ArticleThe Journal of biological chemistry2020
NOTCH3 is non-enzymatically fragmented in inherited cerebral small-vessel disease.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Association Between Vascular NOTCH3 Aggregation and Disease Severity in a CADASIL Cohort - Implications for NOTCH3 Variant-Specific Disease Prediction.Annals of neurology · 2025Article
- Mechanistic advances in factors influencing phenotypic variability in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a review.Frontiers in neurology · 2025Review
- Genomic Insights into Dementia: Precision Medicine and the Impact of Gene-Environment Interaction.Aging and disease · 2024Review
- Article
- Architectural digest: Thermodynamic stability and domain structure of a consensus monomeric globin.Biophysical journal · 2023Article
- Three-tiered EGFr domain risk stratification for individualized NOTCH3-small vessel disease prediction.Brain : a journal of neurology · 2023Article
- Preferential rabbit antibody responses to C-termini of NOTCH3 peptide immunogens.Scientific reports · 2023Article
- Structural changes in NOTCH3 induced by CADASIL mutations: Role of cysteine and non-cysteine alterations.The Journal of biological chemistry · 2023Article
- Article
- Oligomerization, trans-reduction, and instability of mutant NOTCH3 in inherited vascular dementia.Communications biology · 2022Article
- Trans-Reduction of Cerebral Small Vessel Disease Proteins by Notch-Derived EGF-like Sequences.International journal of molecular sciences · 2022Article
- NOTCH3 variant position is associated with NOTCH3 aggregation load in CADASIL vasculature.Neuropathology and applied neurobiology · 2022Article
- Detecting Key Functional Components Group and Speculating the Potential Mechanism of Xiao-Xu-Ming Decoction in Treating Stroke.Frontiers in cell and developmental biology · 2022Article
- Electrophilic and Drug-Induced Stimulation of NOTCH3 N-terminal Fragment Oligomerization in Cerebrovascular Pathology.Translational stroke research · 2021Article
- Overlapping Protein Accumulation Profiles of CADASIL and CAA: Is There a Common Mechanism Driving Cerebral Small-Vessel Disease?The American journal of pathology · 2021Review
- Hydrolysis of a second Asp-Pro site at the N-terminus of NOTCH3 in inherited vascular dementia.Scientific reports · 2021Article
- Thiol-mediated and catecholamine-enhanced multimerization of a cerebrovascular disease enriched fragment of NOTCH3.Experimental neurology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The small-vessel disorder cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) arises from mutations in the human gene encoding NOTCH3 and results in vascular smooth muscle cell degeneration, stroke, and dementia. However, the structural changes in NOTCH3 involved in CADASIL etiology are unclear. Here, we discovered site-specific fragmentation of NOTCH3 protein in pathologically affected vessels of human CADASIL-affected brains. EM-based experiments to pinpoint NOTCH3 localization in these brains indicated accumulation of NOTCH3 fragmentation products in the basement membrane, collagen fibers, and granular osmiophilic material within the cerebrovasculature. Using antibodies generated against a disease-linked neo-epitope found in degenerating vascular medium of CADASIL brains, we mapped the site of fragmentation to the NOTCH3 N terminus at the peptide bond joining Asp
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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.