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Article

Targeting ubiquitin signaling vulnerabilities in KEAP1-inactivated lung cancer.

The EMBO journal - 1 May 2026

Shah Varun Jayeshkumar, Hartmann Oliver, Wegner Martin, Prieto-Garcia Cristian, Kazi Rubina, von Heyl Zu Herrnsheim Viktoria, Wanli Amin, Mačinković Igor, Bohnacker Bianka, Husnjak Koraljka, Namgaladze Dmitry, Rosenfeldt Mathias, Kaulich Manuel, Diefenbacher Markus E, Dikic Ivan

Abstract excerpt

Lung cancer cells rely on protein homeostasis regulators, particularly the ubiquitin-proteasome system (UPS), to sustain malignancy. Genetic alterations in UPS components, such as E3 ubiquitin ligases (E3s) and deubiquitinating enzymes (DUBs), are common and create context-dependent therapeutic dependencies. To investigate how these genetic alterations drive tumor formation, we conducted CRISPR screens on...

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Topics

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Share to Cell Line, Tumor
Share to Carcinoma, Non-Small-Cell Lung

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation, Neoplastic

Share to Kelch-Like ECH-Associated Protein 1

Share to Lung Neoplasms

Share to NF-E2-Related Factor 2

Share to Ubiquitin

Share to Ubiquitin-Protein Ligases

Source

Open in PubMed Open full text

Identifiers

PMID: 41862643
DOI: 10.1038/s44318-026-00737-9
PMCID: PMC13144482

Genes

KEAP1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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Targeting ubiquitin signaling vulnerabilities in KEAP1-inactivated lung cancer.PMID 41862643Read ↗

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