RIPOR2

Chr 6ARAD

RHO family interacting cell polarization regulator 2

Also known as: C6orf32, DFNA21, DFNB104, DIFF40, DIFF48, FAM65B, MYONAP, PL48

The protein acts as an inhibitor of the small GTPase RHOA and is essential for normal development and structural organization of hair cell stereocilia within the cochlea, which is required for normal hearing. Mutations cause autosomal recessive deafness (DFNB104) or autosomal dominant deafness (DFNA21). The gene is highly constrained against loss-of-function variants, indicating that such mutations are likely to be pathogenic.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismAR/ADLOEUF 0.332 OMIM phenotypes
Clinical SummaryRIPOR2
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Gene-Disease Validity (ClinGen)
autosomal dominant nonsyndromic hearing loss · ADLimited

Limited evidence — not for standalone diagnostic reporting

2 total gene-disease associations curated

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.92). One damaged copy is likely sufficient to cause disease.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.33LOEUF
pLI 0.923
Z-score 5.21
OE 0.19 (0.110.33)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
2.37Z-score
OE missense 0.72 (0.660.78)
400 obs / 557.3 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.19 (0.110.33)
00.351.4
Missense OE0.72 (0.660.78)
00.61.4
Synonymous OE0.84
01.21.6
LoF obs/exp: 9 / 47.9Missense obs/exp: 400 / 557.3Syn Z: 1.86
DN
0.6161th %ile
GOF
0.6444th %ile
LOF
0.55top 25%

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

LOFLOEUF 0.33
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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

RIPOR2 · 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.

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Clinical Literature
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