ArticleeLife2022
Integrating multi-omics data reveals function and therapeutic potential of deubiquitinating enzymes.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Global analysis of cancer cell responses to USP9X inhibition.The EMBO journal · 2026Article
- Article
- Targeting protein protein interactions and their modulators to enable new therapeutic strategies for human diseases.NPJ systems biology and applications · 2026Review
- Ubiquitin-Modifying Enzymes as Cell-Fate Regulators in Intestinal Inflammation.International journal of biological sciences · 2026Review
- USP38 functions as an oncoprotein by downregulating the p53 pathway through deubiquitination and stabilization of MDM2.Cell death and differentiation · 2025Article
- Review
- Chemical tools to define and manipulate interferon-inducible Ubl protease USP18.Nature communications · 2025Article
- From Lab to Clinic: Success Stories of Repurposed Drugs in Treating Major Diseases.Advances in pharmacological and pharmaceutical sciences · 2025Review
- Disrupting USP39 deubiquitinase function impairs the survival and migration of multiple myeloma cells through ZEB1 degradation.Journal of experimental & clinical cancer research : CR · 2024Article
- Comprehensive pan-cancer analysis indicates UCHL5 as a novel cancer biomarker and promotes cervical cancer progression through the Wnt signaling pathway.Biology direct · 2024Article
- Open-source electrophilic fragment screening platform to identify chemical starting points for UCHL1 covalent inhibitors.SLAS discovery : advancing life sciences R & D · 2024Article
- PTPN23-dependent ESCRT machinery functions as a cell death checkpoint.Nature communications · 2024Article
- Introducing dysfunctional Protein-Protein Interactome (dfPPI) - A platform for systems-level protein-protein interaction (PPI) dysfunction investigation in disease.Current opinion in structural biology · 2024Review
- Loss of the proteasomal deubiquitinase USP14 induces growth defects and a senescence phenotype in colorectal cancer cells.Scientific reports · 2024Article
- Chemical tools to define and manipulate interferon-inducible Ubl protease USP18.bioRxiv : the preprint server for biology · 2024Article
- Characterization of MYBL1 Gene in Triple-Negative Breast Cancers and the Genes' Relationship to Alterations Identified at the Chromosome 8q Loci.International journal of molecular sciences · 2024Article
- Potential Otubain1 Inhibitor, an Approach for a Treatment against Breast Cancer.International journal of molecular and cellular medicine · 2024Article
- Ubiquitin-specific peptidase 1: assessing its role in cancer therapy.Clinical and experimental medicine · 2023Review
- Multi-Omics Integration for the Design of Novel Therapies and the Identification of Novel Biomarkers.Proteomes · 2023Review
- USP32 deubiquitinase: cellular functions, regulatory mechanisms, and potential as a cancer therapy target.Cell death discovery · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Deubiquitinating enzymes (DUBs), ~100 of which are found in human cells, are proteases that remove ubiquitin conjugates from proteins, thereby regulating protein turnover. They are involved in a wide range of cellular activities and are emerging therapeutic targets for cancer and other diseases. Drugs targeting USP1 and USP30 are in clinical development for cancer and kidney disease respectively. However, the majority of substrates and pathways regulated by DUBs remain unknown, impeding efforts to prioritize specific enzymes for research and drug development. To assemble a knowledgebase of DUB activities, co-dependent genes, and substrates, we combined targeted experiments using CRISPR libraries and inhibitors with systematic mining of functional genomic databases. Analysis of the Dependency Map, Connectivity Map, Cancer Cell Line Encyclopedia, and multiple protein-protein interaction databases yielded specific hypotheses about DUB function, a subset of which were confirmed in follow-on experiments. The data in this paper are browsable online in a newly developed DUB Portal and promise to improve understanding of DUBs as a family as well as the activities of incompletely characterized DUBs (e.g. USPL1 and USP32) and those already targeted with investigational cancer therapeutics (e.g. USP14, UCHL5, and USP7).
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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.