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Identifying Therapeutic Targets for Complex Notch1 Mutations of Hypoplastic Left Heart Syndrome

https://doi.org/10.2139/ssrn.5390714
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Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1002/stem.2582openalex-snapshot
NOTCH1-Dependent Nitric Oxide Signaling Deficiency in Hypoplastic Left Heart Syndrome Revealed Through Patient-Specific Phenotypes Detected in Bioengineered Cardiogenesis
inferredcites →https://doi.org/10.1007/s00439-015-1582-1openalex-snapshot
Compound heterozygous NOTCH1 mutations underlie impaired cardiogenesis in a patient with hypoplastic left heart syndrome
inferredcites →https://doi.org/10.1007/s40268-015-0083-yopenalex-snapshot
Auranofin: Repurposing an Old Drug for a Golden New Age
inferredcites →https://doi.org/10.1016/j.addr.2015.04.019openalex-snapshot
Maturing human pluripotent stem cell-derived cardiomyocytes in human engineered cardiac tissues
inferredcites →https://doi.org/10.1016/j.devcel.2006.12.011openalex-snapshot
Notch Signaling Is Essential for Ventricular Chamber Development
inferredcites →https://doi.org/10.1016/j.intimp.2021.108272openalex-snapshot
Auranofin: Past to Present, and repurposing
inferredcites →https://doi.org/10.1016/j.jaccao.2022.12.005openalex-snapshot
Cardiovascular Toxicity of Proteasome Inhibitors: Underlying Mechanisms and Management Strategies
inferredcites →https://doi.org/10.1016/j.stem.2020.07.015openalex-snapshot
Intrinsic Endocardial Defects Contribute to Hypoplastic Left Heart Syndrome
inferredcites →https://doi.org/10.1016/j.stem.2022.03.003openalex-snapshot
Uncompensated mitochondrial oxidative stress underlies heart failure in an iPSC-derived model of congenital heart disease
inferredcites →https://doi.org/10.1016/j.xpro.2022.101560openalex-snapshot
A review of protocols for human iPSC culture, cardiac differentiation, subtype-specification, maturation, and direct reprogramming
inferredcites →https://doi.org/10.1016/s0070-2153(10)92011-5openalex-snapshot
Notch Signaling in Cardiac Development and Disease
inferredcites →https://doi.org/10.1016/s0735-1097(01)01272-4openalex-snapshot
Task Force 1: the changing profile of congenital heart disease in adult life
inferredcites →https://doi.org/10.1038/gim.2015.193openalex-snapshot
Cardiovascular malformations caused by NOTCH1 mutations do not keep left: data on 428 probands with left-sided CHD and their families
inferredcites →https://doi.org/10.1038/nature03940openalex-snapshot
Mutations in NOTCH1 cause aortic valve disease
inferredcites →https://doi.org/10.1038/s41467-017-01741-8openalex-snapshot
NOTCH1 is a mechanosensor in adult arteries
inferredcites →https://doi.org/10.1038/s41467-022-33678-yopenalex-snapshot
Mitochondrial network configuration influences sarcomere and myosin filament structure in striated muscles
inferredcites →https://doi.org/10.1038/s41586-022-04989-3openalex-snapshot
Integrated multi-omic characterization of congenital heart disease
inferredcites →https://doi.org/10.1038/s41598-020-66845-6openalex-snapshot
Robust detection of undifferentiated iPSC among differentiated cells
inferredcites →https://doi.org/10.1074/jbc.m101343200openalex-snapshot
Functional Interaction between SEL-10, an F-box Protein, and the Nuclear Form of Activated Notch1 Receptor
inferredcites →https://doi.org/10.1074/jbc.m103992200openalex-snapshot
The Notch Intracellular Domain Is Ubiquitinated and Negatively Regulated by the Mammalian Sel-10 Homolog
inferredcites →https://doi.org/10.1093/hmg/ddx140openalex-snapshot
Induced pluripotent stem cell modelling of HLHS underlines the contribution of dysfunctional NOTCH signalling to impaired cardiogenesis
inferredcites →https://doi.org/10.1101/cshperspect.a013953openalex-snapshot
Complex Genetics and the Etiology of Human Congenital Heart Disease
inferredcites →https://doi.org/10.1101/gad.276304openalex-snapshot
Notch promotes epithelial-mesenchymal transition during cardiac development and oncogenic transformation
inferredcites →https://doi.org/10.1111/febs.15792openalex-snapshot
Regulation of Notch signaling by E3 ubiquitin ligases
inferredcites →https://doi.org/10.1111/j.1399-0004.2011.01674.xopenalex-snapshot
Identification of de novo mutations and rare variants in hypoplastic left heart syndrome
inferredcites →https://doi.org/10.1128/mcb.21.21.7403-7415.2001openalex-snapshot
SEL-10 Is an Inhibitor of Notch Signaling That Targets Notch for Ubiquitin-Mediated Protein Degradation
inferredcites →https://doi.org/10.1161/circresaha.115.305350openalex-snapshot
Endocardial Notch Signaling in Cardiac Development and Disease
inferredcites →https://doi.org/10.1161/circulationaha.119.045317openalex-snapshot
Patient-Specific Induced Pluripotent Stem Cells Implicate Intrinsic Impaired Contractility in Hypoplastic Left Heart Syndrome
inferredcites →https://doi.org/10.1371/journal.pone.0102796openalex-snapshot
Directed Differentiation of Patient-Specific Induced Pluripotent Stem Cells Identifies the Transcriptional Repression and Epigenetic Modification of NKX2-5, HAND1, and NOTCH1 in Hypoplastic Left Heart Syndrome
inferredcites →https://doi.org/10.18632/oncotarget.2113openalex-snapshot
Clinically used antirheumatic agent auranofin is a proteasomal deubiquitinase inhibitor and inhibits tumor growth
inferredcites →https://doi.org/10.3389/fcell.2020.00440openalex-snapshot
Contractility of Induced Pluripotent Stem Cell-Cardiomyocytes With an MYH6 Head Domain Variant Associated With Hypoplastic Left Heart Syndrome
inferredcites →https://doi.org/10.3389/fped.2021.635776openalex-snapshot
The Improved Prognosis of Hypoplastic Left Heart: A Population-Based Register Study of 343 Cases in England and Wales
inferredcites →https://doi.org/10.5966/sctm.2013-0105openalex-snapshot
An Induced Pluripotent Stem Cell Model of Hypoplastic Left Heart Syndrome (HLHS) Reveals Multiple Expression and Functional Differences in HLHS-Derived Cardiac Myocytes
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