KDM5A

Chr 12AR

lysine demethylase 5A

Also known as: NEDEHC, RBBP-2, RBBP2, RBP2

The KDM5A protein is a histone demethylase that specifically removes methyl groups from lysine 4 of histone H3, playing a central role in gene regulation and transcriptional control of developmental genes including Hox proteins and circadian rhythm genes. Mutations cause El Hayek-Chahrour neurodevelopmental syndrome, which follows an autosomal recessive inheritance pattern. This gene is extremely intolerant to loss-of-function variants, indicating that functional copies are critical for normal development.

OMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismARLOEUF 0.161 OMIM phenotype
Clinical SummaryKDM5A
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Gene-Disease Validity (ClinGen)
congenital heart disease · ADLimited

Limited evidence — not for standalone diagnostic reporting

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.
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ClinVar Variants
74 unique Pathogenic / Likely Pathogenic· 231 VUS of 397 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.16LOEUF
pLI 1.000
Z-score 7.94
OE 0.09 (0.050.16)
Highly constrained

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

Missense Constraint
2.25Z-score
OE missense 0.79 (0.740.84)
718 obs / 908.6 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.09 (0.050.16)
00.351.4
Missense OE0.79 (0.740.84)
00.61.4
Synonymous OE1.19
01.21.6
LoF obs/exp: 8 / 88.7Missense obs/exp: 718 / 908.6Syn Z: -2.66
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedKDM5A-related intellectual developmental disorderOTHERAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.2798th %ile
GOF
0.4085th %ile
LOF
0.74top 10%

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

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

397 submitted variants in ClinVar

Classification Summary

Pathogenic66
Likely Pathogenic8
VUS231
Likely Benign34
Benign12
Conflicting2
66
Pathogenic
8
Likely Pathogenic
231
VUS
34
Likely Benign
12
Benign
2
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
4
1
61
0
66
Likely Pathogenic
3
2
3
0
8
VUS
9
197
25
0
231
Likely Benign
0
4
13
17
34
Benign
0
7
2
3
12
Conflicting
2
Total1621110420353

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

View in ClinVar →

Protein Context — Lollipop Plot

KDM5A · 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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