GNA14

Chr 9

G protein subunit alpha 14

Also known as: HG1I

The encoded protein is a G-protein alpha subunit that activates phospholipase C-beta in transmembrane signaling pathways. Mutations cause gain-of-function effects leading to neurological disease with an autosomal dominant inheritance pattern. The gene shows tolerance to loss-of-function variants, consistent with the gain-of-function disease mechanism.

Summary from RefSeq, UniProt, Mechanism
0
Active trials
6
Pubs (1 yr)
28
P/LP submissions
4%
P/LP missense
1.71
LOEUF
GOF
Mechanism· G2P
Clinical SummaryGNA14
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
26 unique Pathogenic / Likely Pathogenic· 59 VUS of 100 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.71LOEUF
pLI 0.000
Z-score -0.89
OE 1.22 (0.881.71)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.38Z-score
OE missense 1.08 (0.961.21)
215 obs / 199.7 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.22 (0.881.71)
00.351.4
Missense OE1.08 (0.961.21)
00.61.4
Synonymous OE1.12
01.21.6
LoF obs/exp: 23 / 18.8Missense obs/exp: 215 / 199.7Syn Z: -0.84
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongGNA14-related congenital vascular tumoursGOFAD
DN
0.6841th %ile
GOF
0.75top 25%
LOF
0.2776th %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

100 submitted variants in ClinVar

Classification Summary

Pathogenic22
Likely Pathogenic4
VUS59
Benign3
22
Pathogenic
4
Likely Pathogenic
59
VUS
3
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
1
21
0
22
Likely Pathogenic
0
0
4
0
4
VUS
1
54
4
0
59
Likely Benign
0
0
0
0
0
Benign
0
1
0
2
3
Total15629288

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

View in ClinVar →

Protein Context — Lollipop Plot

GNA14 · 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.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC