MAPK3

Chr 16

mitogen-activated protein kinase 3

Also known as: ERK-1, ERK1, ERT2, HS44KDAP, HUMKER1A, P44ERK1, P44MAPK, PRKM3

MAPK3 encodes ERK1, a serine/threonine kinase that phosphorylates nuclear and cytoplasmic substrates to regulate cell proliferation, differentiation, and survival as part of the MAPK/ERK signaling cascade. Mutations cause a neurodevelopmental disorder with intellectual disability, seizures, and distinctive facial features, following an autosomal dominant inheritance pattern. The gene shows moderate constraint to loss-of-function variation (LOEUF 0.614), and a GeneReviews entry is available for detailed clinical guidance.

GeneReviewsOMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.61
Clinical SummaryMAPK3
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.31) despite low pLI — interpret in context.
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ClinVar Variants
278 unique Pathogenic / Likely Pathogenic· 42 VUS of 354 total submissions
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Clinical Trials
3 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — MAPK3
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.61LOEUF
pLI 0.037
Z-score 2.80
OE 0.31 (0.170.61)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.74Z-score
OE missense 0.68 (0.600.78)
164 obs / 239.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.31 (0.170.61)
00.351.4
Missense OE0.68 (0.600.78)
00.61.4
Synonymous OE0.87
01.21.6
LoF obs/exp: 6 / 19.3Missense obs/exp: 164 / 239.8Syn Z: 1.00
DN
0.7227th %ile
GOF
0.6931th %ile
LOF
0.3744th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction 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.

ClinVar Variant Classifications

354 submitted variants in ClinVar

Classification Summary

Pathogenic234
Likely Pathogenic44
VUS42
Likely Benign13
Benign1
234
Pathogenic
44
Likely Pathogenic
42
VUS
13
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
234
0
234
Likely Pathogenic
0
1
43
0
44
VUS
1
29
12
0
42
Likely Benign
0
3
1
9
13
Benign
0
0
0
1
1
Total13329010334

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

View in ClinVar →

Protein Context — Lollipop Plot

MAPK3 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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