Stress-induced Eukaryotic Translational Regulatory Mechanisms.


Journal

ArXiv
ISSN: 2331-8422
Titre abrégé: ArXiv
Pays: United States
ID NLM: 101759493

Informations de publication

Date de publication:
02 May 2024
Historique:
medline: 15 5 2024
pubmed: 15 5 2024
entrez: 15 5 2024
Statut: epublish

Résumé

The eukaryotic protein synthesis process entails intricate stages governed by diverse mechanisms to tightly regulate translation. Translational regulation during stress is pivotal for maintaining cellular homeostasis, ensuring the accurate expression of essential proteins crucial for survival. This selective translational control mechanism is integral to cellular adaptation and resilience under adverse conditions. This review manuscript explores various mechanisms involved in selective translational regulation, focusing on mRNA-specific and global regulatory processes. Key aspects of translational control include translation initiation, which is often a rate-limiting step, and involves the formation of the eIF4F complex and recruitment of mRNA to ribosomes. Regulation of translation initiation factors, such as eIF4E, eIF4E2, and eIF2, through phosphorylation and interactions with binding proteins, modulates translation efficiency under stress conditions. This review also highlights the control of translation initiation through factors like the eIF4F complex and the ternary complex and also underscores the importance of eIF2{\alpha} phosphorylation in stress granule formation and cellular stress responses. Additionally, the impact of amino acid deprivation, mTOR signaling, and ribosome biogenesis on translation regulation and cellular adaptation to stress is also discussed. Understanding the intricate mechanisms of translational regulation during stress provides insights into cellular adaptation mechanisms and potential therapeutic targets for various diseases, offering valuable avenues for addressing conditions associated with dysregulated protein synthesis.

Identifiants

pubmed: 38745702
pii: 2405.01664
pmc: PMC11092689
pii:

Types de publication

Preprint

Langues

eng

Auteurs

Classifications MeSH