ArticleMolecular & cellular proteomics : MCP2020
Molecular Basis of the Mechanisms Controlling MASTL.
Article in Molecular & cellular proteomics : MCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- A Comparative Analysis of the Action Mechanisms of Cannabidiol, Cannabigerol, and Cannabinol in Human Cholangiocarcinoma Cell Lines.Molecules (Basel, Switzerland) · 2026Article
- MAST Kinases' Function and Regulation: Insights from Structural Modeling and Disease Mutations.Biomedicines · 2025Article
- Computational analysis of regulatory regions in human protein kinases.Protein science : a publication of the Protein Society · 2023Article
- Role of Bile-Derived Extracellular Vesicles in Hepatocellular Proliferation after Partial Hepatectomy in Rats.International journal of molecular sciences · 2023Article
- The MASTL/PP2A cell cycle kinase-phosphatase module restrains PI3K-Akt activity in an mTORC1-dependent manner.The EMBO journal · 2023Article
- SILAC kinase screen identifies potential MASTL substrates.Scientific reports · 2022Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human MASTL (Microtubule-associated serine/threonine kinase-like) gene encodes an essential protein in the cell cycle. MASTL is a key factor preventing early dephosphorylation of M-phase targets of Cdk1/CycB. Little is known about the mechanism of MASTL activation and regulation. MASTL contains a non-conserved insertion of 550 residues within its activation loop, splitting the kinase domain, and making it unique. Here, we show that this non-conserved middle region (NCMR) of the protein is crucial for target specificity and activity. We performed a phosphoproteomic assay with different MASTL constructs identifying key phosphorylation sites for its activation and determining whether they arise from autophosphorylation or exogenous kinases, thus generating an activation model. Hydrogen/deuterium exchange data complements this analysis revealing that the C-lobe in full-length MASTL forms a stable structure, whereas the N-lobe is dynamic and the NCMR and C-tail contain few localized regions with higher-order structure. Our results indicate that truncated versions of MASTL conserving a cryptic C-Lobe in the NCMR, display catalytic activity and different targets, thus establishing a possible link with truncated mutations observed in cancer-related databases.
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