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A model for the recovery kinetics of rod phototransduction, based on the enzymatic deactivation of rhodopsin.一种基于视紫红质酶促失活的视杆光转导恢复动力学模型。
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2
Recovery kinetics of human rod phototransduction inferred from the two-branched alpha-wave saturation function.从双分支α波饱和函数推断的人类视杆光转导恢复动力学
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3
Does rod phototransduction involve the delayed transition of activated rhodopsin to a second, more active catalytic state?视杆细胞的光转导过程是否涉及激活的视紫红质向第二种更活跃的催化状态的延迟转变?
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Light scattering methods to monitor interactions between rhodopsin-containing membranes and soluble proteins.用于监测含视紫红质膜与可溶性蛋白质之间相互作用的光散射方法。
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本文引用的文献

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GTP-binding-protein-coupled receptor kinases--two mechanistic models.GTP结合蛋白偶联受体激酶——两种作用机制模型
Eur J Biochem. 1997 Sep 1;248(2):261-9. doi: 10.1111/j.1432-1033.1997.00261.x.
2
Functional differences in the interaction of arrestin and its splice variant, p44, with rhodopsin.抑制蛋白及其剪接变体p44与视紫红质相互作用的功能差异。
Biochemistry. 1997 Jul 29;36(30):9253-60. doi: 10.1021/bi970772g.
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Structure and function of proteins in G-protein-coupled signal transfer.G蛋白偶联信号转导中蛋白质的结构与功能
Biochim Biophys Acta. 1996 Oct 29;1286(3):285-322. doi: 10.1016/s0304-4157(96)00013-5.
4
Stochastic simulation of the transducin GTPase cycle.转导素GTP酶循环的随机模拟。
Biophys J. 1996 Dec;71(6):3051-63. doi: 10.1016/S0006-3495(96)79499-7.
5
Responses of the phototransduction cascade to dim light.光转导级联反应对暗光的响应。
Proc Natl Acad Sci U S A. 1996 May 14;93(10):4677-82. doi: 10.1073/pnas.93.10.4677.
6
Novel mechanism for the activation of rhodopsin kinase: implications for other G protein-coupled receptor kinases (GRK's).视紫红质激酶激活的新机制:对其他G蛋白偶联受体激酶(GRK)的启示
Biochemistry. 1996 May 14;35(19):6164-72. doi: 10.1021/bi952480q.
7
Recovery kinetics of human rod phototransduction inferred from the two-branched alpha-wave saturation function.从双分支α波饱和函数推断的人类视杆光转导恢复动力学
J Opt Soc Am A Opt Image Sci Vis. 1996 Mar;13(3):586-600. doi: 10.1364/josaa.13.000586.
8
Recovery phase of the murine rod photoresponse reconstructed from electroretinographic recordings.从视网膜电图记录重建的小鼠视杆光反应的恢复阶段。
J Neurosci. 1996 Jan 15;16(2):563-71. doi: 10.1523/JNEUROSCI.16-02-00563.1996.
9
Interaction between photoactivated rhodopsin and its kinase: stability and kinetics of complex formation.光激活视紫红质与其激酶之间的相互作用:复合物形成的稳定性和动力学
Biochemistry. 1993 Dec 28;32(51):14082-8. doi: 10.1021/bi00214a002.
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Structure and mechanism of the G protein-coupled receptor kinases.G蛋白偶联受体激酶的结构与机制
J Biol Chem. 1993 Nov 15;268(32):23735-8.

一种基于视紫红质酶促失活的视杆光转导恢复动力学模型。

A model for the recovery kinetics of rod phototransduction, based on the enzymatic deactivation of rhodopsin.

作者信息

Laitko U, Hofmann K P

机构信息

Institut für Medizinische Physik und Biophysik, Medizinische Fakultät Charité der Humboldt-Universität zu Berlin, Germany.

出版信息

Biophys J. 1998 Feb;74(2 Pt 1):803-15. doi: 10.1016/S0006-3495(98)74005-6.

DOI:10.1016/S0006-3495(98)74005-6
PMID:9533693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1302561/
Abstract

We propose a model for the recovery of the retinal rod photoresponse after a short stimulus. The approach describes the enzymatic deactivation of the photoactivated receptor, rhodopsin, by simple enzyme kinetics. An important feature of this description is that the R* deactivation obeys different time laws, depending on the numbers of R* formed per disc membrane and available enzyme molecules. If the enzyme works below substrate saturation, the rate of deactivation depends linearly on the number of R*, whereas for substrate saturation a hyperbolic relation--the well-known Michaelis-Menten equation--applies. This dichotomy is used to explain experimental finding that the relation between the saturation time of the photoresponse after short illumination and the flash strength has two sharply separated branches for low and high flash intensities (up to approximately 10% bleaching). By relating both branches to properties of the enzymatic rhodopsin deactivation, the new model transcends the classical notion of a constant characteristic lifetime of activated rhodopsin. With parameters that are plausible in the light of the available data and the additional information that the deactivating enzyme, rhodopsin kinase, and the signaling G-protein, transducin, compete for the active receptor, the slopes of the saturation function are correctly reproduced.

摘要

我们提出了一个用于描述短刺激后视网膜视杆光反应恢复的模型。该方法通过简单的酶动力学描述了光激活受体视紫红质的酶促失活过程。此描述的一个重要特征是,视紫红质*(R*)的失活遵循不同的时间规律,这取决于每个盘膜形成的R数量以及可用的酶分子数量。如果酶在底物饱和浓度以下起作用,失活速率与R数量呈线性关系,而在底物饱和时,则适用双曲线关系——即著名的米氏方程。这种二分法用于解释实验发现:短时间光照后光反应的饱和时间与闪光强度之间的关系在低闪光强度和高闪光强度(高达约10%漂白)时具有两个明显分开的分支。通过将两个分支与视紫红质酶促失活的特性相关联,新模型超越了激活视紫红质具有恒定特征寿命的经典概念。根据现有数据以及失活酶视紫红质激酶和信号转导G蛋白转导素竞争活性受体的额外信息,该模型合理设置参数,正确再现了饱和函数的斜率。