ArticleScientific reports2016
Structural basis for autoinhibition and its relief of MOB1 in the Hippo pathway.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Understanding the Mechanisms of Human Liver Regeneration via Characterization of Circulating Extracellular Vesicles.BioMed research international · 2026Article
- Evaluation of Quantification and Normalization Strategies for Phosphoprotein Phosphatase Affinity Proteomics: Application to Breast Cancer Signaling.Journal of proteome research · 2023Article
- Molecular Alterations in Malignant Pleural Mesothelioma: A Hope for Effective Treatment by Targeting YAP.Targeted oncology · 2022Review
- Oxidative stress-CBP axis modulates MOB1 acetylation and activates the Hippo signaling pathway.Nucleic acids research · 2022Article
- Hippo signaling pathway in companion animal diseases, an under investigated signaling cascade.The veterinary quarterly · 2021Article
- Cryo-EM structure of the Hippo signaling integrator human STRIPAK.Nature structural & molecular biology · 2021Article
- RNA-binding protein Musashi2 regulates Hippo signaling via SAV1 and MOB1 in pancreatic cancer.Medical oncology (Northwood, London, England) · 2020Article
- TheProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Ndr/Lats Kinases Bind Specific Mob-Family Coactivators through a Conserved and Modular Interface.Biochemistry · 2020Article
- Lysine demethylase 2 (KDM2B) regulates hippo pathway via MOB1 to promote pancreatic ductal adenocarcinoma (PDAC) progression.Journal of experimental & clinical cancer research : CR · 2020Article
- Mob Family Proteins: Regulatory Partners in Hippo and Hippo-Like Intracellular Signaling Pathways.Frontiers in cell and developmental biology · 2020Review
- Review
- Polarity in Ciliate Models: From Cilia to Cell Architecture.Frontiers in cell and developmental biology · 2019Review
- Activation mechanisms of the Hippo kinase signaling cascade.Bioscience reports · 2018Review
- Structural Basis for Auto-Inhibition of the NDR1 Kinase Domain by an Atypically Long Activation Segment.Structure (London, England : 1993) · 2018Article
- Stable MOB1 interaction with Hippo/MST is not essential for development and tissue growth control.Nature communications · 2017Article
- Regulation of Protein Interactions byMolecular & cellular proteomics : MCP · 2017Article
- MST1/MST2 Protein Kinases: Regulation and Physiologic Roles.Biochemistry · 2016Review
- CORO7 functions as a scaffold protein for the core kinase complex assembly of the Hippo pathway.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MOB1 protein is a key regulator of large tumor suppressor 1/2 (LATS1/2) kinases in the Hippo pathway. MOB1 is present in an autoinhibited form and is activated by MST1/2-mediated phosphorylation, although the precise mechanisms responsible for autoinhibition and activation are unknown due to lack of an autoinhibited MOB1 structure. Here, we report on the crystal structure of full-length MOB1B in the autoinhibited form and a complex between the MOB1B core domain and the N-terminal regulation (NTR) domain of LATS1. The structure of full-length MOB1B shows that the N-terminal extension forms a short β-strand, the SN strand, followed by a long conformationally flexible positively-charged linker and α-helix, the Switch helix, which blocks the LATS1 binding surface of MOB1B. The Switch helix is stabilized by β-sheet formation of the SN strand with the S2 strand of the MOB1 core domain. Phosphorylation of Thr12 and Thr35 residues structurally accelerates dissociation of the Switch helix from the LATS1-binding surface by the "pull-the-string" mechanism, thereby enabling LATS1 binding.
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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.