ArticleMolecular cell2020
Structural Insights into Pseudokinase Domains of Receptor Tyrosine Kinases.
Article in Molecular cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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Who cites it
58 citing papers in PubMed.
- PTK7 scaffolds DNA-PKcs to promote DNA damage response and immune evasion in triple-negative breast cancer.Oncogene · 2026Article
- SLV-404, an anti-RYK antibody-drug conjugate, is effective in Richter transformation patient-derived xenografts.HemaSphere · 2026Article
- Modulating pseudokinase conformation from the ATP-binding site.Structure (London, England : 1993) · 2026Article
- Black Sheep: Pseudokinases Bucking the Trend to Reveal Non-Catalytic Kinase Functions.IUBMB life · 2026Review
- Quantum Reactivity-Guided Optimization of ATP-Competitive Ligands through Multiscale Simulation.ACS physical chemistry Au · 2026Article
- The multifaceted roles of receptor tyrosine pseudokinases in cellular signalling.Biochemical Society transactions · 2026Review
- Structure-Based Design, Synthesis, and Evaluation of Novel Ponatinib Derivatives With a Significantly Altered Selectivity Profile.ChemMedChem · 2026Article
- Targeting ROR1 with humanized antibody drug conjugates and cytokine fusion proteins for cancer therapy.iScience · 2026Article
- ROR1-PI3K/AKT signaling drives adaptive resistance to cell cycle blockade in TP53 mutated ovarian cancer.Cell death & disease · 2026Article
- ROR1 protein: a pseudokinase at the crossroads of cancer progression and therapy.Molecular biology reports · 2026Review
- Structural basis for MEKK2 dimerization and substrate recognition.Nature communications · 2025Article
- Therapeutic targeting of the protein tyrosine kinase-7 in cancer: an overview.The oncologist · 2025Review
- Novel Para-Phenylenediamine-Based Derivatives as Receptor Tyrosine Kinase-like Orphan Receptor 1 (ROR1) Inhibitors: An In Vitro Preliminary Characterization.ChemMedChem · 2025Article
- The Rho GEF Trio functions in contact inhibition of locomotion of neural crest cells by interacting with Ptk7.Development (Cambridge, England) · 2025Article
- The Medicago truncatula LYR4 intracellular domain serves as a scaffold in immunity signaling independent of its phosphorylation activity.The New phytologist · 2025Article
- Article
- The Multi-Kinase Inhibitor GZD824 (Olverembatinib) Shows Pre-Clinical Efficacy in Endometrial Cancer.Cancer medicine · 2025Article
- Unlocking the potential: advancements and future horizons in ROR1-targeted cancer therapies.Science China. Life sciences · 2024Review
- Non-canonical Wnt signaling triggered by WNT2B drives adrenal aldosterone production.bioRxiv : the preprint server for biology · 2024Article
- Allosteric activation of the co-receptor BAK1 by the EFR receptor kinase initiates immune signaling.eLife · 2024Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Despite their apparent lack of catalytic activity, pseudokinases are essential signaling molecules. Here, we describe the structural and dynamic properties of pseudokinase domains from the Wnt-binding receptor tyrosine kinases (PTK7, ROR1, ROR2, and RYK), which play important roles in development. We determined structures of all pseudokinase domains in this family and found that they share a conserved inactive conformation in their activation loop that resembles the autoinhibited insulin receptor kinase (IRK). They also have inaccessible ATP-binding pockets, occluded by aromatic residues that mimic a cofactor-bound state. Structural comparisons revealed significant domain plasticity and alternative interactions that substitute for absent conserved motifs. The pseudokinases also showed dynamic properties that were strikingly similar to those of IRK. Despite the inaccessible ATP site, screening identified ATP-competitive type-II inhibitors for ROR1. Our results set the stage for an emerging therapeutic modality of "conformational disruptors" to inhibit or modulate non-catalytic functions of pseudokinases deregulated in disease.
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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.