Liu Yanqing, Xiang Jiani, Gong Hang, Yu Tianxiong, Gao Meng, Huang Yongqi
Cooperative Innovation Center of Industrial Fermentation (Ministry of Education & Hubei Province), Hubei University of Technology, Wuhan, 430068, China.
Hubei Key Laboratory of Industrial Microbiology, Hubei University of Technology, Wuhan, 430068, China.
Protein J. 2025 Apr;44(2):113-132. doi: 10.1007/s10930-025-10261-0. Epub 2025 Feb 22.
The transactive response DNA binding protein 43 (TDP-43) is an RNA/DNA-binding protein that is involved in a number of cellular functions, including RNA processing and alternative splicing, RNA transport and translation, and stress granule assembly. It has attracted significant attention for being the primary component of cytoplasmic inclusions in patients with amyotrophic lateral sclerosis or frontotemporal dementia. Mounting evidence suggests that both cytoplasmic aggregation of TDP-43 and loss of nuclear TDP-43 function contribute to TDP-43 pathology. Furthermore, recent studies have demonstrated that TDP-43 is an important component of many constitutive or stress-induced biomolecular condensates. Dysregulation or liquid-to-gel transition of TDP-43 condensates can lead to alterations in TDP-43 function and the formation of TDP-43 amyloid fibrils. In this review, we summarize recent research progress on the structural characterization of TDP-43 and the TDP-43 phase transition. In particular, the roles that disease-associated genetic mutations, post-translational modifications, and extrinsic stressors play in the transitions among TDP-43 monomers, liquid condensates, solid condensates, and fibrils are discussed. Finally, we discuss the effectiveness of available regulators of TDP-43 phase separation and aggregation. Understanding the underlying mechanisms that drive the pathological transformation of TDP-43 could help develop therapeutic strategies for TDP-43 pathology.
反式激活反应DNA结合蛋白43(TDP - 43)是一种RNA/DNA结合蛋白,参与多种细胞功能,包括RNA加工和可变剪接、RNA运输与翻译以及应激颗粒组装。它因作为肌萎缩侧索硬化症或额颞叶痴呆患者细胞质内含物的主要成分而备受关注。越来越多的证据表明,TDP - 43的细胞质聚集和核TDP - 43功能丧失都促成了TDP - 43病理学。此外,最近的研究表明,TDP - 43是许多组成型或应激诱导的生物分子凝聚物的重要成分。TDP - 43凝聚物的失调或从液态到凝胶态的转变可导致TDP - 43功能改变以及TDP - 43淀粉样原纤维的形成。在这篇综述中,我们总结了TDP - 43结构表征和TDP - 43相变的最新研究进展。特别讨论了疾病相关基因突变、翻译后修饰和外在应激源在TDP - 43单体、液态凝聚物、固态凝聚物和原纤维之间转变中所起的作用。最后,我们讨论了现有的TDP - 43相分离和聚集调节剂的有效性。了解驱动TDP - 43病理转变的潜在机制有助于开发针对TDP - 43病理学的治疗策略。