Angelman syndrome due to maternal 15q11q13 deletion

disease
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Also known as Angelman syndrome due to maternal monosomy 15q11q13

Summary

Angelman syndrome due to maternal 15q11q13 deletion (MONDO:0020302) is a disease. A subtype of Angelman syndrome — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

  • Phenotypes (HPO): 50

Clinical features

Signs & symptoms

Clinical features (HPO)

50 HPO clinical features (Orphanet curated; top 50 by frequency):

HPO IDTermFrequency
HP:0002353EEG abnormalityVery frequent (80-99%)
HP:0004485Cessation of head growthVery frequent (80-99%)
HP:0005484Secondary microcephalyVery frequent (80-99%)
HP:0011203EEG with abnormally slow frequenciesVery frequent (80-99%)
HP:0012758Neurodevelopmental delayVery frequent (80-99%)
HP:0001250SeizureVery frequent (80-99%)
HP:0001263Global developmental delayVery frequent (80-99%)
HP:0000154Wide mouthFrequent (30-79%)
HP:0000486StrabismusFrequent (30-79%)
HP:0000687Widely spaced teethFrequent (30-79%)
HP:0000729Autistic behaviorFrequent (30-79%)
HP:0000736Short attention spanFrequent (30-79%)
HP:0000748Inappropriate laughterFrequent (30-79%)
HP:0000752HyperactivityFrequent (30-79%)
HP:0001010Hypopigmentation of the skinFrequent (30-79%)
HP:0001513ObesityFrequent (30-79%)
HP:0002019ConstipationFrequent (30-79%)
HP:0002033Poor suckFrequent (30-79%)
HP:0002079Hypoplasia of the corpus callosumFrequent (30-79%)
HP:0002167Abnormality of speech or vocalizationFrequent (30-79%)
HP:0002307DroolingFrequent (30-79%)
HP:0002395Lower limb hyperreflexiaFrequent (30-79%)
HP:0002650ScoliosisFrequent (30-79%)
HP:0004302Functional motor deficitFrequent (30-79%)
HP:0005469Flat occiputFrequent (30-79%)
HP:0005599Hypopigmentation of hairFrequent (30-79%)
HP:0007730Iris hypopigmentationFrequent (30-79%)
HP:0008947Floppy infantFrequent (30-79%)
HP:0010808Protruding tongueFrequent (30-79%)
HP:0010864Intellectual disability, severeFrequent (30-79%)
HP:0011968Feeding difficultiesFrequent (30-79%)
HP:0012448Delayed myelinationFrequent (30-79%)
HP:0040082Happy demeanorFrequent (30-79%)
HP:0100703Tongue thrustingFrequent (30-79%)
HP:0100738Abnormal eating behaviorFrequent (30-79%)
HP:0000303Mandibular prognathiaOccasional (5-29%)
HP:0001251AtaxiaOccasional (5-29%)
HP:0001336MyoclonusOccasional (5-29%)
HP:0001337TremorOccasional (5-29%)
HP:0001344Absent speechOccasional (5-29%)
HP:0002015DysphagiaOccasional (5-29%)
HP:0002046Heat intoleranceOccasional (5-29%)
HP:0002136Broad-based gaitOccasional (5-29%)
HP:0002141Gait imbalanceOccasional (5-29%)
HP:0002465Poor speechOccasional (5-29%)
HP:0010505Limitation of movement at anklesOccasional (5-29%)
HP:0033063Shortened sleep cycleOccasional (5-29%)
HP:0040196Mild microcephalyOccasional (5-29%)
HP:0100022Abnormality of movementOccasional (5-29%)
HP:0100023Recurrent hand flappingOccasional (5-29%)

Identifiers

Disease identifiers

FieldValue
Canonical nameAngelman syndrome due to maternal 15q11q13 deletion
Mondo IDMONDO:0020302
Orphanet98794
UMLSC5566334
MedGen1797757
GARD0019577
Is cancer (heuristic)no

Also known as: Angelman syndrome due to maternal monosomy 15q11q13

Disease family

This is a subtype of Angelman syndrome. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: disease › human disease › disease by body system or component › syndromic diseaseAngelman syndromeAngelman syndrome due to maternal 15q11q13 deletion

Related subtypes (3): Angelman syndrome due to a point mutation, Angelman syndrome due to imprinting defect in 15q11-q13, Angelman syndrome due to paternal uniparental disomy of chromosome 15

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.

No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.