The NOTCH3 protein functions as a receptor for membrane-bound ligands (Jagged1, Jagged2, and Delta1) that regulates cell-fate determination and affects differentiation, proliferation, and apoptotic programs. Mutations cause cerebral arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), lateral meningocele syndrome, infantile myofibromatosis, and familial partial lipodystrophy, with both autosomal dominant and recessive inheritance patterns reported. The gene shows high constraint against loss-of-function variants (LOEUF 0.32), indicating intolerance to protein-disrupting mutations.

OMIMResearchSummary from RefSeq, OMIM, UniProt
GOFmechanismAD/ARLOEUF 0.325 OMIM phenotypes
Clinical SummaryNOTCH3
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Gene-Disease Validity (ClinGen)
pulmonary arterial hypertension · ADDisputed

Disputed — evidence questions this relationship

2 total gene-disease associations curated

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.23) despite low pLI — interpret in context.
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Clinical Trials
9 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.32LOEUF
pLI 0.408
Z-score 7.09
OE 0.23 (0.160.32)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
3.53Z-score
OE missense 0.74 (0.700.77)
1037 obs / 1410.4 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.23 (0.160.32)
00.351.4
Missense OE0.74 (0.700.77)
00.61.4
Synonymous OE0.92
01.21.6
LoF obs/exp: 22 / 97.6Missense obs/exp: 1037 / 1410.4Syn Z: 1.51
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedNOTCH3-related infantile myofibromatosisGOFAD
definitiveNOTCH3-related cerebral arteiopathy with subcortical infarcts and leukencephalopathyGOFAD
DN
0.4388th %ile
GOF
0.6052th %ile
LOF
0.52top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function, gain-of-function and dominant-negative). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFLOEUF 0.32
GOF1 literature citation
DN1 literature citation

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Literature Evidence

DNIn a follow-up to the study of Joutel et al. (2004), Monet-Lepretre et al. (2009) found that the C428S mutation exerted a dominant-negative effect in transgenic mice, and antagonized the function of wildtype Notch3 when coexpressed.PMID:19293235
GOFInvestigation of CADASIL mutant Notch3 shows that the majority of mutations do not change CBF1/JBP-Jkappa mediated classic Notch activation, so the pathological consequences of NOTCH3 mutations in CADASIL patients can not be simply explained by loss- or gain-of-function in the classic Notch signalliPMID:17854869

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

NOTCH3 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

Cardiovascular DiseaseArterial StiffnessGermline Mutation in the NOTCH 3 Gene

Natural History Study of CADASIL

RECRUITING
NCT05072483National Heart, Lung, and Blood Institute (NHLBI)Started 2022-04-18
MRI
LeukodystrophyWhite Matter DiseaseLeukoencephalopathies

The Myelin Disorders Biorepository Project

RECRUITING
NCT03047369Children's Hospital of PhiladelphiaStarted 2016-12-08
Cerebral Small Vessel DiseasesCadasilHTRA1-Related Autosomal Dominant Cerebral Angiopathy

Taiwan Associated Genetic and Nongenetic Small Vessel Disease

RECRUITING
NCT05473637National Taiwan University HospitalStarted 2019-01-01
MRI
CADASILCADASIL (Diagnosis)

Genotype, Clinical Features and Imaging of Neuroradiological Abnormalities in CADASIL

RECRUITING
NCT06938100Fondazione I.R.C.C.S. Istituto Neurologico Carlo BestaStarted 2023-11-21
CADASIL

Development and Validation of a Functional MRI Biomarker of Cerebral Small Vessel Dysfunction in CADASIL

NOT YET RECRUITING
NCT06859658Assistance Publique - Hôpitaux de ParisStarted 2025-04-01
Functional MRI at 3TFunctional MRI at 3TFunctional MRI at 3T
Cadasil

AusCADASIL: An Australian Cohort of CADASIL

RECRUITING
NCT06148051Perminder SachdevStarted 2023-11-25
CADASILCerebral Autosomal Dominant Arteriopatie With Subcortical Infarcts and Leukoencephalopathy

Long-term Prospective Study of Korean CADASIL Patients

RECRUITING
NCT07497867Jeju National University HospitalStarted 2023-07-10
Migraine With Aura

Neurogenetic And Hemodynamic Of Migraine Aura And Pfo

RECRUITING
NCT07349004Azienda Usl di BolognaStarted 2025-11-24
Intervention
CADASIL

Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) Study

RECRUITING
NCT05677880University of Wisconsin, MadisonStarted 2022-06-03
Study Procedures
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
CADASIL.
Wang MM·Handb Clin Neurol
2018Review
Notch3 in Development, Health and Disease.
Hosseini-Alghaderi S et al.·Biomolecules
2020Review
Top 5 results · since 2015Search PubMed ↗