ArticleNature communications2016
β-Catenin C-terminal signals suppress p53 and are essential for artery formation.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- The β-catenin C terminus links Wnt and sphingosine-1-phosphate signaling pathways to promote vascular remodeling and atherosclerosis.Science advances · 2024Article
- Orally administered sodium nitrite prevents the increased α-1 adrenergic vasoconstriction induced by hypertension and promotes the S-nitrosylation of calcium/calmodulin-dependent protein kinase II.Biochemical pharmacology · 2023Article
- Mechanisms of fibrous cap formation in atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
- CKD-581 Downregulates Wnt/β-Catenin Pathway by DACT3 Induction in Hematologic Malignancy.Biomolecules & therapeutics · 2022Article
- The interaction of canonical Wnt/β-catenin signaling with protein lysine acetylation.Cellular & molecular biology letters · 2022Article
- The Atypical Cadherin FAT1 Limits Mitochondrial Respiration and Proliferation of Vascular Smooth Muscle Cells.Frontiers in cardiovascular medicine · 2022Review
- Direct targeting of β-catenin in the Wnt signaling pathway: Current progress and perspectives.Medicinal research reviews · 2021Review
- Inverse and reciprocal regulation of p53/p21 and Bmi-1 modulates vasculogenic differentiation of dental pulp stem cells.Cell death & disease · 2021Article
- Wnt/ß-catenin-mediated p53 suppression is indispensable for osteogenesis of mesenchymal progenitor cells.Cell death & disease · 2021Article
- Thyroid Cancer Stem-Like Cells: From Microenvironmental Niches to Therapeutic Strategies.Journal of clinical medicine · 2021Review
- PPARγ-p53-Mediated Vasculoregenerative Program to Reverse Pulmonary Hypertension.Circulation research · 2021Article
- Three-Dimensional Imaging Provides Detailed Atherosclerotic Plaque Morphology and Reveals Angiogenesis After Carotid Artery Ligation.Circulation research · 2020Article
- Notch pathway: a bistable inducer of biological noise?Cell communication and signaling : CCS · 2019Review
- Gene Co-expression Network and Copy Number Variation Analyses Identify Transcription Factors Associated With Multiple Myeloma Progression.Frontiers in genetics · 2019Article
- MicroRNA profiling of diabetic atherosclerosis in a rat model.European journal of medical research · 2018Article
- Role of p53 in the Regulation of the Inflammatory Tumor Microenvironment and Tumor Suppression.Cancers · 2018Review
- Inhibiting β-Catenin by β-Carboline-Type MDM2 Inhibitor for Pancreatic Cancer Therapy.Frontiers in pharmacology · 2018Article
- Inhibition of Smooth Muscle β-Catenin Hinders Neointima Formation After Vascular Injury.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- MicroRNA-27a promotes podocyte injury via PPARγ-mediated β-catenin activation in diabetic nephropathy.Cell death & disease · 2017Article
- Polycistronic tRNA and CRISPR guide-RNA enables highly efficient multiplexed genome engineering in human cells.Biochemical and biophysical research communications · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Increased activity of the tumour suppressor p53 is incompatible with embryogenesis, but how p53 is controlled is not fully understood. Differential requirements for p53 inhibitors Mdm2 and Mdm4 during development suggest that these control mechanisms are context-dependent. Artery formation requires investment of nascent endothelial tubes by smooth muscle cells (SMCs). Here, we find that embryos lacking SMC β-catenin suffer impaired arterial maturation and die by E12.5, with increased vascular wall p53 activity. β-Catenin-deficient SMCs show no change in p53 levels, but greater p53 acetylation and activity, plus impaired growth and survival. In vivo, SMC p53 inactivation suppresses phenotypes caused by loss of β-catenin. Mechanistically, β-catenin C-terminal interactions inhibit Creb-binding protein-dependent p53 acetylation and p53 transcriptional activity, and are required for artery formation. Thus in SMCs, the β-catenin C-terminus indirectly represses p53, and this function is essential for embryogenesis. These findings have implications for angiogenesis, tissue engineering and vascular disease.
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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.