CAMK4

Chr 5

calcium/calmodulin dependent protein kinase IV

Also known as: CaMK IV, CaMK-GR, CaMKIV, caMK

CAMK4 encodes a calcium/calmodulin-dependent protein kinase that phosphorylates transcription factors including CREB1, MEF2D, and JUN to regulate gene expression in immune cells and neurons, particularly contributing to memory consolidation and hippocampal long-term potentiation. Mutations cause intellectual disability and developmental delay with autosomal recessive inheritance. The gene shows significant constraint against loss-of-function variants (LOEUF 0.47), indicating intolerance to protein-disrupting mutations.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.47
Clinical SummaryCAMK4
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.51) — some intolerance to loss-of-function variants.
📋
ClinVar Variants
27 unique Pathogenic / Likely Pathogenic· 94 VUS of 139 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.47LOEUF
pLI 0.510
Z-score 3.23
OE 0.21 (0.100.47)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.81Z-score
OE missense 0.68 (0.600.77)
177 obs / 259.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.21 (0.100.47)
00.351.4
Missense OE0.68 (0.600.77)
00.61.4
Synonymous OE0.95
01.21.6
LoF obs/exp: 4 / 19.3Missense obs/exp: 177 / 259.0Syn Z: 0.39
DN
0.6259th %ile
GOF
0.73top 25%
LOF
0.4430th %ile

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

GOFprediction above median
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.

ClinVar Variant Classifications

139 submitted variants in ClinVar

Classification Summary

Pathogenic27
VUS94
Likely Benign7
Benign5
27
Pathogenic
94
VUS
7
Likely Benign
5
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
1
25
0
27
Likely Pathogenic
0
0
0
0
0
VUS
9
69
16
0
94
Likely Benign
0
4
2
1
7
Benign
0
2
2
1
5
Total1076452133

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

View in ClinVar →

Protein Context — Lollipop Plot

CAMK4 · 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.

Search ClinicalTrials.gov →
Clinical Literature
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