ZNF462

Chr 9AD

zinc finger protein 462

Also known as: WSKA, ZFPIP, Zfp462

This zinc finger transcription factor regulates chromatin structure and controls key developmental genes including SOX2, POU5F1/OCT4, and NANOG, while also regulating neuronal development and neural cell differentiation. Mutations cause Weiss-Kruszka syndrome, an autosomal dominant developmental disorder with intellectual disability, distinctive facial features, and growth abnormalities. The gene is extremely intolerant to loss-of-function variation (pLI >0.99, LOEUF 0.085), indicating that functional copies are critical for normal development.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismADLOEUF 0.091 OMIM phenotype
Clinical SummaryZNF462
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Gene-Disease Validity (ClinGen)
Weiss-Kruszka syndrome · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

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
42 unique Pathogenic / Likely Pathogenic· 339 VUS of 500 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — ZNF462
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.09LOEUF
pLI 1.000
Z-score 8.56
OE 0.03 (0.010.09)
Highly constrained

Among the most LoF-intolerant genes (~top 3%)

Missense Constraint
3.35Z-score
OE missense 0.75 (0.710.79)
1058 obs / 1412.4 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.03 (0.010.09)
00.351.4
Missense OE0.75 (0.710.79)
00.61.4
Synonymous OE1.08
01.21.6
LoF obs/exp: 3 / 91.2Missense obs/exp: 1058 / 1412.4Syn Z: -1.40
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongZNF462-related craniofacial anomalies, corpus callosum dysgenesis, ptosis, and developmental delayLOFAD
DN
0.17100th %ile
GOF
0.1899th %ile
LOF
0.87top 5%

The highest-scoring mechanism for this gene is loss-of-function (haploinsufficiency).

LOFprediction above median · 1 literature citation · 93% of P/LP variants are LoF · LOEUF 0.09

Literature Evidence

LOFHaploinsufficiency of ZNF462 is associated with craniofacial anomalies, corpus callosum dysgenesis, ptosis, and developmental delay.PMID:28513610

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

500 submitted variants in ClinVar

Classification Summary

Pathogenic23
Likely Pathogenic19
VUS339
Likely Benign89
Benign2
Conflicting9
23
Pathogenic
19
Likely Pathogenic
339
VUS
89
Likely Benign
2
Benign
9
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
20
0
3
0
23
Likely Pathogenic
19
0
0
0
19
VUS
3
328
7
1
339
Likely Benign
0
50
1
38
89
Benign
0
2
0
0
2
Conflicting
9
Total423801139481

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

View in ClinVar →

Protein Context — Lollipop Plot

ZNF462 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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