ArticleCurrent molecular pharmacology2019
Convergence of Canonical and Non-Canonical Wnt Signal: Differential Kat3 Coactivator Usage.
Article in Current molecular pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- A Model of Butyrate Activity and Resistance in CRC.Journal of cellular and molecular medicine · 2025Review
- Significance of the Wnt signaling pathway in coronary artery atherosclerosis.Frontiers in cardiovascular medicine · 2024Article
- β-catenin inhibitors in cancer therapeutics: intricacies and way forward.Bioengineered · 2023Review
- Anti-inflammatory and antifibrotic effects of CBP/β-catenin inhibitor for hepatocytes: small molecular inhibitor, OP-724 possibly improves liver function.Medical molecular morphology · 2023Article
- ME2 Promotes Hepatocellular Carcinoma Cell Migration through Pyruvate.Metabolites · 2023Article
- Wnt4 increases the thickness of the epidermis in burn wounds by activating canonical Wnt signalling and decreasing the cell junctions between epidermal cells.Burns & trauma · 2023Article
- Roles of lncRNAs Mediating Wnt/β-Catenin Signaling in HCC.Frontiers in oncology · 2022Review
- Phosphorylation-Dependent Regulation of WNT/Beta-Catenin Signaling.Frontiers in oncology · 2022Review
- Differential Kat3 Usage Orchestrates the Integration of Cellular Metabolism with Differentiation.Cancers · 2021Article
- Morphological neurite changes induced by porcupine inhibition are rescued by Wnt ligands.Cell communication and signaling : CCS · 2021Article
- Pharmacologically Targeting the WNT/β-Catenin Signaling Cascade: Avoiding the Sword of Damocles.Handbook of experimental pharmacology · 2021Article
- Targeting the CBP/β-Catenin Interaction to Suppress Activation of Cancer-Promoting Pancreatic Stellate Cells.Cancers · 2020Article
- Enhanced Kat3A/Catenin transcription: a common mechanism of therapeutic resistance.Cancer drug resistance (Alhambra, Calif.) · 2019Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe ancient and highly evolutionarily conserved Wnt signaling pathway is critical in nearly all tissues and organs for an organism to develop normally from embryo through adult. Wnt signaling is generally parsed into "canonical" or Wnt-β-catenin-dependent or "non-canonical" β-catenin-independent signaling. Even though designating Wnt signaling as either canonical or noncanonical allows for easier conceptual discourse about this signaling pathway, in fact canonical and non-canonical Wnt crosstalk regulates complex nonlinear networks.
objectiveIn this perspective, we discuss the integration of canonical and non-canonical Wnt signaling via differential Kat3 (CBP and p300) coactivator usage, thereby regulating and coordinating gene expression programs associated with both proliferation and cellular differentiation and morphogenesis.
methodsPharmacologic inhibitors, cell culture, real-time PCR, chromatin immunoprecipitation, protein immunoprecipitation, Western blotting, reporter-luciferase, protein purification, site-directed mutagenesis, in vitro phosphorylation and binding assays, and immunofluorescence were utilized.
conclusionCoordinated integration between both canonical and non-canonical Wnt pathways appears to be crucial not only in the control of fundamental morphologic processes but also in the regulation of normal as well as pathologic events. Such integration between both canonical and non-canonical Wnt signaling is presumably effected via reversible phosphorylation mechanism (e.g., protein kinase C) to regulate differential β -catenin/Kat3 coactivator usage in order to coordinate proliferation with differentiation and adhesion.
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