GORASP1

Chr 3

golgi reassembly stacking protein 1

Also known as: GOLPH5, GRASP65, P65

The protein encoded by this gene is a key structural protein required for formation and maintenance of the Golgi apparatus ribbon structure and mediates docking of transport vesicles with Golgi membranes. Pathogenic variants in GORASP1 cause autosomal recessive genitopatellar syndrome, a rare developmental disorder characterized by genital anomalies, absent or hypoplastic patellae, intellectual disability, and distinctive facial features with early childhood onset. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.675), affecting multiple organ systems including skeletal, genitourinary, and neurological development.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.68
Clinical SummaryGORASP1
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.34) despite low pLI — interpret in context.
📋
ClinVar Variants
9 unique Pathogenic / Likely Pathogenic· 67 VUS of 98 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.68LOEUF
pLI 0.020
Z-score 2.55
OE 0.34 (0.190.68)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.67Z-score
OE missense 0.88 (0.790.98)
216 obs / 245.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.34 (0.190.68)
00.351.4
Missense OE0.88 (0.790.98)
00.61.4
Synonymous OE0.82
01.21.6
LoF obs/exp: 6 / 17.5Missense obs/exp: 216 / 245.5Syn Z: 1.42
DN
0.7130th %ile
GOF
0.75top 25%
LOF
0.3261th %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

98 submitted variants in ClinVar

Classification Summary

Pathogenic8
Likely Pathogenic1
VUS67
Likely Benign4
Benign4
8
Pathogenic
1
Likely Pathogenic
67
VUS
4
Likely Benign
4
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
8
0
8
Likely Pathogenic
0
0
1
0
1
VUS
1
66
0
0
67
Likely Benign
0
4
0
0
4
Benign
0
1
1
2
4
Total17110284

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

View in ClinVar →

Protein Context — Lollipop Plot

GORASP1 · 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
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC

No open access results found