ArticleDevelopment (Cambridge, England)2015
UXT potentiates angiogenesis by attenuating Notch signaling.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Zebrafish model for studying vascular development and vascular-related disease.Frontiers in cell and developmental biology · 2026Review
- Targeting the Notch signaling pathway: molecular mechanisms and therapeutic strategies for cardiac repair after myocardial infarction.Frontiers in cardiovascular medicine · 2025Review
- UXT attenuates the CGAS-STING1 signaling by targeting STING1 for autophagic degradation.Autophagy · 2023Article
- Genomic architecture and functional unit of mimicry supergene in female limited Batesian mimicPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Mice deficient in UXT exhibit retinitis pigmentosa-like features via aberrant autophagy activation.Autophagy · 2021Article
- UXT chaperone prevents proteotoxicity by acting as an autophagy adaptor for p62-dependent aggrephagy.Nature communications · 2021Article
- The SARS-CoV-2 receptor and other key components of the Renin-Angiotensin-Aldosterone System related to COVID-19 are expressed in enterocytes in larval zebrafish.Biology open · 2021Article
- Rab5c-mediated endocytic trafficking regulates hematopoietic stem and progenitor cell development via Notch and AKT signaling.PLoS biology · 2020Article
- Parallel evolution of Batesian mimicry supergene in twoScience advances · 2018Article
- The Transcription Factor Bach1 Suppresses the Developmental Angiogenesis of Zebrafish.Oxidative medicine and cellular longevity · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenesis is spatially and temporally orchestrated by a myriad of signaling pathways, including the Notch signaling pathway. Here, we identified UXT as an evolutionarily conserved and developmentally expressed protein, indispensable for intersegmental vessel (ISV) formation in zebrafish. Deficiency of UXT in zebrafish embryos results in shorter ISVs, loss of tip cell behavior, and impairment of endothelial cell migration and division. Significantly, UXT attenuates the expression of the Notch-responsive genes in vitro and in vivo. Mechanistically, UXT binds to the promoters of the Notch signaling target genes and specifically interacts with the transactivation region domain of the Notch intracellular domain (NICD), impairing the interaction between NICD and the transcription factor RBP-Jκ endogenously. This prevents RBP-Jκ/CSL from activation and thus inhibits the consequent gene inductions. Furthermore, blockade of Notch signaling rescues the angiogenesis defect caused by UXT knockdown both in vitro and in vivo. Taken together, the data presented in this study characterize UXT as a novel repressor of Notch signaling, shedding new light on the molecular regulation of angiogenesis.
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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.