ArticleStructure (London, England : 1993)2019
Structural Basis for Recruitment of DAPK1 to the KLHL20 E3 Ligase.
Article in Structure (London, England : 1993), 2019. 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, 36 citations in OpenAlex.
- De Novo-Designed Bifunctional Proteins for Targeted Protein Degradation.Journal of the American Chemical Society · 2026Article
- Identification of KLHL12 Ligands Using Fragment-Based Methods.Journal of medicinal chemistry · 2026Article
- Identification of ZFTA as a Novel KLHL20 Substrate and Mechanistic Insights Into Fuzzy Binding of Disordered Peptides via Biosensor Analysis and Computational Modelling.Chembiochem : a European journal of chemical biology · 2026Article
- Diverse and Bioactive Lactones from the Sri Lankan Mangrove-Derived FungusMarine drugs · 2026Article
- Temporal and Spatial Characterization of CUL3ACS chemical biology · 2025Article
- Structural mimicry of UM171 and neomorphic cancer mutants co-opts E3 ligase KBTBD4 for HDAC1/2 recruitment.Nature communications · 2025Article
- Article
- Proteolysis-targeting influenza vaccine strains induce broad-spectrum immunity and in vivo protection.Nature microbiology · 2025Article
- Modulation of DAPK1 expression by its alternative splice variant DAPK1-215 in cancer.Journal of translational medicine · 2025Article
- Predictive Role of Cluster Bean (Genes · 2024Article
- Sanggenon C inhibits cell proliferation and induces apoptosis by regulating the MIB1/DAPK1 axis in glioblastoma.MedComm · 2023Article
- A covalent BTK ternary complex compatible with targeted protein degradation.Nature communications · 2023Article
- A Perspective on Newly Emerging Proteolysis-Targeting Strategies in Antimicrobial Drug Discovery.Antibiotics (Basel, Switzerland) · 2022Review
- Disease-associated KBTBD4 mutations in medulloblastoma elicit neomorphic ubiquitylation activity to promote CoREST degradation.Cell death and differentiation · 2022Article
- A synthetic KLHL20 ligand to validate CUL3Genes & development · 2022Article
- Structural Model for Recruitment of RIT1 to the LZTR1 E3 Ligase: Evidences from an Integrated Computational Approach.Journal of chemical information and modeling · 2021Article
- E3 Ligase Ligands for PROTACs: How They Were Found and How to Discover New Ones.SLAS discovery : advancing life sciences R & D · 2021Review
- Challenges and Limitations of Targeting the Keap1-Nrf2 Pathway for Neurotherapeutics: Bach1 De-Repression to the Rescue.Frontiers in aging neuroscience · 2021Review
- Identification of a PGXPP degron motif in dishevelled and structural basis for its binding to the E3 ligase KLHL12.Open biology · 2020Article
- PROTACs- a game-changing technology.Expert opinion on drug discovery · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BTB-Kelch proteins form the largest subfamily of Cullin-RING E3 ligases, yet their substrate complexes are mapped and structurally characterized only for KEAP1 and KLHL3. KLHL20 is a related CUL3-dependent ubiquitin ligase linked to autophagy, cancer, and Alzheimer's disease that promotes the ubiquitination and degradation of substrates including DAPK1, PML, and ULK1. We identified an "LPDLV"-containing motif in the DAPK1 death domain that determines its recruitment and degradation by KLHL20. A 1.1-Å crystal structure of a KLHL20 Kelch domain-DAPK1 peptide complex reveals DAPK1 binding as a loose helical turn that inserts deeply into the central pocket of the Kelch domain to contact all six blades of the β propeller. Here, KLHL20 forms salt-bridge and hydrophobic interactions including tryptophan and cysteine residues ideally positioned for covalent inhibitor development. The structure highlights the diverse binding modes of β-propeller domains versus linear grooves and suggests a new target for structure-based drug design.
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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.