ArticleBiochemical Society transactions2014
New strategies to inhibit KEAP1 and the Cul3-based E3 ubiquitin ligases.
Article in Biochemical Society transactions, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Interplay between NRF2 post-translational modifications and protein-protein interactions: Perspectives from emerging structural and functional evidence.Archives of biochemistry and biophysics · 2026Review
- Galectin 3-binding protein suppresses PRRSV replication via Cullin3-mediated ubiquitination degradation of non-structural protein 12.Journal of virology · 2025Article
- Vesicular mechanisms of drug resistance in apicomplexan parasites.Microbiology and molecular biology reviews : MMBR · 2025Review
- Article
- Nrf2-mediated ferroptosis inhibition: a novel approach for managing inflammatory diseases.Inflammopharmacology · 2024Review
- Structural and biochemical characterization establishes a detailed understanding of KEAP1-CUL3 complex assembly.Free radical biology & medicine · 2023Article
- Mitigation of Cardiovascular Disease and Toxicity through NRF2 Signalling.International journal of molecular sciences · 2023Review
- Single-cell transcriptomics of human iPSC differentiation dynamics reveal a core molecular network of Parkinson's disease.Communications biology · 2022Article
- Review
- Discovery of a Nitric Oxide-Responsive Protein inMolecules (Basel, Switzerland) · 2019Article
- Article
- AMP-activated protein kinase protects against necroptosis via regulation of Keap1-PGAM5 complex.International journal of cardiology · 2018Article
- High-throughput RNA sequencing reveals structural differences of orthologous brain-expressed genes between western lowland gorillas and humans.The Journal of comparative neurology · 2016Article
- Nrf2 Is an Attractive Therapeutic Target for Retinal Diseases.Oxidative medicine and cellular longevity · 2016Review
- Structural basis of Keap1 interactions with Nrf2.Free radical biology & medicine · 2015Review
- Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia.EMBO molecular medicine · 2015Article
- Expression profile of a Caenorhabditis elegans model of adult neuronal ceroid lipofuscinosis reveals down regulation of ubiquitin E3 ligase components.Scientific reports · 2015Article
- Non-electrophilic modulators of the canonical Keap1/Nrf2 pathway.Bioorganic & medicinal chemistry letters · 2015Review
- Targeting Cullin-RING E3 ubiquitin ligases for drug discovery: structure, assembly and small-molecule modulation.The Biochemical journal · 2015Review
- Structural and biochemical characterization of the KLHL3-WNK kinase interaction important in blood pressure regulation.The Biochemical journal · 2014Article
Corrections and comments
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2 authors.
Funding
Abstract
E3 ubiquitin ligases that direct substrate proteins to the ubiquitin-proteasome system are promising, though largely unexplored drug targets both because of their function and their remarkable specificity. CRLs [Cullin-RING (really interesting new gene) ligases] are the largest group of E3 ligases and function as modular multisubunit complexes constructed around a Cullin-family scaffold protein. The Cul3-based CRLs uniquely assemble with BTB (broad complex/tramtrack/bric-à-brac) proteins that also homodimerize and perform the role of both the Cullin adapter and the substrate-recognition component of the E3. The most prominent member is the BTB-BACK (BTB and C-terminal Kelch)-Kelch protein KEAP1 (Kelch-like ECH-associated protein 1), a master regulator of the oxidative stress response and a potential drug target for common conditions such as diabetes, Alzheimer's disease and Parkinson's disease. Structural characterization of BTB-Cul3 complexes has revealed a number of critical assembly mechanisms, including the binding of an N-terminal Cullin extension to a bihelical '3-box' at the C-terminus of the BTB domain. Improved understanding of the structure of these complexes should contribute significantly to the effort to develop novel therapeutics targeted to CRL3-regulated pathways.
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