...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Chemical Society >Alkylated Hydroxylamine Derivatives Eliminate Peripheral Retinylidene Schiff Bases but Cannot Enter the Retinal Binding Pocket of Light-Activated Rhodopsin
【24h】

Alkylated Hydroxylamine Derivatives Eliminate Peripheral Retinylidene Schiff Bases but Cannot Enter the Retinal Binding Pocket of Light-Activated Rhodopsin

机译：烷基化羟胺衍生物消除了周围的视黄醛席夫碱，但不能进入光激活的视紫红质的视网膜结合口袋

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Besides Lys-296 in the binding pocket of opsin, all-trans-retinal forms adducts with peripheral lysine residues and phospholipids, thereby mimicking the spectral and chemical properties of metarhodopsin species. These pseudophotoproducts composed of nonspecific retinylidene Schiff bases have long plagued the investigation of rhodopsin deactivation and identification of decay products. We discovered that, while hydroxylamine can enter the retinal binding pocket of light-activated rhodopsin, the modified hydroxylamine compounds o-methylhydroxylamine (mHA), o-ethylhydroxylamine (eHA), o-tert-butylhydroxylamine (t-bHA), and o-(carboxymethyl)hydroxylamine (cmHA) are excluded. However, the alkylated hydroxylamines react quickly and efficiently with exposed retinylidene Schiff bases to form their respective retinal oximes. We further investigated how t-bHA affects light-activated rhodopsin and its interaction with binding partners. We found that both metarhodopsin II (Meta II) and Meta III are resistant to t-bHA, and neither arrestin nor transducin binding is affected by t-bHA. This discovery suggests that the hypothetical solvent channel that opens in light-activated rhodopsin is extremely stringent with regard to size and/or polarity. We believe that alkylated hydroxylamines will prove to be extremely useful reagents for the investigation of rhodopsin activation and decay mechanisms. Furthermore, the use of alkylated hydroxylamines should not be limited to in vitro studies and could help elucidate visual signal transduction mechanisms in the living cells of the retina.
机译：除了视蛋白结合口袋中的Lys-296外，全反式视网膜形式还带有外周赖氨酸残基和磷脂加合物，从而模仿了视紫红质的光谱和化学性质。这些由非特异性视黄叉基席夫碱组成的伪光产物长期困扰着视紫红质失活的研究和衰变产物的鉴定。我们发现，虽然羟胺可以进入光活化视紫红质的视网膜结合口袋，但改性羟胺化合物包括邻甲基羟胺（mHA），邻乙基羟胺（eHA），邻叔丁基羟胺（t-bHA）和邻-排除（羧甲基）羟胺（cmHA）。但是，烷基化的羟胺与暴露的视黄叉基席夫碱快速有效地反应，形成各自的视网膜肟。我们进一步研究了t-bHA如何影响光激活的视紫红质及其与结合伴侣的相互作用。我们发现，金属视紫红质II（Meta II）和Meta III都对t-bHA具有抗性，并且t-bHA均不抑制抑制素或转导蛋白。该发现表明，在光激活的视紫红质中打开的假设溶剂通道在尺寸和/或极性方面极为严格。我们相信，烷基化羟胺将被证明是用于视紫红质活化和衰变机理研究的极其有用的试剂。此外，烷基化羟胺的使用不应仅限于体外研究，而是可以帮助阐明视网膜活细胞中的视觉信号转导机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号