Role of G-Proteins and GPCR-Mediated Signalling in Neuropathophysiology.

IF 2.7 4区 医学 Q3 NEUROSCIENCES CNS & neurological disorders drug targets Pub Date : 2023-01-01 DOI:10.2174/1871527321666220430142722
Md Mominur Rahman, Sadia Afsana Mim, Md Rezaul Islam, Nasrin Sultana, Muniruddin Ahmed, Mohammad Amjad Kamal
{"title":"Role of G-Proteins and GPCR-Mediated Signalling in Neuropathophysiology.","authors":"Md Mominur Rahman,&nbsp;Sadia Afsana Mim,&nbsp;Md Rezaul Islam,&nbsp;Nasrin Sultana,&nbsp;Muniruddin Ahmed,&nbsp;Mohammad Amjad Kamal","doi":"10.2174/1871527321666220430142722","DOIUrl":null,"url":null,"abstract":"<p><p>G-protein-coupled receptors (GPCRs) are activated by manifold neurotransmitters, and their activation, in turn, evokes slow synaptic transmission. They are profoundly related to numerous psychiatric and neurological disorders such as schizophrenia and Parkinson's disease. The significant malady indications for GPCR modulators demonstrate a change towards obesity, diabetes, and Alzheimer's disease, while other central nervous system disorders persist highly represented. GPR52, GPR6, and GPR8 are recognised as orphan GPCRs, co-exist either with both the dopamine D2 and D1 receptors in neurons of the basal ganglia or with the dopamine D2 receptor alone, and recommend that between these orphan receptors, GPR52 has the maximum potential of being a therapeutic psychiatric receptor. Genetically modified creature models and molecular biological investigations have suggested that these improved GPCRs could be potential therapeutic psychiatric receptors. In this perspective, the role of molecular targets in GPCR-mediated signalling has been discussed that would be novel drug design and discovery options for a scientist to elaborate previous knowledge with modern techniques.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"CNS & neurological disorders drug targets","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/1871527321666220430142722","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 5

Abstract

G-protein-coupled receptors (GPCRs) are activated by manifold neurotransmitters, and their activation, in turn, evokes slow synaptic transmission. They are profoundly related to numerous psychiatric and neurological disorders such as schizophrenia and Parkinson's disease. The significant malady indications for GPCR modulators demonstrate a change towards obesity, diabetes, and Alzheimer's disease, while other central nervous system disorders persist highly represented. GPR52, GPR6, and GPR8 are recognised as orphan GPCRs, co-exist either with both the dopamine D2 and D1 receptors in neurons of the basal ganglia or with the dopamine D2 receptor alone, and recommend that between these orphan receptors, GPR52 has the maximum potential of being a therapeutic psychiatric receptor. Genetically modified creature models and molecular biological investigations have suggested that these improved GPCRs could be potential therapeutic psychiatric receptors. In this perspective, the role of molecular targets in GPCR-mediated signalling has been discussed that would be novel drug design and discovery options for a scientist to elaborate previous knowledge with modern techniques.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
g蛋白和gpcr介导的信号传导在神经病理生理中的作用。
g蛋白偶联受体(gpcr)被多种神经递质激活,而它们的激活反过来又引起缓慢的突触传递。它们与精神分裂症和帕金森氏症等许多精神和神经疾病密切相关。GPCR调节剂的显着疾病适应症显示肥胖,糖尿病和阿尔茨海默病的变化,而其他中枢神经系统疾病仍然高度代表。GPR52, GPR6和GPR8被认为是孤儿gprcrs,与基底神经节神经元中的多巴胺D2和D1受体或单独与多巴胺D2受体共存,并建议在这些孤儿受体之间,GPR52具有最大的潜力成为治疗精神病学受体。转基因生物模型和分子生物学研究表明,这些改进的gpcr可能是潜在的治疗精神疾病的受体。从这个角度来看,分子靶点在gpcr介导的信号传导中的作用已经被讨论,这将是科学家用现代技术阐述先前知识的新药物设计和发现选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
5.10
自引率
3.30%
发文量
158
审稿时长
6-12 weeks
期刊介绍: Aims & Scope CNS & Neurological Disorders - Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular targets involved in neurological and central nervous system (CNS) disorders e.g. disease specific proteins, receptors, enzymes, genes. CNS & Neurological Disorders - Drug Targets publishes guest edited thematic issues written by leaders in the field covering a range of current topics of CNS & neurological drug targets. The journal also accepts for publication original research articles, letters, reviews and drug clinical trial studies. As the discovery, identification, characterization and validation of novel human drug targets for neurological and CNS drug discovery continues to grow; this journal is essential reading for all pharmaceutical scientists involved in drug discovery and development.
期刊最新文献
Association between Frequency of Seizures and Number of Antiseizure Medications (ASM) in Patients with Epilepsy. Choice and Timing of Antithrombotic after Ischemic Stroke, Intracerebral Hemorrhage or Cerebral Venous Thrombosis. New Psychometric Strategies for the Evaluation of Affective, Cognitive, and Psychosocial Functioning in Unipolar versus Bipolar Depression: Impact of Drug Treatment. Curbing Rhes Actions: Mechanism-based Molecular Target for Huntington's Disease and Tauopathies. G Protein-coupled Receptors (GPCRs) as Potential Therapeutics for Psychiatric Disorders.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1