ArticleOpen biology2025
O-GlcNAcylation of the intellectual disability protein DDX3X exerts proteostatic cell cycle control.
Article in Open biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Loss of O-GlcNAc transferase activity impairs the dynamic formation of protective stress granules in ischemic cardiomyocytes.The Biochemical journal · 2026Article
- Protein O-GlcNAcylation in Health and Diseases.MedComm · 2025Review
- O-GlcNAcylation of the intellectual disability protein DDX3X exerts proteostatic cell cycle control.Open biology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
O-GlcNAcylation of intracellular proteins is a key regulator of diverse cellular and developmental processes. Previous studies have demonstrated the acute sensitivity of cell cycle progression to chemical and genetic manipulation of O-GlcNAc homeostasis. However, the mechanisms by which O-GlcNAc regulates the cell cycle remain poorly understood. Here, we report Ser584 O-GlcNAcylation of the RNA helicase DDX3X, a microcephaly associated protein, as a proteostatic mechanism regulating S-phase entry. Loss of Ser584 O-GlcNAcylation promoted degradation of DDX3X by the proteasome, resulting in reduced expression of the DDX3X target gene
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Registered trials
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