NEK6

Chr 9

NIMA related kinase 6

Also known as: SID6-1512

The protein is a kinase that regulates mitotic cell cycle progression by phosphorylating multiple substrates required for chromosome segregation, spindle formation, and cytokinesis. Loss-of-function mutations cause a neurodevelopmental disorder with intellectual disability, developmental delay, and seizures, inherited in an autosomal dominant pattern. The pathogenic mechanism involves dominant-negative effects that disrupt normal mitotic processes in developing neurons.

OMIMResearchSummary from RefSeq, UniProt, Mechanism
MultiplemechanismLOEUF 0.61
Clinical SummaryNEK6
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
28 unique Pathogenic / Likely Pathogenic· 43 VUS of 95 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.61LOEUF
pLI 0.039
Z-score 2.82
OE 0.31 (0.170.61)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.95Z-score
OE missense 0.62 (0.540.72)
131 obs / 210.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.31 (0.170.61)
00.351.4
Missense OE0.62 (0.540.72)
00.61.4
Synonymous OE0.95
01.21.6
LoF obs/exp: 6 / 19.4Missense obs/exp: 131 / 210.8Syn Z: 0.39
DN
0.77top 25%
GOF
0.6736th %ile
LOF
0.3454th %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

95 submitted variants in ClinVar

Classification Summary

Pathogenic27
Likely Pathogenic1
VUS43
Likely Benign3
Benign1
27
Pathogenic
1
Likely Pathogenic
43
VUS
3
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
27
0
27
Likely Pathogenic
0
0
1
0
1
VUS
0
42
1
0
43
Likely Benign
0
3
0
0
3
Benign
0
0
0
1
1
Total04529175

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

View in ClinVar →

Protein Context — Lollipop Plot

NEK6 · 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
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC