Posttranslational modifications in retinal degeneration diseases: An update on the molecular basis and treatment

Brain-X Pub Date : 2024-10-15 DOI:10.1002/brx2.70005
Ke Yao, Qianxue Mou, Zhen Jiang, Yin Zhao
{"title":"Posttranslational modifications in retinal degeneration diseases: An update on the molecular basis and treatment","authors":"Ke Yao,&nbsp;Qianxue Mou,&nbsp;Zhen Jiang,&nbsp;Yin Zhao","doi":"10.1002/brx2.70005","DOIUrl":null,"url":null,"abstract":"<p>Noninherited diseases and age-associated vision loss are often associated with retinal degeneration. The retina is a postmitotic neural tissue lacking endogenous regeneration capacity. Therefore, understanding the mechanism of retinal degeneration in diseases is pivotal. Posttranslational modifications (PTMs) determine protein function during physiological and pathological processes, including signal transduction, protein localization, and protein activation. Advanced detection technologies have revealed over 400 different PTMs including acetylation, methylation, phosphorylation, ubiquitination and SUMOylation. Here, we discuss PTMs in retinal degeneration diseases to aid in our understanding of their molecular basis and suggest potential future clinical treatment.</p>","PeriodicalId":94303,"journal":{"name":"Brain-X","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brx2.70005","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain-X","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/brx2.70005","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Noninherited diseases and age-associated vision loss are often associated with retinal degeneration. The retina is a postmitotic neural tissue lacking endogenous regeneration capacity. Therefore, understanding the mechanism of retinal degeneration in diseases is pivotal. Posttranslational modifications (PTMs) determine protein function during physiological and pathological processes, including signal transduction, protein localization, and protein activation. Advanced detection technologies have revealed over 400 different PTMs including acetylation, methylation, phosphorylation, ubiquitination and SUMOylation. Here, we discuss PTMs in retinal degeneration diseases to aid in our understanding of their molecular basis and suggest potential future clinical treatment.

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
视网膜变性疾病中的翻译后修饰:分子基础和治疗的最新进展
非遗传性疾病和老年性视力丧失通常与视网膜变性有关。视网膜是一种后凋亡神经组织,缺乏内源性再生能力。因此,了解疾病导致视网膜退化的机制至关重要。翻译后修饰(PTM)决定了蛋白质在生理和病理过程中的功能,包括信号转导、蛋白质定位和蛋白质活化。先进的检测技术已经发现了 400 多种不同的 PTM,包括乙酰化、甲基化、磷酸化、泛素化和 SUMOylation。在此,我们将讨论视网膜变性疾病中的 PTMs,以帮助我们了解这些疾病的分子基础,并为未来潜在的临床治疗提供建议。
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
自引率
0.00%
发文量
0
期刊最新文献
Posttranslational modifications in retinal degeneration diseases: An update on the molecular basis and treatment Reconstructing continuous language from brain signals measured by fMRI based brain-computer interface A novel neuronal circuit: Tanycytes mediate defensive metabolic responses following acute high-temperature exposure A systematic review on investigating major depressive disorder and bipolar disorder using MRI and genetic data from 2018 to 2024 Music therapy for depression: A narrative review
×
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