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International Union of Pharmacology LVIII: update on the P2Y G protein-coupled nucleotide receptors: from molecular mechanisms and pathophysiology to therapy.
Pharmacological Reviews ( IF 19.3 ) Pub Date : 2006-09-01 , DOI: 10.1124/pr.58.3.3
Maria P Abbracchio 1 , Geoffrey Burnstock , Jean-Marie Boeynaems , Eric A Barnard , José L Boyer , Charles Kennedy , Gillian E Knight , Marta Fumagalli , Christian Gachet , Kenneth A Jacobson , Gary A Weisman
Affiliation  

There have been many advances in our knowledge about different aspects of P2Y receptor signaling since the last review published by our International Union of Pharmacology subcommittee. More receptor subtypes have been cloned and characterized and most orphan receptors de-orphanized, so that it is now possible to provide a basis for a future subdivision of P2Y receptor subtypes. More is known about the functional elements of the P2Y receptor molecules and the signaling pathways involved, including interactions with ion channels. There have been substantial developments in the design of selective agonists and antagonists to some of the P2Y receptor subtypes. There are new findings about the mechanisms underlying nucleotide release and ectoenzymatic nucleotide breakdown. Interactions between P2Y receptors and receptors to other signaling molecules have been explored as well as P2Y-mediated control of gene transcription. The distribution and roles of P2Y receptor subtypes in many different cell types are better understood and P2Y receptor-related compounds are being explored for therapeutic purposes. These and other advances are discussed in the present review.

中文翻译:


国际药理学联合会 LVIII:P2Y G 蛋白偶联核苷酸受体的最新进展:从分子机制和病理生理学到治疗。



自国际药理学联盟小组委员会发表上一篇综述以来,我们对 P2Y 受体信号转导不同方面的认识取得了许多进展。更多的受体亚型已被克隆和表征,并且大多数孤儿受体已去孤儿化,因此现在可以为 P2Y 受体亚型的未来细分提供基础。人们对 P2Y 受体分子的功能元件和所涉及的信号传导途径(包括与离子通道的相互作用)了解更多。一些 P2Y 受体亚型的选择性激动剂和拮抗剂的设计已经取得了实质性进展。关于核苷酸释放和胞外酶核苷酸分解的机制有了新的发现。人们已经探索了 P2Y 受体与其他信号分子受体之间的相互作用以及 P2Y 介导的基因转录控制。人们更好地了解了 P2Y 受体亚型在许多不同细胞类型中的分布和作用,并且正在探索用于治疗目的的 P2Y 受体相关化合物。本综述讨论了这些和其他进展。
更新日期:2019-11-01
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