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G736R

Category 3/4 — Most DruggablePathogenicLumenal · predictedσ-1 candidateEditorial
GlycineArginine at position 736 · C-terminal lumenal domain (653-869) · WFS1 (Wolframin)

Glycine → Arginine at position 736 in wolframin's C-terminal lumenal domain. ClinVar Pathogenic. AlphaMissense 0.984, DynaMut2 ΔΔG -0.92 kcal/mol (destabilising). Another glycine-removal variant — paralleling the G674 cluster mechanism.

Interactive 3D Structure

Wild-type reference
Wild-type G736 — hydrogen bond to R732
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DynaMut2 mutant · G736R
Mutant R736 — energy-minimized; 9 new contacts formed
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Bond changes · DynaMut2 interaction analysis

0 lost9 gained5 preserved
Interaction typeWild-type partnerMutant partnerStatus
Ionic bondE717Gained
Hydrogen bondE717Gained
Hydrogen bondR732R732Preserved
Polar contactE717Gained
Polar contactR732R732Preserved
Polar contactC765Gained
Polar contactH766H766Preserved
CarbonylR732Gained
CarbonylC733Gained
CarbonylH766H766Preserved
Van der WaalsR732Gained
Van der WaalsH766H766Preserved
HydrophobicR732Gained
HydrophobicI767Gained

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
-0.92kcal/mol
Destabilising — mild
AlphaMissense
0.984
LPath
AlphaFold pLDDT
88
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 classificationPathogenic
Review statuscriteria provided, single submitter
Associated conditions(no specific conditions catalogued for G736R — ClinVar Pathogenic by review evidence)
InheritanceInheritance not specified. ClinVar Pathogenic classification with multiple submitters.
Population frequency (gnomAD v4)Ultra-rare · AF 0.00066%
cDNA changec.2206G>C
ClinVar accessionVCV002734647
Last evaluated2022/10/26 00:00

Observed at very low frequency in gnomAD.

Classified for1★ unverified submission

ClinVar classifies this variant as Pathogenic, but does not state what it is classified for. ClinVar records the condition only as "not provided". A classification without a phenotype and an inheritance mode cannot be read as a statement about Wolfram syndrome risk or severity.

  • 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 0.00066% · 1 / 152,202 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-sampled0.021%1 / 4,8320

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 736 sits in wolframin's C-terminal lumenal domain. The AlphaFold model places G736 within 5 Å of GLU737 (2.4 Å), TYR735 (2.5 Å), ARG732 (3.1 Å — a four-residue-back contact), HIS766 (3.3 Å — long-range), and ILE767 (4.1 Å). The local environment combines polar (E737, Y735), basic (R732), and titratable (H766) residues with a hydrophobic contact (I767).

The wild-type glycine at 736 plays the same backbone-flexibility role described for the G674 cluster. The neighbor analysis shows particularly tight packing — multiple residues within 4 Å — suggesting the local fold is geometrically constrained, and glycine's lack of side chain is what enables that geometry. Notably, ARG732 sits 3.1 Å away; the wild-type G736 plus R732 form a tight cluster where a single basic residue dominates the local electrostatic character.

Replacing glycine with arginine adds a second positive charge at 3.1 Å from the existing R732. This produces a two-arginine cluster similar to the G674R case — local electrostatic repulsion between adjacent positive charges plus the loss of glycine's backbone flexibility.

The |ΔΔG| of 0.92 reflects this combined cost. AlphaMissense's 0.984 score captures the severe functional consequence — likely disruption of a specific lumenal interaction surface where R732 alone served as the recognized positive charge.

Amino-acid chemistry
Glycine (G) → Arginine (R) — smallest amino acid replaced by a large, positively-charged guanidinium-bearing residue. Same chemistry shift as G674R but at a different position.
Position in the protein
C-terminal lumenal domain · position 736 sits in the ER lumen (pLDDT 88).

Druggability Assessment

Category 3/4 — Most Druggable. |ΔΔG| = 0.92 kcal/mol — fold survives. AlphaMissense 0.984 confirms severe functional consequence.

The mechanism is loss of glycine flexibility plus introduction of a second positive charge adjacent to R732 — disrupting a likely partner-recognition surface where R732 alone was the wild-type signature.

Therapeutic strategy: site-directed small molecules at the R732-G736-Y735 microregion. Pharmacological chaperones biasing the local backbone toward the wild-type glycine-enabled geometry.

Why this matters

G736R parallels the G674R mechanism — glycine removal in a tightly-packed loop adjacent to an existing arginine. The Atlas's per-variant analysis shows that this 'glycine-adjacent-to-arginine' pattern repeats multiple times across the WFS1 lumenal domain, and substitutions at the glycine positions are consistently pathogenic. The class is a coherent therapeutic target — drug discovery against the geometric niche of these glycines.
Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the G736R 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 G736R PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.

UniProt Domain Annotation

Chain1890 · Wolframin
Topological domain653869 · Lumenal
Natural variant736736 · in WFS1; dbSNP:rs71532864