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百日咳毒素催化的ADP-核糖基化对转导素及腺苷酸环化酶抑制性GTP结合蛋白与鸟苷核苷酸相互作用的影响。

Effects of pertussis toxin-catalyzed ADP-ribosylation on interactions of transducin and the inhibitory GTP-binding protein of adenylate cyclase with guanyl nucleotides.

作者信息

Bruni P, Hewlett E L, Moss J

出版信息

Biochem Biophys Res Commun. 1985 Mar 29;127(3):999-1006. doi: 10.1016/s0006-291x(85)80043-7.

DOI:10.1016/s0006-291x(85)80043-7
PMID:3921021
Abstract

Release of bound [3H]Gpp(NH)p from NG108-15 cell membranes was induced by carbamylcholine, enkephalinamide, and norepinephrine, all of which inhibit adenylate cyclase. Release was blocked by antagonist, was greater with multiple agonists than with one, and required guanyl nucleotides. With membranes from pertussis toxin-treated cells, both total [3H] Gpp(NH)p binding and agonist-induced [3H]Gpp(NH)p release was decreased. ADP-ribosylation by toxin of transducin, the retinal GTP-binding protein which is similar in structure and function to that in cyclase, decreased [3H]Gpp(NH)p binding. Thus, the inability to demonstrate agonist-induced [3H]Gpp(NH)p release from toxin-treated NG108-15 membranes may result in part from absence of bound [3H]Gpp(NH)p.

摘要

氨甲酰胆碱、脑啡肽酰胺和去甲肾上腺素可诱导NG108 - 15细胞膜中结合的[³H]Gpp(NH)p释放，这些物质均抑制腺苷酸环化酶。拮抗剂可阻断释放，多种激动剂诱导的释放比单一激动剂诱导的释放更大，且需要鸟苷核苷酸。对于百日咳毒素处理过的细胞的膜，总的[³H]Gpp(NH)p结合以及激动剂诱导的[³H]Gpp(NH)p释放均减少。转导蛋白是视网膜GTP结合蛋白，其结构和功能与环化酶中的相似，毒素对转导蛋白进行的ADP - 核糖基化作用降低了[³H]Gpp(NH)p结合。因此，无法证明毒素处理过的NG108 - 15细胞膜存在激动剂诱导的[³H]Gpp(NH)p释放，这可能部分是由于缺乏结合的[³H]Gpp(NH)p所致。

相似文献

1
Effects of pertussis toxin-catalyzed ADP-ribosylation on interactions of transducin and the inhibitory GTP-binding protein of adenylate cyclase with guanyl nucleotides.百日咳毒素催化的ADP-核糖基化对转导素及腺苷酸环化酶抑制性GTP结合蛋白与鸟苷核苷酸相互作用的影响。
Biochem Biophys Res Commun. 1985 Mar 29;127(3):999-1006. doi: 10.1016/s0006-291x(85)80043-7.
2
Altered activity of the inhibitory guanyl nucleotide-binding component (Ni) induced by pertussis toxin. Uncoupling of Ni from receptor with continued coupling of Ni to the catalytic unit.百日咳毒素诱导的抑制性鸟苷酸结合成分（Ni）活性改变。Ni与受体解偶联，而Ni与催化单元持续偶联。
J Biol Chem. 1984 Jul 25;259(14):8693-8.
3
ADP-ribosylation of adenylate cyclase by pertussis toxin. Effects on inhibitory agonist binding.百日咳毒素对腺苷酸环化酶的ADP-核糖基化作用。对抑制性激动剂结合的影响。
J Biol Chem. 1984 Jan 25;259(2):1086-90.
4
Effects of guanyl nucleotides and rhodopsin on ADP-ribosylation of the inhibitory GTP-binding component of adenylate cyclase by pertussis toxin.鸟苷酸和视紫红质对百日咳毒素催化的腺苷酸环化酶抑制性GTP结合成分ADP核糖基化的影响。
J Biol Chem. 1984 Dec 25;259(24):15320-3.
5
The interaction of nucleotides with pertussis toxin. Direct evidence for a nucleotide binding site on the toxin regulating the rate of ADP-ribosylation of Ni, the inhibitory regulatory component of adenylyl cyclase.核苷酸与百日咳毒素的相互作用。毒素上存在核苷酸结合位点的直接证据，该位点调节腺苷酸环化酶抑制性调节成分Ni的ADP核糖基化速率。
J Biol Chem. 1986 Aug 25;261(24):11173-9.
6
Pertussis toxin-catalyzed ADP-ribosylation of adenylate cyclase. Effects of guanyl nucleotides and rhodopsin.百日咳毒素催化的腺苷酸环化酶的ADP-核糖基化。鸟苷核苷酸和视紫红质的作用。
Dev Biol Stand. 1985;61:43-9.
7
[Receptor-adenylate cyclase coupling--receptor-GTP binding protein(N) coupling and ADP-ribosylation of N by bacterial toxins].[受体 - 腺苷酸环化酶偶联——受体 - GTP 结合蛋白（N）偶联以及细菌毒素对 N 的 ADP 核糖基化作用]
Tanpakushitsu Kakusan Koso. 1985 Apr;30(4):303-13.
8
NaF and guanine nucleotides modulate adenylate cyclase activity in NG108-15 cells by interacting with both Gs and Gi.氟化钠和鸟嘌呤核苷酸通过与Gs和Gi相互作用来调节NG108-15细胞中的腺苷酸环化酶活性。
Br J Pharmacol. 1990 Jun;100(2):223-30. doi: 10.1111/j.1476-5381.1990.tb15786.x.
9
Determination of G-protein levels, ADP-ribosylation by cholera and pertussis toxins and the regulation of adenylyl cyclase activity in liver plasma membranes from lean and genetically diabetic (db/db) mice.测定瘦型和遗传性糖尿病（db/db）小鼠肝细胞膜中G蛋白水平、霍乱毒素和百日咳毒素介导的ADP核糖基化作用以及腺苷酸环化酶活性的调节。
Biochim Biophys Acta. 1991 Oct 21;1097(3):193-204. doi: 10.1016/0925-4439(91)90035-8.
10
Loss of the inhibitory function of the guanine nucleotide regulatory component of adenylate cyclase due to its ADP ribosylation by islet-activating protein, pertussis toxin, in adipocyte membranes.在脂肪细胞膜中，由于胰岛激活蛋白百日咳毒素使其发生ADP核糖基化，导致腺苷酸环化酶的鸟嘌呤核苷酸调节成分的抑制功能丧失。
J Biol Chem. 1983 Mar 10;258(5):3319-26.

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Mol Cell Biochem. 2001 Dec;228(1-2):91-8. doi: 10.1023/a:1013320625846.
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Biochem J. 1987 Dec 15;248(3):749-54. doi: 10.1042/bj2480749.
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