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Article

Progress to Clarify How NOTCH3 Mutations Lead to CADASIL, a Hereditary Cerebral Small Vessel Disease.

Biomolecules - 18 Jan 2024

Mizuta Ikuko, Nakao-Azuma Yumiko, Yoshida Hideki, Yamaguchi Masamitsu, Mizuno Toshiki

Abstract excerpt

Notch signaling is conserved in C. elegans, Drosophila, and mammals. Among the four NOTCH genes in humans, NOTCH1, NOTCH2, and NOTCH3 are known to cause monogenic hereditary disorders. Most NOTCH-related disorders are congenital and caused by a gain or loss of Notch signaling activity. In contrast, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) caused by...

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Identifiers

PMID: 38254727
DOI: 10.3390/biom14010127
PMCID: PMC10813265

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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.

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Progress to Clarify How NOTCH3 Mutations Lead to CADASIL, a Hereditary Cerebral Small Vessel Disease.PMID 38254727Read ↗

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Novel human pathological mutations. Gene symbol: NOTCH3. Disease: cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL).Semantic proximity Read ↗

Novel human pathological mutations. Gene symbol: NOTCH3. Disease: cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL).Semantic proximity Read ↗

Novel human pathological mutations. Gene symbol: NOTCH3. Disease: cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL).Semantic proximity Read ↗

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