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C765R

Category 3/4 — Most DruggableConflictingLumenal · predictedσ-1 candidateEditorial
CysteineArginine at position 765 · C-terminal lumenal domain (653-869) · WFS1 (Wolframin)

Cysteine → Arginine at position 765 in wolframin's C-terminal lumenal domain. ClinVar Conflicting classifications including Wolfram syndrome 1. AlphaMissense 0.991 (near-maximum), DynaMut2 ΔΔG -1.06 kcal/mol (destabilising). The C765 partner residue of the C733 inferred disulfide.

Interactive 3D Structure

Wild-type reference
Wild-type C765 — hydrogen bond to A738
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DynaMut2 mutant · C765R
Mutant R765 — hydrogen bond to A738 lost (2 contacts lost)
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Bond changes · DynaMut2 interaction analysis

2 lost3 gained6 preserved
Interaction typeWild-type partnerMutant partnerStatus
Hydrogen bondC733Gained
Hydrogen bondA738Lost
Polar contactC733C733Preserved
Polar contactE737E737Preserved
CarbonylE737E737Preserved
Van der WaalsE737E737Preserved
Van der WaalsA738Gained
Van der WaalsH763H763Preserved
HydrophobicR732Lost
HydrophobicC733C733Preserved
HydrophobicA738Gained

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
-1.06kcal/mol
Destabilising — moderate
AlphaMissense
0.991
LPath
AlphaFold pLDDT
89
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 classificationConflicting classifications of pathogenicity
Review statuscriteria provided, conflicting classifications
Associated conditionsWolfram syndrome 1
InheritanceWolfram syndrome 1 documented.
Population frequency (gnomAD v4)Ultra-rare · AF 0.000068%
cDNA changec.2293T>C
ClinVar accessionVCV000166604
Last evaluated2014/11/17 00:00

Observed at very low frequency in gnomAD.

Classified for1★ unverified submission

ClinVar classifies this variant as Conflicting classifications of pathogenicity for Wolfram syndrome (classic) (autosomal recessive, OMIM 222300). Classic Wolfram syndrome is recessive: a single copy does not produce it, and this classification says nothing about a carrier's own risk.

  • 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 0.000068% · 1 / 1,460,554 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 / 1,111,9860

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 765 sits in wolframin's C-terminal lumenal domain. The AlphaFold model places C765 within 5 Å of HIS766 (2.4 Å — partner of D771H Atlas card region), PRO764 (2.5 Å), GLU737 (3.2 Å — same E737 as G736R/G736S neighbor), ALA738 (4.0 Å), and TYR739 (4.2 Å).

C765 was the partner residue identified in the C733G Atlas card (3.5 Å distance — possible disulfide). C765R replaces the cysteine at the OTHER end of this potential disulfide. The combination of C733G (cysteine removed) + C765R (cysteine replaced by arginine) at the inferred disulfide pair confirms both cysteines are pathogenic when mutated.

The |ΔΔG| of 1.06 reflects substantial fold cost. AlphaMissense's 0.991 (near-maximum) confirms severe functional consequence.

Amino-acid chemistry
Cysteine (C) → Arginine (R) — thiol-bearing residue replaced by large positively-charged guanidinium. Loss of disulfide potential plus charge introduction.
Position in the protein
C-terminal lumenal domain · position 765 in the ER lumen (pLDDT 89).

Druggability Assessment

Category 3/4 — Most Druggable. |ΔΔG| = 1.06 — fold survives. AlphaMissense 0.991 confirms severe functional consequence.

Mechanism is loss of the inferred C733-C765 disulfide bond plus charge introduction. Therapeutic strategy: site-directed at the C733-C765 microregion (same target as C733G).

Why this matters

C765R + C733G are the two pathogenic variants at opposite ends of the inferred C733-C765 disulfide. Two convergent variant targets at the same disulfide pair.
Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the C765R 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 C765R PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.

UniProt Domain Annotation

Chain1890 · Wolframin
Topological domain653869 · Lumenal