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E462G

Category 3/4 — Most DruggableLikely pathogenicTransmembrane · predictedEditorial
GlutamateGlycine at position 462 · Connecting loop · WFS1 (Wolframin)

Glutamate → Glycine at position 462 in a connecting loop. ClinVar Likely pathogenic. AlphaMissense 0.805, DynaMut2 ΔΔG -1.10 kcal/mol (destabilising). Loss of charge plus loss of side chain entirely.

Interactive 3D Structure

Wild-type reference
Wild-type E462 — hydrogen bond to A458
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DynaMut2 mutant · E462G
Mutant G462 — hydrogen bond to L459 lost (12 contacts lost)
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Bond changes · DynaMut2 interaction analysis

12 lost0 gained8 preserved
Interaction typeWild-type partnerMutant partnerStatus
Hydrogen bondA458A458Preserved
Hydrogen bondL459L459Preserved
Hydrogen bondA465Lost
Hydrogen bondG466G466Preserved
Hydrogen bondF538Lost
Hydrogen bondC541Lost
Hydrogen bondE542Lost
Polar contactA458A458Preserved
Polar contactL459L459Preserved
Polar contactT464Lost
Polar contactA465A465Preserved
Polar contactG466G466Preserved
Polar contactY534Lost
Polar contactF538Lost
Polar contactC541Lost
Van der WaalsT464T464Preserved
Van der WaalsA465Lost
Van der WaalsF538Lost
HydrophobicL511Lost
HydrophobicF538Lost

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
-1.10kcal/mol
Destabilising — moderate
AlphaMissense
0.805
LPath
AlphaFold pLDDT
85
model confidence
Schema
Cat 3/4
Category 3/4 — Most Druggable
ΔΔG confidence: Reduced confidence · Transmembrane
  • transmembrane position; predictor benchmarked on soluble proteins

This variant sits in the transmembrane band. The stability value was computed with a predictor benchmarked on water-soluble proteins. Published benchmarks of ddG predictors on membrane proteins report correlation below 0.4. Treat the magnitude as unreliable and the sign as weak evidence only.

Do not rank this value against a variant from a different region on ΔΔG alone.

Clinical Evidence

ClinVar classificationLikely pathogenic
Review statuscriteria provided, single submitter
Associated conditions(no specific conditions catalogued)
InheritanceInheritance not specified.
Population frequency (gnomAD v4)Absent from gnomAD v4
cDNA changec.1385A>G
ClinVar accessionVCV000092252
Last evaluated2024/07/01 00:00

Not observed in ~730k individuals — consistent with a rare allele (ACMG PM2_supporting).

Classified for1★ unverified submission

ClinVar classifies this variant as Likely 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)
Absent from gnomAD v4
Homozygotes
Not available

No population breakdown — the variant is absent from gnomAD v4, so no ancestry group has an observed frequency.

No homozygotes — the variant is absent from gnomAD v4 altogether.

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 462 sits in a connecting loop. The AlphaFold model places E462 within 5 Å of VAL463 (2.5 Å), THR461 (2.5 Å), LEU459 (3.7 Å), ALA458 (3.8 Å), and THR464 (4.3 Å). The local environment is hydrophobic-leaning with two threonines providing H-bond options.

The wild-type glutamate's carboxylate likely engages T461 or T464 through H-bonding while extending the negative charge toward solvent. Replacing E462 with glycine eliminates both the charge and the side chain — substantial loss for a single substitution.

The |ΔΔG| of 1.10 reflects this. AlphaMissense's 0.805 confirms pathogenic functional consequence. Mechanism is loss of E462's H-bonding role in the loop's polar network plus introduction of backbone flexibility where the wild-type constrained.

Amino-acid chemistry
Glutamate (E) → Glycine (G) — negatively-charged carboxylate replaced by smallest amino acid. Loss of charge and side-chain mass.
Position in the protein
Connecting loop · position 462 in a loop region (pLDDT 85).

Druggability Assessment

Category 3/4 — Most Druggable. |ΔΔG| = 1.10 — fold survives. AlphaMissense 0.805 confirms severe functional consequence.

Mechanism is loss of E462 H-bonding plus backbone flexibility gain. Therapeutic strategy: site-directed at the loop polar network.

Why this matters

E462G is one of several charge-loss-to-glycine variants in the Atlas — substantial structural and functional cost from a single substitution removing both charge and side chain.
Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the E462G 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 E462G PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.

UniProt Domain Annotation

Chain1890 · Wolframin
Natural variant461463 · in WFS1
Natural variant462462 · in CTRCT41; dbSNP:rs398123066