ArticlePloS one2015
Galnt1 is required for normal heart valve development and cardiac function.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 50 citations in OpenAlex.
- O-GlcNAcylation as a Metabolic Integrator in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2026Review
- Decoding the complex substrate specificities of GalNAc-Ts.Glycobiology · 2025Review
- ADAMTS7, a target in atherosclerosis, cooperates with its homolog ADAMTS12 to protect against myxomatous valve degeneration.Journal of molecular and cellular cardiology plus · 2025Article
- A cardiac transcriptional enhancer is repurposed during regeneration to activate an anti-proliferative program.Development (Cambridge, England) · 2025Article
- An unusual dual sugar-binding lectin domain controls the substrate specificity of a mucin-type O-glycosyltransferase.Science advances · 2024Article
- Functional dissection of human cardiac enhancers and noncoding de novo variants in congenital heart disease.Nature genetics · 2024Article
- Screening and regulatory mechanism exploration of M1 macrophage polarization and efferocytosis-related biomarkers in coronary heart disease.Frontiers in cardiovascular medicine · 2024Article
- Comparative Proteomic and Phosphoproteomic Analyses Reveal Molecular Signatures of Myocardial Infarction and Transverse Aortic Constriction in Aged Mouse Models.Cardiology research and practice · 2024Article
- Dynamic expression of mucins and the genes controlling mucin-type O-glycosylation within the mouse respiratory system.Glycobiology · 2023Article
- Identification of global inhibitors of cellular glycosylation.Nature communications · 2023Article
- In vivo models of mucin biosynthesis and function.Advanced drug delivery reviews · 2022Review
- GRASP depletion-mediated Golgi fragmentation impairs glycosaminoglycan synthesis, sulfation, and secretion.Cellular and molecular life sciences : CMLS · 2022Article
- PolypeptideMolecules (Basel, Switzerland) · 2021Review
- Detection of selection signatures for response to Aleutian mink disease virus infection in American mink.Scientific reports · 2021Article
- An Overview of Glycosylation and its Impact on Cardiovascular Health and Disease.Frontiers in molecular biosciences · 2021Review
- Mucin-Type O-GalNAc Glycosylation in Health and Disease.Advances in experimental medicine and biology · 2021Article
- Ser and Thr acceptor preferences of the GalNAc-Ts vary among isoenzymes to modulate mucin-type O-glycosylation.Glycobiology · 2020Article
- O-glycan initiation directs distinct biological pathways and controls epithelial differentiation.EMBO reports · 2020Article
- Predicting mucin-type O-Glycosylation using enhancement value products from derived protein features.Journal of theoretical & computational chemistry · 2020Article
- Genome-wide Identification of Foxf2 Target Genes in Palate Development.Journal of dental research · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Congenital heart valve defects in humans occur in approximately 2% of live births and are a major source of compromised cardiac function. In this study we demonstrate that normal heart valve development and cardiac function are dependent upon Galnt1, the gene that encodes a member of the family of glycosyltransferases (GalNAc-Ts) responsible for the initiation of mucin-type O-glycosylation. In the adult mouse, compromised cardiac function that mimics human congenital heart disease, including aortic and pulmonary valve stenosis and regurgitation; altered ejection fraction; and cardiac dilation, was observed in Galnt1 null animals. The underlying phenotype is aberrant valve formation caused by increased cell proliferation within the outflow tract cushion of developing hearts, which is first detected at developmental stage E11.5. Developing valves from Galnt1 deficient animals displayed reduced levels of the proteases ADAMTS1 and ADAMTS5, decreased cleavage of the proteoglycan versican and increased levels of other extracellular matrix proteins. We also observed increased BMP and MAPK signaling. Taken together, the ablation of Galnt1 appears to disrupt the formation/remodeling of the extracellular matrix and alters conserved signaling pathways that regulate cell proliferation. Our study provides insight into the role of this conserved protein modification in cardiac valve development and may represent a new model for idiopathic valve 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.