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R703H

Category 4 — Stable Fold, Function DisruptedConflictingLumenal · predictedσ-1 candidateEditorial
ArginineHistidine at position 703 · C-terminal lumenal domain (653-869) · WFS1 (Wolframin)

Arg→His p703 lumenal AM=0.10 ddg=-1.21 pLDDT=89. ClinVar Conflicting evidence. Atlas mechanism: see structural analysis.

Interactive 3D Structure

Wild-type reference
Wild-type R703 — ionic bond to E795
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DynaMut2 mutant · R703H
Mutant H703 — ionic bond to E795 lost (6 contacts lost)
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Bond changes · DynaMut2 interaction analysis

6 lost2 gained6 preserved
Interaction typeWild-type partnerMutant partnerStatus
Ionic bondE795Lost
Hydrogen bondV779Lost
Hydrogen bondG780G780Preserved
Hydrogen bondE795Lost
Hydrogen bondG820Gained
Hydrogen bondS821S821Preserved
Polar contactK705K705Preserved
Polar contactG780G780Preserved
Polar contactE795Lost
Polar contactS821S821Preserved
CarbonylS821S821Preserved
Van der WaalsE795Lost
Van der WaalsS821Gained
HydrophobicL822Lost

Lost / gained / preserved interatomic contacts at the variant residue, from the DynaMut2 (Arpeggio) interaction analysis of the wild-type and energy-minimized mutant structures.

Computational Predictions

DynaMut2 ΔΔG
-1.21kcal/mol
Destabilising — moderate
AlphaMissense
0.104
LBen
AlphaFold pLDDT
89
model confidence
Schema
Cat 4
Category 4 — Stable Fold, Function Disrupted
ΔΔG confidence: Standard confidence · Lumenal

This variant is in a water-facing region, which is the regime the stability predictor was built and benchmarked for. Ordinary predictor error still applies.

Clinical Evidence

ClinVar classificationConflicting classifications of pathogenicity
Review statuscriteria provided, conflicting classifications
Associated conditions(no specific conditions catalogued)
InheritanceConflicting ClinVar classifications.
Population frequency (gnomAD v4)Ultra-rare · AF 0.00012%
cDNA changec.2108G>A
ClinVar accessionVCV001297606
Last evaluated2026/03/19 00:00

Observed at very low frequency in gnomAD.

Classified for1★ unverified submission

ClinVar classifies this variant as Conflicting classifications of pathogenicity for Hearing loss, inheritance unstated (inheritance not specified); Nonsyndromic hearing loss (DFNA6/14/38) (autosomal dominant, OMIM 600965); Cataract 41 (autosomal dominant, OMIM 116400); Wolfram-like syndrome (autosomal dominant, OMIM 614296); WFS1-related diabetes (autosomal dominant); Wolfram syndrome (classic) (autosomal recessive, OMIM 222300). These are two clinically distinct disease families: classic Wolfram syndrome requires two affected copies, while the dominant WFS1-related disorders do not. One label covers both, and it does not tell you which applies to a given person.

  • Hearing loss, inheritance unstatedinheritance not specifiedsubmitted as: Monogenic hearing loss
  • Nonsyndromic hearing loss (DFNA6/14/38)autosomal dominant · OMIM 600965submitted as: Autosomal dominant nonsyndromic hearing loss 6
  • Cataract 41autosomal dominant · OMIM 116400submitted as: Cataract 41
  • Wolfram-like syndromeautosomal dominant · OMIM 614296submitted as: Wolfram-like syndrome; Wolfram-like syndrome
  • WFS1-related diabetesautosomal dominantsubmitted as: Type 2 diabetes mellitus
  • Wolfram syndrome (classic)autosomal recessive · OMIM 222300submitted as: Wolfram syndrome 1
  • Submitters conflict on this classification (1★). Treat the conditions above as submitted, not as documented phenotypes.
  • Phenotype scope is interpretation of submitted records. The computed values on this card (AlphaMissense, DynaMut2 ΔΔG, pLDDT) are measurements of the model, not of a patient.
  • Presentation cannot be generalised from neighbouring variants: one nucleotide over can present very differently. Structural similarity supports a mechanistic hypothesis, never a phenotype claim.

Review status: 1★ conflicting classifications. ClinVar "conditions" is the union of all submissions; 0–1★ entries are submitted conditions, not documented phenotypes.

Population frequency
Global (all ancestries)
AF 0.00012% · 2 / 1,612,712 alleles
Homozygotes
0

Every ancestry group with observed alleles falls below the reporting threshold (min 2 alleles, min 500 sampled) — too sparse to name a highest-frequency population.

No homozygotes reported in gnomAD v4. For a recessive allele this is expected and is not, on its own, evidence either way.

Ancestry groupAllele freq.AC / ANHom.Carrier est.
South Asian · under-sampled0.0011%1 / 91,0820
European (non-Finnish) · under-sampled0.000085%1 / 1,179,8360

Source: gnomAD r4, retrieved 2026-08-21. Values are allele frequencies. The carrier estimate is derived from the allele frequency (Hardy-Weinberg, ~2·AF) and is an approximation, not a published figure — where a published carrier frequency exists it outranks this column and is cited on the card.

Structural Context

Position analysis: PHE704 (2.4 Å), GLY702 (2.5 Å — G702S!), SER821 (3.4 Å — long-range). Substantial ΔΔG. Same dense 702-708 cluster. The Atlas's neighbor extraction surfaces this variant's contacts.

Amino-acid chemistry
partial charge reduction
Position in the protein
C-terminal lumenal domain

Druggability Assessment

Cat 3/4 — see structural prose. AlphaMissense below threshold (AM under-call class) but mechanism is structurally clear from neighbor analysis. Therapeutic strategy: site-directed at the contacts identified above.

Why this matters

Continues 702-708 dense cluster.
Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the R703H PDF below and upload it to Wolfram Intelligence to generate therapeutic-strategy proposals — guanidinium mimetics, sigma-1 agonist docking, NAC thiol-capping. NAC is already on the bench-testing list.

Download R703H PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.

UniProt Domain Annotation

Chain1890 · Wolframin
Topological domain653869 · Lumenal
Natural variant703703 · in DFNA6; dbSNP:rs1323852277