ArticleMolecular and cellular biology2004
Notch activation induces endothelial cell cycle arrest and participates in contact inhibition: role of p21Cip1 repression.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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Who cites it
116 citing papers in PubMed, 218 citations in OpenAlex.
- Passive nuclear transport deviates from Fickian behavior in prostate and breast cell types.Nucleus (Austin, Tex.) · 2026Article
- ATP-citrate lyase is a critical regulator of physiological and pathological angiogenesis.Angiogenesis · 2026Article
- Necessity of Notch3 signaling in myofiber maturation in a pluripotent stem cell transplant model.Skeletal muscle · 2026Article
- Same same but different? How blood and lymphatic vessels induce cell contact inhibition.Biochemical Society transactions · 2025Review
- HES1 potentiates high salt stress response as an enhancer of NFAT5-DNA binding.Communications biology · 2024Article
- Migration and proliferation drive the emergence of patterns in co-cultures of differentiating vascular progenitor cells.Mathematical biosciences and engineering : MBE · 2024Article
- Endothelial Cell Flow-Mediated Quiescence Is Temporally Regulated and Utilizes the Cell Cycle Inhibitor p27.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- BMPR2 Loss Activates AKT by Disrupting DLL4/NOTCH1 and PPARγ Signaling in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2024Article
- Exploring the Molecular and Developmental Dynamics of Endothelial Cell Differentiation.International journal of stem cells · 2024Review
- LSD1 Regulates Neurogenesis in Human Neural Stem Cells Through the Repression of Human-Enriched Extracellular Matrix and Cell Adhesion Genes.Stem cells (Dayton, Ohio) · 2024Article
- Disruption of DLL4/NOTCH1 Causes Dysregulated PPARγ/AKT Signaling in Pulmonary Arterial Hypertension.bioRxiv : the preprint server for biology · 2024Article
- Endothelial cell flow-mediated quiescence is temporally regulated and utilizes the cell cycle inhibitor p27.bioRxiv : the preprint server for biology · 2024Article
- FAM222A, Part of the BET-Regulated Basal Endothelial Transcriptome, Is a Novel Determinant of Endothelial Biology and Angiogenesis-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Notch Signaling in the Vasculature: Angiogenesis and Angiocrine Functions.Cold Spring Harbor perspectives in medicine · 2023Review
- Cell cycle exits and U-turns: Quiescence as multiple reversible forms of arrest.Faculty reviews · 2023Review
- Notch activation during early mesoderm induction modulates emergence of the T/NK cell lineage from human iPSCs.Stem cell reports · 2022Article
- Mechanosensitive Stem-Cell Genes and Klotho in Atherosclerotic Aortas: Regulating Spatially Deranged Expression Patterns Using Colchicine Regimens.Journal of clinical medicine · 2022Article
- Metabolic Reprogramming in Tumor Endothelial Cells.International journal of molecular sciences · 2022Review
- Automated in vivo compound screening with zebrafish and the discovery and validation of PD 81,723 as a novel angiogenesis inhibitor.Scientific reports · 2022Article
- Mutations inProceedings of the National Academy of Sciences of the United States of America · 2022Article
56 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Although previous studies demonstrate that appropriate Notch signaling is required during angiogenesis and in vascular homeostasis, the mechanisms by which Notch regulates vascular function remain to be elucidated. Here, we show that activation of the Notch pathway by the ligand Jagged1 reduces the proliferation of endothelial cells. Notch activation inhibits proliferation of endothelial cells in a cell-autonomous manner by inhibiting phosphorylation of the retinoblastoma protein (Rb). During cell cycle entry, p21Cip1 is upregulated in endothelial cells. Activated Notch inhibits mitogen-induced upregulation of p21Cip1 and delays cyclin D-cdk4-mediated Rb phosphorylation. Notch-dependent repression of p21Cip1 prevents nuclear localization of cyclin D and cdk4. The necessity of p21Cip1 for nuclear translocation of cyclin D-cdk4 and S-phase entry in endothelial cells was demonstrated by targeted downregulation of p21Cip1 by using RNA interference. We further demonstrate that when endothelial cells reach confluence, Notch is activated and p21Cip1 is downregulated. Inhibition of the Notch pathway at confluence prevents p21Cip1 downregulation and induces Rb phosphorylation. We suggest that Notch activation contributes to contact inhibition of endothelial cells, in part through repression of p21Cip1 expression.
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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.