MAP3K8

Chr 10

mitogen-activated protein kinase kinase kinase 8

Also known as: AURA2, COT, EST, ESTF, MEKK8, TPL2, Tpl-2, c-COT

MAP3K8 encodes a serine/threonine protein kinase that activates MAPK/ERK and JNK signaling pathways and is required for TLR4-mediated inflammatory responses, T-helper cell differentiation, and cytokine production including TNF-alpha and interleukin-8. The gene is highly constrained against loss-of-function variants, but no Mendelian pediatric disorders have been definitively associated with germline MAP3K8 mutations. Somatic mutations in this gene contribute to lung cancer development.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

Lung cancer, somaticMIM #211980
0
Active trials
26
Pubs (1 yr)
10
P/LP submissions
0%
P/LP missense
0.32
LOEUF· LoF intol.
Multiple*
Mechanism· predicted
Clinical SummaryMAP3K8
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.97). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
10 unique Pathogenic / Likely Pathogenic· 144 VUS of 297 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.32LOEUF
pLI 0.968
Z-score 3.67
OE 0.10 (0.040.32)
Highly constrained

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

Missense Constraint
2.29Z-score
OE missense 0.61 (0.540.69)
165 obs / 271.2 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.10 (0.040.32)
00.351.4
Missense OE0.61 (0.540.69)
00.61.4
Synonymous OE1.16
01.21.6
LoF obs/exp: 2 / 19.5Missense obs/exp: 165 / 271.2Syn Z: -1.23
DN
0.4190th %ile
GOF
0.79top 25%
LOF
0.55top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). 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
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

297 submitted variants in ClinVar

Classification Summary

Pathogenic9
Likely Pathogenic1
VUS144
Likely Benign107
Benign24
9
Pathogenic
1
Likely Pathogenic
144
VUS
107
Likely Benign
24
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
9
0
9
Likely Pathogenic
0
0
1
0
1
VUS
1
129
12
2
144
Likely Benign
0
1
29
77
107
Benign
0
1
15
8
24
Total11316687285

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

View in ClinVar →

Protein Context — Lollipop Plot

MAP3K8 · protein map & ClinVar variants

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

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
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