The nuts-and-bolts of ribosomal protein s6 kinase 1 regulation: A shared responsibility for mTOR complexes 1 and 2

IF 4.2 The FEBS journal Pub Date : 2026-10-01 Epub Date: 2026-06-05 DOI:10.1111/febs.70612
Sheikh Tahir Majeed, Rabiya Majeed, Khurshid I. Andrabi
{"title":"The nuts-and-bolts of ribosomal protein s6 kinase 1 regulation: A shared responsibility for mTOR complexes 1 and 2","authors":"Sheikh Tahir Majeed,&nbsp;Rabiya Majeed,&nbsp;Khurshid I. Andrabi","doi":"10.1111/febs.70612","DOIUrl":null,"url":null,"abstract":"<p>Ribosomal protein S6 kinase 1 (S6K1) is a master regulator of cell growth and metabolism and a primary effector of the mTOR signaling pathway. Given its central role in cancer and metabolic diseases, S6K1 is a high-priority therapeutic target; however, developing effective treatments requires a definitive understanding of how the enzyme is activated. This review provides a comprehensive synthesis of S6K1 biology, covering its structural domains, various chemical modifications like acetylation and ubiquitination, and its regulation by noncoding RNAs. We specifically highlight the transition from traditional ‘canonical’ models to an emerging ‘non-canonical’ paradigm. Central to this shift is the proposal that S6K1 activation is a shared responsibility between two complexes: mTORC1 and mTORC2. We detail a two-step mechanism where mTORC1 first ‘primes’ the enzyme by relieving internal constraints, allowing mTORC2 to complete the activation process. By reconciling these different models and addressing long-standing questions about drug sensitivity, this review establishes a modern framework for S6K1 biology and identifies new opportunities for precise therapeutic intervention.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":"293 19","pages":"5669-5685"},"PeriodicalIF":4.2000,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/febs.70612","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The FEBS journal","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/febs.70612","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/6/5 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Ribosomal protein S6 kinase 1 (S6K1) is a master regulator of cell growth and metabolism and a primary effector of the mTOR signaling pathway. Given its central role in cancer and metabolic diseases, S6K1 is a high-priority therapeutic target; however, developing effective treatments requires a definitive understanding of how the enzyme is activated. This review provides a comprehensive synthesis of S6K1 biology, covering its structural domains, various chemical modifications like acetylation and ubiquitination, and its regulation by noncoding RNAs. We specifically highlight the transition from traditional ‘canonical’ models to an emerging ‘non-canonical’ paradigm. Central to this shift is the proposal that S6K1 activation is a shared responsibility between two complexes: mTORC1 and mTORC2. We detail a two-step mechanism where mTORC1 first ‘primes’ the enzyme by relieving internal constraints, allowing mTORC2 to complete the activation process. By reconciling these different models and addressing long-standing questions about drug sensitivity, this review establishes a modern framework for S6K1 biology and identifies new opportunities for precise therapeutic intervention.

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
核糖体蛋白s6激酶1调控的具体细节:mTOR复合物1和2的共同责任。
核糖体蛋白S6激酶1 (S6K1)是细胞生长和代谢的主要调节因子,也是mTOR信号通路的主要效应因子。鉴于其在癌症和代谢性疾病中的核心作用,S6K1是一个高度优先的治疗靶点;然而,开发有效的治疗方法需要明确了解酶是如何被激活的。本文综述了S6K1生物学的全面合成,包括其结构域,各种化学修饰,如乙酰化和泛素化,以及非编码rna对其的调控。我们特别强调了从传统的“规范”模式到新兴的“非规范”范式的转变。这一转变的核心是提出S6K1激活是两个复合物mTORC1和mTORC2之间的共同责任。我们详细介绍了一个两步机制,其中mTORC1首先通过解除内部约束来“启动”酶,允许mTORC2完成激活过程。通过协调这些不同的模型和解决长期存在的药物敏感性问题,本综述建立了S6K1生物学的现代框架,并确定了精确治疗干预的新机会。
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
Breaking the ice: multiple origins of ice-binding/antifreeze proteins. The physiological roles and pathological implications of metabolic communication via tunneling nanotubes in immune cells. Structural and functional insights into rhodopsin-like and secretin-like GPCR-arrestin interactions and regulation. Kinetic signatures of RAS-BRAF engagement reveal isoform selectivity, oncogenic amplification, and mutation-dependent inhibitor resistance. RLIM-associated neurodevelopmental disorders: From clinical spectrum to molecular mechanisms.
wanfang
×
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学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
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