YWHAE

Chr 17

tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein epsilon

Also known as: 14-3-3E, HEL2, KCIP-1, MDCR, MDS

The protein mediates signal transduction by binding to phosphoserine-containing proteins and interacts with key regulators of cell division and insulin sensitivity including CDC25 phosphatases, RAF1, and IRS1. Heterozygous mutations cause autosomal dominant developmental and epileptic encephalopathy with intellectual disability, seizures, and developmental delay. The high pLI score (0.98) and low LOEUF score (0.24) indicate the pathogenic mechanism involves haploinsufficiency, where loss of one functional copy is sufficient to cause disease.

GeneReviewsResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.23
Clinical SummaryYWHAE
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.98). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
125 unique Pathogenic / Likely Pathogenic· 45 VUS of 250 total submissions
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GeneReview available — YWHAE
Authoritative clinical overview · Recommended first read
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Some data sources returned errors (1)

omim: Error: OMIM fetch failed: 429

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.23LOEUF
pLI 0.985
Z-score 3.30
OE 0.00 (0.000.23)
Highly constrained

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

Missense Constraint
2.83Z-score
OE missense 0.34 (0.270.43)
49 obs / 145.0 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.00 (0.000.23)
00.351.4
Missense OE0.34 (0.270.43)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 0 / 12.7Missense obs/exp: 49 / 145.0Syn Z: -0.42
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
moderateYWHAE-related developmental delay, seizures, hypotonia and brain abnormalitiesOTHERAD
DN
0.6648th %ile
GOF
0.3887th %ile
LOF
0.4627th %ile

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and dominant-negative). The Badonyi & Marsh model scores dominant-negative 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 0.23
DNprediction above median

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.

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

250 submitted variants in ClinVar

Classification Summary

Pathogenic97
Likely Pathogenic28
VUS45
Likely Benign35
Benign23
97
Pathogenic
28
Likely Pathogenic
45
VUS
35
Likely Benign
23
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
97
0
97
Likely Pathogenic
1
0
27
0
28
VUS
0
11
34
0
45
Likely Benign
0
0
23
12
35
Benign
0
0
22
1
23
Total11120313228

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

YWHAE · 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

No active trials found for this gene.

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Clinical Literature
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