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R708L

Category 3/4 — Most DruggableLikely pathogenicLumenal · predictedσ-1 candidateEditorial
ArginineLeucine at position 708 · C-terminal lumenal domain (653-869) · WFS1 (Wolframin)

Arginine → Leucine at position 708 in wolframin's C-terminal lumenal domain. ClinVar Likely pathogenic, auditory neuropathy. AlphaMissense 0.954, DynaMut2 ΔΔG +0.20 kcal/mol — STABILISING. A charge-loss variant where the fold tightens slightly.

Interactive 3D Structure

Wild-type reference
Wild-type R708 — ionic bond to E776
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DynaMut2 mutant · R708L
Mutant L708 — ionic bond to E776 lost (5 contacts lost)
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Bond changes · DynaMut2 interaction analysis

5 lost2 gained5 preserved
Interaction typeWild-type partnerMutant partnerStatus
Ionic bondE776Lost
Hydrogen bondF775F775Preserved
Hydrogen bondE776E776Preserved
Polar contactT710Gained
Polar contactF775Lost
Polar contactE776E776Preserved
CarbonylF775Lost
Van der WaalsF775Lost
Van der WaalsE776E776Preserved
HydrophobicY706Gained
HydrophobicT710Lost
HydrophobicE776E776Preserved

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
0.20kcal/mol
Stabilising — mild
AlphaMissense
0.954
LPath
AlphaFold pLDDT
93
model confidence
Schema
Cat 3/4
Category 3/4 — Most Druggable
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 classificationLikely pathogenic
Review statuscriteria provided, single submitter
Associated conditionsAuditory neuropathy
InheritanceAuditory neuropathy documented.
Population frequency (gnomAD v4)Ultra-rare · AF 0.000068%
cDNA changec.2123G>T
ClinVar accessionVCV002683858
Last evaluated2023/12/22 00:00

Observed at very low frequency in gnomAD.

Classified for1★ unverified submission

ClinVar classifies this variant as Likely pathogenic for Hearing loss, inheritance unstated (inheritance not specified).

  • Hearing loss, inheritance unstatedinheritance not specifiedsubmitted as: Auditory neuropathy
  • This rests on a single submitter (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★ single submitter. ClinVar "conditions" is the union of all submissions; 0–1★ entries are submitted conditions, not documented phenotypes.

Population frequency
Global (all ancestries)
AF 0.000068% · 1 / 1,460,618 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.
European (non-Finnish) · under-sampled0.000090%1 / 1,111,8920

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 708 sits in wolframin's C-terminal lumenal domain. The AlphaFold model places R708 within 5 Å of VAL709 (2.4 Å), VAL707 (2.5 Å — same V707 as V707F Atlas card), and GLU776 (3.8 Å — likely salt-bridge partner).

The wild-type arginine likely forms an intramolecular salt bridge with E776 across the lumenal fold. Replacing R708 with leucine eliminates that salt bridge entirely. The DynaMut2 ΔΔG of +0.20 (stabilising) reflects that the leucine packs more efficiently into the hydrophobic V707-V709 local environment than the long arginine side chain did.

AlphaMissense's 0.954 + auditory neuropathy clinical evidence confirm severe functional consequence. The mechanism is loss of the R708-E776 salt bridge that the wild-type fold relied on, even though the local packing improves.

Amino-acid chemistry
Arginine (R) → Leucine (L) — large positively-charged guanidinium replaced by branched hydrophobic. Loss of charge entirely.
Position in the protein
C-terminal lumenal domain · position 708 in the ER lumen (pLDDT 93).

Druggability Assessment

Category 4 — Stable Fold, Function Disrupted. ΔΔG = +0.20 stabilising. AlphaMissense 0.954 + auditory neuropathy confirm severe functional consequence.

Mechanism is loss of R708-E776 salt bridge. Therapeutic strategy: bridge restoration through site-directed small molecules at the E776 microregion. Combined with V707F (adjacent position), drug discovery has convergent targets.

Why this matters

R708L is another Atlas stabilising-but-pathogenic variant. Combined with V707F at the adjacent position, the 707-708 microregion has two convergent therapeutic targets.
Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the R708L 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 R708L PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.

UniProt Domain Annotation

Chain1890 · Wolframin
Topological domain653869 · Lumenal
Natural variant708708 · in dbSNP:rs200099217