DHX38

更新于：2025-05-07

基本信息

别名

ATP-dependent RNA helicase DHX38、DDX38、DEAH box protein 38

+ [7]

简介

Probable ATP-binding RNA helicase (Probable). Involved in pre-mRNA splicing as component of the spliceosome (PubMed:29301961, PubMed:9524131).

关联

100 项与 DHX38 相关的临床结果

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100 项与 DHX38 相关的转化医学

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0 项与 DHX38 相关的专利（医药）

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113

项与 DHX38 相关的文献（医药）

2025-12-31·RNA Biology

Prp16 enables efficient splicing of introns with diverse exonic consensus elements in the short-intron rich Cryptococcus neoformans transcriptome

Article

作者: Saraf, Niharika ; Negi, Manendra Singh ; Vijayraghavan, Usha ; Krishnan, Vishnu Priya

DEAH box splicing helicase Prp16 in budding yeast governs spliceosomal remodelling from the branching conformation (C complex) to the exon ligation conformation (C* complex). In this study, we examined the genome-wide functions of Prp16 in the short intron-rich genome of the basidiomycete yeast Cryptococcus neoformans. The presence of multiple introns per transcript with intronic features that are more similar to those of higher eukaryotes makes it a promising model for studying spliceosomal splicing. Using a promoter-shutdown conditional Prp16 knockdown strain, we uncovered genome-wide but substrate-specific roles in C. neoformans splicing. The splicing functions of Prp16 are dependent on helicase motifs I and II, which are conserved motifs for helicase activity. A small subset of introns spliced independent of Prp16 activity was investigated to discover that exonic sequences at the 5' splice site (5'SS) and 3' splice site (3'SS) with stronger affinity for U5 loop 1 are a common feature in these introns. Furthermore, short (60-100nts) and ultrashort introns (<60nts) prevalent in the C. neoformans transcriptome were more sensitive to Prp16 knockdown than longer introns, indicating that Prp16 is required for the efficient splicing of short and ultrashort introns. We propose that stronger U5 snRNA-pre-mRNA interactions enable efficient transition of the spliceosome from the first to the second catalytic confirmation in Prp16 knockdown, particularly for short introns and introns with suboptimal features. This study provides insights into fine-tuning spliceosomal helicase function with variations in cis-element features.

2025-01-01·Zoological Research

Single-cell sequencing analysis reveals the essential role of the m<sup>6</sup>A reader YTHDF1 in retinal visual function by regulating TULP1 and DHX38 translation

Article

作者: Jiang, Xiao-Yan ; Fan, Yu-Di ; Zhu, Xian-Jun ; Yang, Ye-Ming ; Liu, Wen-Jing ; Liu, Guo ; Lei, Bo ; Yao, Shun ; Sun, Kuan-Xiang ; Chen, Jun-Yao

mRNA的N6-甲基腺苷（m6A）修饰作为一种重要的转录后修饰方式，在mRNA代谢调控中发挥关键作用。m6A阅读蛋白YTHDF1已被证实能增强大脑中被m6A修饰mRNA的翻译效率，从而在学习记忆过程中至关重要。然而，其在成熟视网膜和视觉中的作用仍不明确。该研究利用基因敲除模型揭示了YTHDF1在维持视网膜功能中的新作用：YTHDF1缺失导致暗适应视网膜电生理（ERG）反应受损，并伴随进行性视网膜变性。进一步深入分析发现，Ythdf1缺失主要引起视杆细胞病变丢失，但其纤毛功能未受影响。单细胞RNA测序（scRNA-seq）分析揭示了YTHDF1缺失导致视网膜中各类细胞的分子水平变化。通过结合甲基化RNA免疫共沉淀测序（MeRIP-seq）和RNA免疫共沉淀测序（RIP-seq），最终确定了遗传性视网膜变性疾病关键基因Tulp1和Dhx38作为YTHDF1在视网膜中的调控靶点。YTHDF1能够识别并结合 Tulp1和 Dhx38 mRNA编码区（CDS）上的m6A修饰位点，从而增强其翻译效率。该研究揭示了YTHDF1在维持视功能中的重要作用，阐明了m6A读取蛋白在视网膜变性中的新型调控机制，并为视网膜病变的治疗策略开发提供了潜在靶点。.

2024-12-04·RNA Biology3区 · 生物学

Blocking late stages of splicing quickly limits pre-spliceosome assembly in vivo

3区 · 生物学

Article

作者: Mendoza-Ochoa, Gonzalo I. ; Beggs, Jean D. ; Barrass, J. David ; Maudlin, Isabella E.

Pre-messenger RNA splicing involves multi-step assembly of the large spliceosome complexes that catalyse the two consecutive trans-esterification reactions, resulting in intron removal. There is evidence that proof-reading mechanisms monitor the fidelity of this complex process. Transcripts that fail these fidelity tests are thought to be directed to degradation pathways, permitting the splicing factors to be recycled. While studying the roles of splicing factors in vivo, in budding yeast, we performed targeted depletion of individual proteins, and analysed the effect on co-transcriptional spliceosome assembly and splicing efficiency. Unexpectedly, depleting factors such as Prp16 or Prp22, that are known to function at the second catalytic step or later in the splicing pathway, resulted in a defect in the first step of splicing, and accumulation of arrested spliceosomes. Through a kinetic analysis of newly synthesized RNA, we observed that a second step splicing defect (the primary defect) was rapidly followed by the first step of splicing defect. Our results show that knocking down a splicing factor can quickly lead to a recycling defect with splicing factors sequestered in stalled complexes, thereby limiting new rounds of splicing. We demonstrate that this 'feed-back' effect can be minimized by depleting the target protein more gradually or only partially, allowing a better separation between primary and secondary effects. Our findings indicate that splicing surveillance mechanisms may not always cope with spliceosome assembly defects, and suggest that work involving knock-down of splicing factors or components of other large complexes should be carefully monitored to avoid potentially misleading conclusions.

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