ArticleDevelopment (Cambridge, England)2016
Reck enables cerebrovascular development by promoting canonical Wnt signaling.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 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
33 citing papers in PubMed, 65 citations in OpenAlex.
- Cellular and signalling mechanisms that regulate the blood-brain barrier.Nature reviews. Molecular cell biology · 2026Review
- Conformational cycling of the Wntless transporter drives trafficking and secretion of Wnt morphogens.Nature communications · 2026Article
- Article
- The Roles of the Membrane-Anchored Glycoprotein RECK in Animal Development, Tumor Suppression, and Beyond.Life (Basel, Switzerland) · 2026Review
- Activation of Wnt/β-catenin in neural progenitor cells regulates blood-brain barrier development and promotes neuroinflammation.Scientific reports · 2025Article
- RECK as a Potential Crucial Molecule for the Targeted Treatment of Sepsis.Journal of inflammation research · 2025Review
- IL-1β disrupts the initiation of blood-brain barrier development by inhibiting endothelial Wnt/β-catenin signaling.iScience · 2024Article
- Article
- Postnatal Maturation of the Blood-Brain Barrier in Senescence-Accelerated OXYS Rats, Which Are Prone to an Alzheimer's Disease-like Pathology.International journal of molecular sciences · 2023Article
- A Frizzled4-LRP5 agonist promotes blood-retina barrier function by inducing a Norrin-like transcriptional response.iScience · 2023Article
- Brain endothelial cells acquire blood-brain barrier properties in the absence of Vegf-dependent CNS angiogenesis.Developmental biology · 2023Article
- Historical and current perspectives on blood endothelial cell heterogeneity in the brain.Cellular and molecular life sciences : CMLS · 2022Review
- Structure and Function of the Blood-Brain Barrier (BBB).Handbook of experimental pharmacology · 2022Article
- Molecular and Cellular Mechanisms of Vascular Development in Zebrafish.Life (Basel, Switzerland) · 2021Review
- Impact of Reck expression and promoter activity in neuronal in vitro differentiation.Molecular biology reports · 2021Article
- Controlling Wnt Signaling Specificity and Implications for Targeting WNTs Pharmacologically.Handbook of experimental pharmacology · 2021Article
- Structure of the RECK CC domain, an evolutionary anomaly.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Norrin restores blood-retinal barrier properties after vascular endothelial growth factor-induced permeability.The Journal of biological chemistry · 2020Article
- Cellular and Molecular Mechanisms of Spinal Cord Vascularization.Frontiers in physiology · 2020Review
- RECK in Neural Precursor Cells Plays a Critical Role in Mouse Forebrain Angiogenesis.iScience · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
20 authors at 5 institutions in 2 countries.
Funding
Abstract
The cerebral vasculature provides the massive blood supply that the brain needs to grow and survive. By acquiring distinctive cellular and molecular characteristics it becomes the blood-brain barrier (BBB), a selectively permeable and protective interface between the brain and the peripheral circulation that maintains the extracellular milieu permissive for neuronal activity. Accordingly, there is great interest in uncovering the mechanisms that modulate the formation and differentiation of the brain vasculature. By performing a forward genetic screen in zebrafish we isolated no food for thought (nft (y72)), a recessive late-lethal mutant that lacks most of the intracerebral central arteries (CtAs), but not other brain blood vessels. We found that the cerebral vascularization deficit of nft (y72) mutants is caused by an inactivating lesion in reversion-inducing cysteine-rich protein with Kazal motifs [reck; also known as suppressor of tumorigenicity 15 protein (ST15)], which encodes a membrane-anchored tumor suppressor glycoprotein. Our findings highlight Reck as a novel and pivotal modulator of the canonical Wnt signaling pathway that acts in endothelial cells to enable intracerebral vascularization and proper expression of molecular markers associated with BBB formation. Additional studies with cultured endothelial cells suggest that, in other contexts, Reck impacts vascular biology via the vascular endothelial growth factor (VEGF) cascade. Together, our findings have broad implications for both vascular and cancer biology.
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What OpenQuestion holds
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.