DRP2

Chr X

dystrophin related protein 2

Also known as: DRP-2

DRP2 encodes a dystrophin family protein required for normal myelination and organization of cytoplasm in myelinating Schwann cells, where it helps localize PRX protein at specific membrane sites. Mutations cause Charcot-Marie-Tooth disease type 4J, an autosomal recessive peripheral neuropathy. The gene is highly constrained against loss-of-function variants, indicating that complete loss of DRP2 function is likely pathogenic.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
4
Pubs (1 yr)
22
P/LP submissions
0%
P/LP missense
0.63
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryDRP2
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
22 unique Pathogenic / Likely Pathogenic· 170 VUS of 300 total submissions
📖
GeneReview available — DRP2
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.63LOEUF
pLI 0.000
Z-score 3.38
OE 0.41 (0.280.63)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.70Z-score
OE missense 0.76 (0.690.83)
292 obs / 386.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.41 (0.280.63)
00.351.4
Missense OE0.76 (0.690.83)
00.61.4
Synonymous OE0.88
01.21.6
LoF obs/exp: 16 / 38.7Missense obs/exp: 292 / 386.0Syn Z: 1.15
DN
0.76top 25%
GOF
0.78top 25%
LOF
0.2970th %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

300 submitted variants in ClinVar

Classification Summary

Pathogenic21
Likely Pathogenic1
VUS170
Likely Benign77
Benign3
Conflicting2
21
Pathogenic
1
Likely Pathogenic
170
VUS
77
Likely Benign
3
Benign
2
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
2
0
19
0
21
Likely Pathogenic
1
0
0
0
1
VUS
2
151
14
3
170
Likely Benign
0
2
37
38
77
Benign
0
0
3
0
3
Conflicting
2
Total51537341274

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

View in ClinVar →

Protein Context — Lollipop Plot

DRP2 · 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 →