ArticleNature communications2025
Anti-proteolytic regulation of KRAS by USP9X/NDRG3 in KRAS-driven cancer development.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Rewiring KRAS-driven cancers through the ubiquitin-proteasome system: therapeutic opportunities with a focus on deubiquitinase.Experimental & molecular medicine · 2026Review
- Bioinformatics screening identifies USP9X as a pathogenic gene underlying thyroid and breast cancer comorbidity.Journal of molecular histology · 2026Article
- NDRG3 is essential for sustaining antigen-driven T cell responses by protecting against restimulation-induced cell death.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Cancers with activating mutations of KRAS show a high prevalence but remain intractable, requiring innovative strategies to overcome the poor targetability of KRAS. Here, we report that KRAS expression is post-translationally up-regulated through deubiquitination when the scaffolding function of NDRG3 (N-Myc downstream-regulated gene 3) promotes specific interaction between KRAS and a deubiquitinating enzyme, USP9X. In KRAS-mutant cancer cells KRAS protein expression, downstream signaling, and cell growth are highly dependent on NDRG3. In conditional Kras
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