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Rhodopsin phosphorylation: 30 years later.
Progress in Retinal and Eye Research ( IF 17.8 ) Pub Date : 2003-05-14 , DOI: 10.1016/s1350-9462(03)00017-x
Tadao Maeda 1 , Yoshikazu Imanishi , Krzysztof Palczewski
Affiliation  

Phototransduction in vertebrate photoreceptor cells mediated by rhodopsin is one of the most comprehensively examined G protein-coupled receptor (GPCR) signaling pathways. The signal transduction pathway can be mapped from the initial absorption of light to conformational changes within rhodopsin, through activation of the G protein transducin, and to the ultimate closure of the cation cGMP-gated channels in the plasma membrane. Furthermore, phototransduction has become an intensely studied model system for understanding the desensitizing processes that allow reduced non-linear responses of photoreceptor cells to increasing levels of illumination. Although some general themes appear to occur in GPCR systems, the details of these desensitizing processes are likely to be specific to each of the receptors. These differences are attributed to the fact that each receptor has unique kinetic constraints, amplification levels, tolerance to basal constitutive activity, intracellular internalization and recycling, redundancy of isoforms, and morphologies of the cell of their expression. One of the biochemical processes that are believed to be a common part of this desensitization of the GPCR-mediated cascade is receptor phosphorylation catalyzed by members of a small family of the GPCR kinases. The enzymatic, physiological and genetic aspects of rhodopsin phosphorylation and rhodopsin kinase have been characterized extensively over the last 30 yr. However, new structurally based approaches to examining rhodopsin kinase and rhodopsin phosphorylation are still awaiting further investigations. We present here a summary of the current understanding of rhodopsin phosphorylation and the properties of rhodopsin kinase, along with some expectations of future investigations into these topics.

中文翻译:

视紫红质的磷酸化:30年后。

视紫红质介导的脊椎动物感光细胞中的光转导是最全面检查的G蛋白偶联受体(GPCR)信号通路之一。信号转导途径可以从最初的光吸收到视紫红质内的构象变化(通过激活G蛋白转导素)到质膜中阳离子cGMP门控通道的最终关闭进行映射。此外,光转导已经成为深入研究的模型系统,用于理解脱敏过程,该过程允许减少感光细胞对增加的照明水平的非线性响应。尽管某些通用主题似乎出现在GPCR系统中,但这些脱敏过程的细节可能对每种受体都是特定的。这些差异归因于每个受体具有独特的动力学约束,扩增水平,对基础组成活性的耐受性,细胞内内化和再循环,同工型的冗余以及它们表达的细胞形态的事实。被认为是GPCR介导的级联反应脱敏的常见部分的生化过程之一是由一小部分GPCR激酶成员催化的受体磷酸化。在过去的30年中,视紫红质磷酸化和视紫红质激酶的酶,生理和遗传方面已得到广泛表征。然而,用于检查视紫红质激酶和视紫红质磷酸化的新的基于结构的方法仍在等待进一步的研究。
更新日期:2019-11-01
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