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C426Y

AlphaMissense: likely benign (0.09)Likely benignTransmembrane · predicted
CysteineTyrosine at position 426 · Lumenal loop 2 · WFS1 (Wolframin)

Interactive 3D Structure

Interactive structure
rotate · zoom · variant + 5 Å neighbors
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Computational Predictions

AlphaMissense
0.087
likely benign
AlphaFold pLDDT
83
model confidence
DynaMut2 ΔΔG
pending
not yet computed
ClinVar
Likely benign
Benign/Likely benign

AlphaMissense + AlphaFold card. This variant is mapped from AlphaMissense pathogenicity and AlphaFold confidence. The DynaMut2 ΔΔG stability prediction and the wild-type/mutant structural comparison (dual-pane + bond network) are computed per-variant and backfill here — they require a DynaMut2 submission, unlike the precomputed AlphaMissense score.

Clinical Evidence

ClinVar classificationBenign/Likely benign
Review statuscriteria provided, multiple submitters, no conflicts
Associated conditionsWFS1-Related Spectrum Disorders; Monogenic diabetes; Wolfram syndrome 1
Population frequency (gnomAD v4)Low frequency · AF 0.136%
cDNA changec.1277G>A
ClinVar accessionVCV000045432
Last evaluated2026/01/27 00:00

Observed in the general population.

Classified for2★ documented assertion

ClinVar classifies this variant as Benign/Likely benign for WFS1-related spectrum (unresolved mode) (dominant or recessive); WFS1-related diabetes (autosomal dominant); Wolfram syndrome (classic) (autosomal recessive, OMIM 222300). ClinVar records this under a WFS1-spectrum label that spans both disease families — recessive Wolfram syndrome (biallelic) and the dominant WFS1-related disorders. The label does not resolve which applies, and it is not a severity statement.

  • WFS1-related spectrum (unresolved mode)dominant or recessivesubmitted as: WFS1-Related Spectrum Disorders
  • WFS1-related diabetesautosomal dominantsubmitted as: Monogenic diabetes
  • Wolfram syndrome (classic)autosomal recessive · OMIM 222300submitted as: Wolfram syndrome 1
  • 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: 2★ multiple submitters, no conflicts. ClinVar "conditions" is the union of all submissions; 0–1★ entries are submitted conditions, not documented phenotypes.

Population frequency
Global (all ancestries)
AF 0.136% · 2,195 / 1,613,942 alleles
Homozygotes
41
Highest-frequency population
Ashkenazi Jewish · AF 5.17%

Highest in Ashkenazi Jewish: AF 5.17% (1530 of 29,608 alleles), 38.0x the global figure. The global AF describes the general population, not the at-risk group.

41 homozygotes reported in gnomAD v4 (41 Ashkenazi Jewish). gnomAD excludes individuals with severe pediatric disease, so homozygotes in this dataset argue against a fully penetrant severe recessive phenotype and belong in the clinical picture. This is interpretive signal, not a classification.

Ancestry groupAllele freq.AC / ANHom.Carrier est.
Ashkenazi Jewish5.17%1,530 / 29,60841~1 in 10
Remaining individuals0.363%227 / 62,4860~1 in 140
Middle Eastern0.115%7 / 6,0840~1 in 430
Admixed American0.043%26 / 60,0060~1 in 1150
European (non-Finnish)0.033%392 / 1,180,0320~1 in 1510
South Asian0.0099%9 / 91,0840~1 in 5060
Finnish0.0031%2 / 63,9280~1 in 15980
African / African American0.0027%2 / 74,9220~1 in 18730

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.

Full Variant Card

C426Y — WFS1 Molecular Atlas Card

Variant type: Missense Substitution: Cysteine (C) → Tyrosine (Y) at position 426 Domain context: Lumenal loop 2


AlphaMissense

  • Pathogenicity score: 0.0872
  • Class: likely benign

AlphaFold confidence

  • pLDDT at residue 426: 83.44

DynaMut2 ΔΔG: not yet computed for this variant — AlphaMissense + AlphaFold confidence shown above. Stability ΔΔG and the wild-type/mutant structural comparison backfill behind this note.


Clinical evidence

Inheritance and scope

Benign/Likely benign — for WFS1-related spectrum (unresolved mode) (dominant or recessive); WFS1-related diabetes (autosomal dominant); Wolfram syndrome (classic) (autosomal recessive, OMIM 222300)

ClinVar classifies this variant as Benign/Likely benign for WFS1-related spectrum (unresolved mode) (dominant or recessive); WFS1-related diabetes (autosomal dominant); Wolfram syndrome (classic) (autosomal recessive, OMIM 222300). ClinVar records this under a WFS1-spectrum label that spans both disease families — recessive Wolfram syndrome (biallelic) and the dominant WFS1-related disorders. The label does not resolve which applies, and it is not a severity statement.

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.

  • Classification: Benign/Likely benign
  • Review status: criteria provided, multiple submitters, no conflicts
  • Associated conditions: WFS1-Related Spectrum Disorders; Monogenic diabetes; Wolfram syndrome 1
  • cDNA change: c.1277G>A
  • ClinVar accession: VCV000045432
  • Last evaluated: 2026/01/27 00:00
  • Submissions: 1

Card generated by wolfram-atlas-batch (missense AlphaMissense mint) on 2026-06-08T02:27:33.528313Z. AlphaMissense (Cheng et al. 2023) · AlphaFold model v6 · UniProt O76024.

Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the C426Y 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 C426Y PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.