ArticleMolecular and cellular biology2012
Loss of endothelial furin leads to cardiac malformation and early postnatal death.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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, 46 citations in OpenAlex.
- Furin inhibition protects against acute lung injury in a mouse model of Pseudomonas aeruginosa infection.American journal of respiratory cell and molecular biology · 2026Article
- Tissue Damage in Rheumatoid Arthritis Is Genetically Linked to Low Peptidylglycine Alpha-Amidating Monooxygenase Activity in Synovial Fibroblasts.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- The proprotein convertase FURIN is a novel aneurysm predisposition gene impairing TGF-β signalling.Cardiovascular research · 2024Article
- Functional Roles of Furin in Cardio-Cerebrovascular Diseases.ACS pharmacology & translational science · 2024Review
- Endothelin signaling in development.Development (Cambridge, England) · 2023Review
- Translational control of furina by an RNA regulon is important for left-right patterning, heart morphogenesis and cardiac valve function.Development (Cambridge, England) · 2023Article
- Association of single nucleotide polymorphisms with dyslipidemia and risk of metabolic disorders in the State of Qatar.Molecular genetics & genomic medicine · 2023Article
- Mouse Models of Human Proprotein Convertase Insufficiency.Endocrine reviews · 2021Review
- Proadrenomedullin N-Terminal 20 Peptides (PAMPs) Are Agonists of the Chemokine Scavenger Receptor ACKR3/CXCR7.ACS pharmacology & translational science · 2021Article
- Identification of Novel Genetic Regulatory Region for Proprotein Convertase FURIN and Interferon Gamma in T Cells.Frontiers in immunology · 2021Article
- Review
- Article
- Genetics of Congenital Heart Disease.Biomolecules · 2019Review
- FURIN Inhibition Reduces Vascular Remodeling and Atherosclerotic Lesion Progression in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Furin-mediated protein processing in infectious diseases and cancer.Clinical & translational immunology · 2019Review
- Furin, a transcriptional target of NKX2-5, has an essential role in heart development and function.PloS one · 2019Article
- Furin inhibitor protects against neuronal cell death induced by activated NMDA receptors.Scientific reports · 2018Article
- Proprotein convertase furin regulates osteocalcin and bone endocrine function.The Journal of clinical investigation · 2017Article
- Proprotein convertase inhibition: Paralyzing the cell's master switches.Biochemical pharmacology · 2017Review
- Thrombin activation of protein C requires prior processing by a liver proprotein convertase.The Journal of biological chemistry · 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 6 institutions in 3 countries.
Funding
Abstract
In mammals, seven proprotein convertases (PCs) cleave secretory proteins after basic residues, and four of them are called furin-like PCs: furin, PC5, PACE4, and PC7. In vitro, they share many substrates. However, furin is essential during development since deficient embryos die at embryonic day 11 and exhibit multiple developmental defects, particularly defects related to the function of endothelial cells. To define the role of furin in endothelial cells, an endothelial cell-specific knockout (ecKO) of the Furin gene was generated. Newborns die shortly after birth, indicating that furin is essential in these cells. Magnetic resonance imaging revealed that ecKO embryos exhibit ventricular septal defects (VSD) and/or valve malformations. In addition, primary cultures of wild-type and ecKO lung endothelial cells revealed that ecKO cells are unable to grow. Growth was efficiently rescued by extracellular soluble furin. Analysis of the processing of precursors of endothelin-1 (ET-1), adrenomedullin (Adm), transforming growth factor β1 (TGF-β1), and bone morphogenetic protein 4 (BMP4) confirmed that ET-1, Adm, and TGF-β1 are in vivo substrates of endothelial furin. Mature ET-1 and BMP4 forms were reduced by ~90% in ecKO purified endothelial cells from lungs.
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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.