ReviewCancer cell international2025
Regulation of disease signaling by YOD1: potential implications for therapeutic strategies.
Review in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed.
- The deubiquitinase YOD1 in renal tubular epithelial cells promotes diabetic kidney disease by stabilizing KEAP1.Acta pharmacologica Sinica · 2026Article
- The comparative diagnostic and therapeutic application value of FAPI PET/CT andFrontiers in oncology · 2026Review
- YOD1 promotes ferroptosis in acute lung injury by deubiquitination of NCOA4.Communications biology · 2025Article
- Integrative bulk and single-cell transcriptome analyses reveal integrated stress response-related biomarkers in periodontitis with experimental validation.Frontiers in immunology · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
YOD1 (OTUD2) is a pivotal deubiquitinating enzyme (DUB) of the Otubain family. It plays an essential role in protein degradation and the regulation of cell signal transduction, influencing various biological processes. The activity of YOD1 is mediated through its three structural domains: the Ubiquitin Regulatory X (UBX) domain, the Zinc Finger (ZNF) domain, and the Ovarian Tumor (OTU) domain. Specifically, the UBX domain regulates protein interactions, mitochondrial quality control, and immune responses. The ZNF domain facilitates protein localization, degradation, and cancer progression. The OTU domain drives deubiquitination, ensuring protein stability and regulating key signaling pathways. In recent years, increasing attention has been paid to the role of YOD1 in various diseases. Studies have demonstrated that YOD1 influences critical cellular activities such as proliferation, apoptosis, migration, and invasion by modulating key signaling pathways, including Hippo and TGF-β. Abnormal YOD1 expression is closely linked to the development of several cancers, including breast, liver, and lung cancer. Moreover, in non-malignant conditions such as inflammation and vascular diseases, YOD1 plays a key role in maintaining tissue homeostasis and repairing damaged tissues. Given its multifaceted roles in both tumorigenic and non-tumorigenic contexts, YOD1 is considered a promising target for therapeutic strategies. This review systematically analyzes the key signaling pathways regulated by YOD1, with a focus on elucidating its potential therapeutic value in cancer and various non-tumor diseases. Additionally, it provides a comprehensive review of the recent research progress in the field of YOD1 inhibitors. Our aim is to underscore the significance of YOD1 as a potential therapeutic target, to provide a theoretical basis for the development of innovative therapeutic strategies, and to offer new perspectives and insights for future related research.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.