴随脱敏。
Mol Pharmacol. 1985 Mar;27(3):325-32.
4
Monoclonal anti-CD23 antibodies induce a rise in [Ca2+]i and polyphosphoinositide hydrolysis in human activated B cells. Involvement of a Gp protein.单克隆抗CD23抗体可诱导人活化B细胞内[Ca2+]i升高及多磷酸肌醇水解。Gp蛋白的参与。
J Immunol. 1990 Jul 15;145(2):429-37.
5
G-protein involvement in central-nervous-system muscarinic-receptor-coupled polyphosphoinositide hydrolysis.G蛋白参与中枢神经系统毒蕈碱受体偶联的多磷酸肌醇水解。
Biochem J. 1988 Dec 15;256(3):995-9. doi: 10.1042/bj2560995.
6
Muscarinic receptor-operated Ca2+ influx in transfected fibroblast cells is independent of inositol phosphates and release of intracellular Ca2+.转染的成纤维细胞中,毒蕈碱受体介导的Ca2+内流与肌醇磷酸及细胞内Ca2+释放无关。
Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):509-13. doi: 10.1073/pnas.89.2.509.
7
Muscarinic receptor-induced phosphoinositide hydrolysis at resting cytosolic Ca2+ concentration in PC12 cells.毒蕈碱受体在PC12细胞静息胞质钙离子浓度下诱导的磷酸肌醇水解作用
J Cell Biol. 1985 Apr;100(4):1330-3. doi: 10.1083/jcb.100.4.1330.
8
Opposing effects of a ras oncogene on growth factor-stimulated phosphoinositide hydrolysis: desensitization to platelet-derived growth factor and enhanced sensitivity to bradykinin.一种原癌基因ras对生长因子刺激的磷酸肌醇水解的相反作用:对血小板衍生生长因子脱敏以及对缓激肽敏感性增强。
Proc Natl Acad Sci U S A. 1987 May;84(9):2648-52. doi: 10.1073/pnas.84.9.2648.
9
Activation of muscarinic receptors in PC12 cells. Correlation between cytosolic Ca2+ rise and phosphoinositide hydrolysis.PC12细胞中M胆碱能受体的激活。胞质Ca2+升高与磷酸肌醇水解之间的相关性。
Biochem J. 1986 Mar 15;234(3):555-62. doi: 10.1042/bj2340555.
10
Scrape-loading of Swiss 3T3 cells with ras protein rapidly activates protein kinase C in the absence of phosphoinositide hydrolysis.在不存在磷酸肌醇水解的情况下,用ras蛋白对瑞士3T3细胞进行刮擦加载可快速激活蛋白激酶C。
Oncogene. 1989 Jan;4(1):27-31.

引用本文的文献

1
p21ras-induced responsiveness of phosphatidylinositol turnover to bradykinin is a receptor number effect.p21ras诱导的磷脂酰肌醇周转率对缓激肽的反应性是一种受体数量效应。
Proc Natl Acad Sci U S A. 1988 Aug;85(16):5774-8. doi: 10.1073/pnas.85.16.5774.
2
The structure and mechanism of neurotransmitter receptors. Implications for the structure and function of the central nervous system.神经递质受体的结构与机制。对中枢神经系统结构和功能的影响。
Biochem J. 1988 Jan 15;249(2):309-18. doi: 10.1042/bj2490309.
3
Arachidonic acid mobilization in platelets: the possible role of protein kinase C and G-proteins.
血小板中花生四烯酸的动员:蛋白激酶C和G蛋白的可能作用。
Experientia. 1988 Feb 15;44(2):101-4. doi: 10.1007/BF01952189.
4
Phospholipase C-mediated hydrolysis of phosphatidylcholine is activated by muscarinic agonists.磷脂酶C介导的磷脂酰胆碱水解由毒蕈碱激动剂激活。
Biochem J. 1989 Oct 1;263(1):115-20. doi: 10.1042/bj2630115.
5
Desensitization of prostaglandin F2 alpha-stimulated inositol phosphate generation in NIH-3T3 fibroblasts transformed by overexpression of normal c-Ha-ras-1, c-Ki-ras-2 and c-N-ras genes.在通过正常c-Ha-ras-1、c-Ki-ras-2和c-N-ras基因过表达而转化的NIH-3T3成纤维细胞中,前列腺素F2α刺激的肌醇磷酸生成的脱敏作用。
Biochem J. 1990 May 1;267(3):809-13. doi: 10.1042/bj2670809.
6
NIH-3T3 cells transformed with a ras oncogene exhibit a protein kinase C-mediated inhibition of agonist-stimulated Ca2+ inflow.用ras癌基因转化的NIH-3T3细胞表现出蛋白激酶C介导的对激动剂刺激的Ca2+内流的抑制作用。
Biochem J. 1990 Oct 15;271(2):309-15. doi: 10.1042/bj2710309.
7
Transformation-specific decrease of phosphorylation of 80K protein, a substrate of protein kinase C, in NIH3T3 cells.NIH3T3细胞中蛋白激酶C的底物80K蛋白磷酸化的转化特异性降低。
Jpn J Cancer Res. 1990 Aug;81(8):799-806. doi: 10.1111/j.1349-7006.1990.tb02648.x.