题名 | Research progress of ubiquitin and ubiquitin-like signaling in Toxoplasma gondii |
作者 | |
发表日期 | 2024-06-30 |
发表期刊 | Acta Tropica 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Journal Article ; Review |
关键词 | Deubiquitinating enzyme Toxoplasma gondii Ubiquitin ligase (E3) Ubiquitin signaling Ubiquitin-conjugating enzyme (E2) Ubiquitin-like proteins, Ubiquitin-activating enzyme (E1) |
其他关键词 | DEUBIQUITINATING ENZYME ; PROTEIN ; DEGRADATION ; PROTEASOME ; MEMBRANE ; LIGASES ; NEDD8 ; PATHOGEN ; EXOSOMES ; SYSTEMS |
摘要 | Toxoplasmosis, a zoonotic parasitic disease caused by Toxoplasma gondii (T. gondii), is prevalent worldwide. The fact should be emphasized that a considerable proportion of individuals infected with T. gondii may remain asymptomatic; nevertheless, the condition can have severe implications for pregnant women or immunocompromised individuals. The current treatment of toxoplasmosis primarily relies on medication; however, traditional anti-toxoplasmosis drugs exhibit significant limitations in terms of efficacy, side effects, and drug resistance. The life cycles of T. gondii are characterized by distinct stages and its body morphology goes through dynamic alterations during the growth cycle that are intricately governed by a wide array of post-translational modifications (PTMs). Ubiquitin (Ub) signaling and ubiquitin-like (Ubl) signaling are two crucial post-translational modification pathways within cells, regulating protein function, localization, stability, or interactions by attaching Ub or ubiquitin-like proteins (Ubls) to target proteins. While these signaling mechanisms share some functional similarities, they have distinct regulatory mechanisms and effects. T. gondii possesses both Ub and Ubls and plays a significant role in regulating the parasite's life cycle and maintaining its morphology through PTMs of substrate proteins. Investigating the role and mechanism of protein ubiquitination in T. gondii will provide valuable insights for preventing and treating toxoplasmosis. This review explores the distinctive characteristics of Ub and Ubl signaling in T. gondii, with the aim of inspiring research ideas for the identification of safer and more effective drug targets against toxoplasmosis. |
资助项目 | National Natural Science Foundation of China [81971962, 82172303, 82372282]; Key Project of Natural Science Foundation of Zhejiang Province [LZ22H190001]; Talent Project of Wenzhou Medical University [89222021] |
出版者 | ELSEVIER |
ISSN | 0001-706X |
EISSN | 1873-6254 |
卷号 | 257 |
DOI | 10.1016/j.actatropica.2024.107283 |
页数 | 9 |
WOS类目 | Parasitology ; Tropical Medicine |
WOS研究方向 | Parasitology ; Tropical Medicine |
WOS记录号 | WOS:001265793600001 |
收录类别 | PUBMED ; SCIE ; SCOPUS |
URL | 查看原文 |
PubMed ID | 38955322 |
SCOPUSEID | 2-s2.0-85197393631 |
通讯作者地址 | [Mou, Ya-ni]Wenzhou Med Univ, Sch Basic Med Sci, Dept Parasitol, Wenzhou 325035, Zhejiang, Peoples R China. |
Scopus学科分类 | Parasitology;Infectious Diseases |
SCOPUS_ID | SCOPUS_ID:85197393631 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/215671 |
专题 | 基础医学院(机能实验教学中心)_病原生物学与免疫学系_医学寄生虫学 |
作者单位 | 1.Department of Parasitology, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang, PR China.; 2.Department of Parasitology, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang, PR China. Electronic address: mouyaniq@163.com. |
第一作者单位 | 基础医学院(机能实验教学中心)_病原生物学与免疫学系_医学寄生虫学 |
通讯作者单位 | 基础医学院(机能实验教学中心)_病原生物学与免疫学系_医学寄生虫学 |
第一作者的第一单位 | 基础医学院(机能实验教学中心)_病原生物学与免疫学系_医学寄生虫学 |
推荐引用方式 GB/T 7714 | Qi-Xin Zhou,Si-Yu Tian,Xiao-Na Liu,et al. Research progress of ubiquitin and ubiquitin-like signaling in Toxoplasma gondii[J]. Acta Tropica,2024,257. |
APA | Qi-Xin Zhou., Si-Yu Tian., Xiao-Na Liu., Shi-Peng Xiang., Xue-Jing Lin., ... & Ya-Ni Mou. (2024). Research progress of ubiquitin and ubiquitin-like signaling in Toxoplasma gondii. Acta Tropica, 257. |
MLA | Qi-Xin Zhou,et al."Research progress of ubiquitin and ubiquitin-like signaling in Toxoplasma gondii".Acta Tropica 257(2024). |
条目包含的文件 | 条目无相关文件。 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论