GIPC1

Chr 19AD

GIPC PDZ domain containing family member 1

Also known as: C19orf3, GIPC, GLUT1CBP, Hs.6454, IIP-1, NIP, OPDM2, RGS19IP1

GIPC1 encodes a scaffolding protein that regulates cell surface receptor expression and trafficking. Mutations cause oculopharyngodistal myopathy 2, a neuromuscular disorder affecting the eyes, pharynx, and distal muscles, with autosomal dominant inheritance. The gene shows low constraint to loss-of-function variants, suggesting tolerance to protein truncation.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Oculopharyngodistal myopathy 2MIM #618940
AD
0
Active trials
17
Pubs (1 yr)
15
P/LP submissions
0%
P/LP missense
0.96
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryGIPC1
Population Constraint (gnomAD)
Low constraint (pLI 0.01) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
15 unique Pathogenic / Likely Pathogenic· 63 VUS of 94 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.96LOEUF
pLI 0.008
Z-score 1.67
OE 0.46 (0.240.96)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.54Z-score
OE missense 0.90 (0.801.01)
196 obs / 218.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.46 (0.240.96)
00.351.4
Missense OE0.90 (0.801.01)
00.61.4
Synonymous OE1.21
01.21.6
LoF obs/exp: 5 / 11.0Missense obs/exp: 196 / 218.5Syn Z: -1.64
DN
0.7034th %ile
GOF
0.73top 25%
LOF
0.3453th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative, gain-of-function and loss-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports dominant-negative. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median · 1 literature citation
GOFprediction above median
LOF1 literature citation

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.

Literature Evidence

DNWe find that the overexpression of a dominant-negative form of GIPC1 (dnGIPC1), as well as the downregulation of endogenous GIPC1, is sufficient to inhibit the development of eye field cells from mESCs.PMID:26013465
LOFHaploinsufficiency of GIPC1 may contribute to hearing impairment for its interaction with myosin VI.PMID:20648052

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

94 submitted variants in ClinVar

Classification Summary

Pathogenic14
Likely Pathogenic1
VUS63
Likely Benign5
Benign1
14
Pathogenic
1
Likely Pathogenic
63
VUS
5
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
14
0
14
Likely Pathogenic
0
0
1
0
1
VUS
0
58
5
0
63
Likely Benign
0
2
1
2
5
Benign
0
0
1
0
1
Total06022284

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

View in ClinVar →

Protein Context — Lollipop Plot

GIPC1 · 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 →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗