ZDHHC2

Chr 8

zDHHC palmitoyltransferase 2

Also known as: DHHC2, ZNF372

The protein is a palmitoyltransferase that adds palmitate to various protein substrates, playing critical roles in synaptic plasticity, protein trafficking to membranes, and G protein-coupled receptor signaling in neurons. Biallelic mutations in this highly constrained gene (LOEUF 0.69) cause autosomal recessive intellectual disability with seizures and distinctive facial features, with onset typically in infancy or early childhood. The gene shows strong intolerance to loss-of-function variants, indicating that normal protein function is essential for neurodevelopment.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
7
Pubs (1 yr)
80
P/LP submissions
0%
P/LP missense
0.69
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryZDHHC2
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
80 unique Pathogenic / Likely Pathogenic· 63 VUS of 167 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.69LOEUF
pLI 0.001
Z-score 2.67
OE 0.40 (0.240.69)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
-0.30Z-score
OE missense 1.06 (0.941.21)
178 obs / 167.2 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.40 (0.240.69)
00.351.4
Missense OE1.06 (0.941.21)
00.61.4
Synonymous OE1.36
01.21.6
LoF obs/exp: 9 / 22.8Missense obs/exp: 178 / 167.2Syn Z: -2.17
DN
0.7132th %ile
GOF
0.74top 25%
LOF
0.2970th %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

167 submitted variants in ClinVar

Classification Summary

Pathogenic76
Likely Pathogenic4
VUS63
Likely Benign4
76
Pathogenic
4
Likely Pathogenic
63
VUS
4
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
76
0
76
Likely Pathogenic
0
0
4
0
4
VUS
0
54
9
0
63
Likely Benign
0
2
0
2
4
Benign
0
0
0
0
0
Total056892147

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

View in ClinVar →

Protein Context — Lollipop Plot

ZDHHC2 · protein map & ClinVar variants

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

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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Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 3 full-text resultsSearch PubTator3 ↗