RGS14

Chr 5

regulator of G protein signaling 14

This protein regulates G protein-coupled receptor signaling by acting as a GTPase activating protein and GDP-dissociation inhibitor, terminating G protein signals and modulating cellular processes including neurite outgrowth and learning/memory. Mutations cause autosomal recessive spinocerebellar ataxia with developmental delay and intellectual disability, typically presenting in childhood. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.58), affecting primarily neurological and cerebellar systems.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
13
Pubs (1 yr)
59
P/LP submissions
0%
P/LP missense
0.58
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryRGS14
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.34) despite low pLI — interpret in context.
📋
ClinVar Variants
57 unique Pathogenic / Likely Pathogenic· 77 VUS of 157 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.58LOEUF
pLI 0.002
Z-score 3.32
OE 0.34 (0.210.58)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
0.54Z-score
OE missense 0.92 (0.831.01)
309 obs / 337.1 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.34 (0.210.58)
00.351.4
Missense OE0.92 (0.831.01)
00.61.4
Synonymous OE0.79
01.21.6
LoF obs/exp: 10 / 29.4Missense obs/exp: 309 / 337.1Syn Z: 2.06
DN
0.6937th %ile
GOF
0.73top 25%
LOF
0.3550th %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

157 submitted variants in ClinVar

Classification Summary

Pathogenic51
Likely Pathogenic6
VUS77
Likely Benign6
Benign2
51
Pathogenic
6
Likely Pathogenic
77
VUS
6
Likely Benign
2
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
51
0
51
Likely Pathogenic
0
0
6
0
6
VUS
0
66
11
0
77
Likely Benign
0
5
1
0
6
Benign
0
1
1
0
2
Total072700142

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

View in ClinVar →

Protein Context — Lollipop Plot

RGS14 · 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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