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鸟苷三磷酸（GTP）对大鼠肝微粒体囊泡中钙离子外流的作用机制。

The mechanism of action of GTP on Ca2+ efflux from rat liver microsomal vesicles.

作者信息

Dawson A P, Hills G, Comerford J G

机构信息

School of Biological Sciences, University of East Anglia, Norwich, U.K.

出版信息

Biochem J. 1987 May 15;244(1):87-92. doi: 10.1042/bj2440087.

DOI:10.1042/bj2440087
PMID:3499139
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1147957/
Abstract
  1. Guanosine 5'-[gamma-thio]triphosphate (GTP[S]), if added before GTP, blocks both Ca2+ efflux promoted by GTP and the effect of GTP on enhancement of inositol 1,4,5-triphosphate (IP3)-promoted Ca2+ release from preloaded microsomal vesicles. If, however, GTP[S] is added after GTP, it does not reverse the Ca2+ efflux promoted by GTP, nor does it inhibit IP3-promoted Ca2+ release. 2. The effect of GTP in enhancing IP3-promoted Ca2+ release is maintained after washing the microsomal vesicles free of added GTP. After this treatment, enhancement of IP3-promoted Ca2+ efflux can be observed in the absence of poly(ethylene glycol). 3. Electron microscopy shows that during GTP treatment of microsomal vesicles there is rapid production of very large vesicular structures, apparently produced by fusion of smaller vesicles. 4. Light-scattering changes are detectable during the fusion process. 5. Both Ca2+ efflux promoted by GTP and the enhancement of IP3-promoted Ca2+ release seen in the presence of GTP can probably be attributed to GTP-dependent vesicle fusion.
摘要
  1. 5'-[γ-硫代]三磷酸鸟苷（GTP[S]）若在鸟苷三磷酸（GTP）之前添加，会阻断由GTP促进的钙离子外流以及GTP对肌醇1,4,5-三磷酸（IP3）促进的预加载微粒体囊泡钙离子释放增强的作用。然而，如果GTP[S]在GTP之后添加，则不会逆转由GTP促进的钙离子外流，也不会抑制IP3促进的钙离子释放。2. 在将微粒体囊泡中添加的GTP洗去后，GTP增强IP3促进的钙离子释放的作用仍然存在。经过这种处理后，在不存在聚乙二醇的情况下，可以观察到IP3促进的钙离子外流增强。3. 电子显微镜显示，在对微粒体囊泡进行GTP处理期间，会迅速产生非常大的囊泡结构，显然是由较小囊泡融合产生的。4. 在融合过程中可检测到光散射变化。5. 由GTP促进的钙离子外流以及在GTP存在下看到的IP3促进的钙离子释放增强，可能都归因于GTP依赖性囊泡融合。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc85/1147957/76338ca8b5a7/biochemj00255-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc85/1147957/76338ca8b5a7/biochemj00255-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc85/1147957/76338ca8b5a7/biochemj00255-0093-a.jpg

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Multiple mechanisms by which protein kinase A potentiates inositol 1,4,5-trisphosphate-induced Ca2+ mobilization in permeabilized hepatocytes.蛋白激酶A增强通透化肝细胞中肌醇1,4,5-三磷酸诱导的Ca2+动员的多种机制。
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Effects of CoA and acyl-CoAs on GTP-dependent Ca2+ release and vesicle fusion in rat liver microsomal vesicles.

本文引用的文献

1
Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
J Biol Chem. 1951 Nov;193(1):265-75.
2
Physiological concentrations of GTP stimulate fusion of the endoplasmic reticulum and the nuclear envelope.生理浓度的鸟苷三磷酸（GTP）可刺激内质网与核膜的融合。
Exp Cell Res. 1984 Apr;151(2):354-66. doi: 10.1016/0014-4827(84)90386-0.
3
Inositol (1,4,5)trisphosphate-promoted Ca2+ release from microsomal fractions of rat liver.肌醇（1,4,5）三磷酸促进大鼠肝脏微粒体组分释放钙离子。
辅酶A和酰基辅酶A对大鼠肝微粒体囊泡中GTP依赖性钙离子释放和囊泡融合的影响。
Biochem J. 1993 Jan 15;289 ( Pt 2)(Pt 2):561-7. doi: 10.1042/bj2890561.
4
Effect of GTP on the dolichol pathway for protein glycosylation in rat liver microsomes.鸟苷三磷酸（GTP）对大鼠肝脏微粒体中蛋白质糖基化的多萜醇途径的影响。
Biochem J. 1993 Dec 15;296 ( Pt 3)(Pt 3):633-7. doi: 10.1042/bj2960633.
5
Effects of CoA and acyl-CoA on Ca(2+)-permeability of endoplasmic-reticulum membranes from rat liver.辅酶A和酰基辅酶A对大鼠肝脏内质网膜钙通透性的影响。
Biochem J. 1995 Mar 15;306 ( Pt 3)(Pt 3):703-8. doi: 10.1042/bj3060703.
6
Characterization of N-ethylmaleimide-sensitive thiol groups required for the GTP-dependent fusion of endoplasmic reticulum membranes.内质网膜的GTP依赖性融合所需的N-乙基马来酰亚胺敏感硫醇基团的表征。
Biochem J. 1995 Nov 15;312 ( Pt 1)(Pt 1):23-30. doi: 10.1042/bj3120023.
7
Calcium entry into the inositol 1,4,5-trisphosphate-releasable calcium pool is mediated by a GTP-regulatory mechanism.钙离子进入肌醇1,4,5-三磷酸可释放钙池是由一种GTP调节机制介导的。
Proc Natl Acad Sci U S A. 1988 Apr;85(8):2499-503. doi: 10.1073/pnas.85.8.2499.
8
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Biochem J. 1987 Dec 15;248(3):741-7. doi: 10.1042/bj2480741.
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Nature. 1983;306(5938):67-9. doi: 10.1038/306067a0.
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J Biol Chem. 1984 Nov 25;259(22):13777-82.
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Release of Ca2+ from a non-mitochondrial store site in peritoneal macrophages treated with saponin by inositol 1,4,5-trisphosphate.用肌醇1,4,5 -三磷酸处理皂素处理的腹膜巨噬细胞后，Ca2+从非线粒体储存位点释放。
Biochem J. 1984 Oct 1;223(1):229-36. doi: 10.1042/bj2230229.
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Rapid mobilization of Ca2+ from rat insulinoma microsomes by inositol-1,4,5-trisphosphate.肌醇-1,4,5-三磷酸促使大鼠胰岛素瘤微粒体中的钙离子快速动员。
Nature. 1984;309(5968):562-4. doi: 10.1038/309562a0.