MAP3K12

Chr 12

mitogen-activated protein kinase kinase kinase 12

Also known as: DLK, HP09298, MEKK12, MUK, ZPK, ZPKP1

This serine/threonine protein kinase is predominantly expressed in neurons and regulates transcription through non-canonical MAPK signaling pathways, forming complexes with transcription factors like CREB. Mutations cause autosomal dominant neurodevelopmental disorders with intellectual disability and seizures. The gene is extremely intolerant to loss-of-function variants (pLI ~1.0), indicating that haploinsufficiency likely underlies the pathogenic mechanism.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.07
Clinical SummaryMAP3K12
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.07LOEUF
pLI 1.000
Z-score 5.96
OE 0.00 (0.000.07)
Highly constrained

Among the most LoF-intolerant genes (~top 3%)

Missense Constraint
2.99Z-score
OE missense 0.63 (0.580.69)
332 obs / 524.7 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.00 (0.000.07)
00.351.4
Missense OE0.63 (0.580.69)
00.61.4
Synonymous OE1.13
01.21.6
LoF obs/exp: 0 / 41.3Missense obs/exp: 332 / 524.7Syn Z: -1.43
DN
0.4488th %ile
GOF
0.6639th %ile
LOF
0.72top 10%

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

LOFprediction above median · LOEUF 0.07
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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

MAP3K12 · 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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