The encoded protein is a kinesin light chain that transports vesicles and organelles along microtubules and recruits kinesin-1 to lysosomes for lysosomal transport. Mutations cause spastic paraplegia, optic atrophy, and neuropathy (SPOAN) syndrome, inherited in an autosomal recessive pattern. The gene is highly constrained against loss-of-function variants (pLI 0.98, LOEUF 0.32), indicating intolerance to protein loss.

OMIMResearchSummary from RefSeq, OMIM, UniProt
ARLOEUF 0.321 OMIM phenotype
Clinical SummaryKLC2
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.98). 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
0.32LOEUF
pLI 0.975
Z-score 4.55
OE 0.15 (0.080.32)
Highly constrained

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

Missense Constraint
2.02Z-score
OE missense 0.72 (0.650.79)
285 obs / 398.4 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.15 (0.080.32)
00.351.4
Missense OE0.72 (0.650.79)
00.61.4
Synonymous OE0.93
01.21.6
LoF obs/exp: 5 / 33.4Missense obs/exp: 285 / 398.4Syn Z: 0.70

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

KLC2 · 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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