Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Sequestration of latent TGF-β binding protein 1 into CADASIL-related Notch3-ECD deposits.

Acta neuropathologica communications - 13 Aug 2014

Kast Jessica, Hanecker Patrizia, Beaufort Nathalie, Giese Armin, Joutel Anne, Dichgans Martin, Opherk Christian, Haffner Christof

Abstract excerpt

INTRODUCTION: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) represents the most common hereditary form of cerebral small vessel disease characterized by early-onset stroke and premature dementia. It is caused by mutations in the transmembrane receptor Notch3, which promote the aggregation and accumulation of the Notch3 extracellular domain (Notch3-ECD) within...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to CADASIL
Share to HEK293 Cells

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Latent TGF-beta Binding Proteins

Share to Receptor, Notch3

Share to Receptors, Notch

Share to Sequence Analysis, Protein

Share to Silver Staining

Share to Statistics, Nonparametric

Source

Open in PubMed Open full text

Identifiers

PMID: 25190493
DOI: 10.1186/s40478-014-0096-8
PMCID: PMC4243959

Genes

ECD

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Sequestration of latent TGF-β binding protein 1 into CADASIL-related Notch3-ECD deposits.PMID 25190493Read ↗

NOTCH3 is non-enzymatically fragmented in inherited cerebral small-vessel disease.Semantic proximity Read ↗

CADASIL brain vessels show a HTRA1 loss-of-function profile.Semantic proximity Read ↗

Blood brain barrier leakage is not a consistent feature of white matter lesions in CADASILSemantic proximity Read ↗

Active immunotherapy reduces NOTCH3 deposition in brain capillaries in a CADASIL mouse model.Semantic proximity Read ↗

NOTCH3 active immunotherapy reduces NOTCH3 deposition in brain capillaries in a CADASIL mouse modelSemantic proximity Read ↗

Heterogeneity of NOTCH3 activation mechanisms uncovers therapeutic potential for targeted therapies for CADASILSemantic proximity Read ↗

Lunatic fringe promotes the aggregation of CADASIL NOTCH3 mutant proteins.Semantic proximity Read ↗

Concentration of non-myocyte proteins in arterial media of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.Semantic proximity Read ↗

Mouse model of CADASIL reveals novel insights into Notch3 function in adult hippocampal neurogenesis.Semantic proximity Read ↗

Transgenic mice expressing mutant Notch3 develop vascular alterations characteristic of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.Semantic proximity Read ↗

NOTCH3 CADASIL Variant Receptor Aggregation Requires NOTCH3 Wild-Type Receptors: Identification of Highly Selective Inhibitors That Block the Process.Semantic proximity Read ↗

The N-acetylglucosaminyltransferase Radical fringe contributes to defects in JAG1-dependent turnover and signaling of NOTCH3 CADASIL mutants.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.