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S855=

SynonymousSilentBenignLumenal · predicted
Synonymous variant · codon at position 855 · C-terminal ER-lumenal (calcium binding, calmodulin, chaperone) · WFS1 (Wolframin)

SilentSilent — no amino-acid change

Interactive 3D Structure

Interactive structure
rotate · zoom · variant + 5 Å neighbors
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AlphaFold wild-type wolframin · the variant site near residue 855 (C-terminal ER-lumenal (calcium binding, calmodulin, chaperone)) is highlighted.

Variant Assessment

Variant type
Synonymous
Schema
Silent
Silent — no amino-acid change
Domain
C-terminal ER-lumenal (calcium binding, calmodulin, chaperone)
Status

Therapeutic Implication · Silent

No amino-acid change (S855 is unchanged): the codon is altered but the protein sequence is identical to wild-type. No structural, stability or AlphaMissense effect applies. Synonymous variants are typically benign unless they affect splicing or regulatory elements; this one is not adjacent to an exon boundary.

Clinical Evidence

ClinVar classificationBenign
Review statuscriteria provided, multiple submitters, no conflicts
Associated conditionsWFS1-Related Spectrum Disorders; Autosomal dominant nonsyndromic hearing loss 6
Population frequency (gnomAD v4)Common · AF 69.92%
cDNA changec.2565A>G
Protein consequenceS855=
ClinVar variantNM_006005.3(WFS1):c.2565A>G (p.Ser855=)
ClinVar accessionVCV000045456
Last evaluated2026/02/04 00:00

Population frequency too high for a penetrant Wolfram allele — stand-alone benign evidence (ACMG BA1).

Classified for2★ documented assertion

ClinVar classifies this variant as Benign for WFS1-related spectrum (unresolved mode) (dominant or recessive); Nonsyndromic hearing loss (DFNA6/14/38) (autosomal dominant, OMIM 600965). 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
  • Nonsyndromic hearing loss (DFNA6/14/38)autosomal dominant · OMIM 600965submitted as: Autosomal dominant nonsyndromic hearing loss 6
  • 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 69.92% · 1,127,544 / 1,612,712 alleles
Homozygotes
397,452
Highest-frequency population
East Asian · AF 95.54%

Highest in East Asian: AF 95.54% (42879 of 44,882 alleles), in line with the global figure.

397452 homozygotes reported in gnomAD v4 (20517 East Asian; 9205 Ashkenazi Jewish; 18182 Admixed American; 26782 South Asian; 21702 African / African American; 1775 Middle Eastern; 16232 Remaining individuals; 271400 European (non-Finnish); 11517 Finnish; 140 Amish). 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.
East Asian95.54%42,879 / 44,88220517~1 in 1
Ashkenazi Jewish78.76%23,307 / 29,5929205~1 in 1
Admixed American77.67%46,596 / 59,99418182~1 in 1
South Asian76.47%69,644 / 91,06826782~1 in 1
African / African American76.05%57,069 / 75,04021702~1 in 1
Middle Eastern75.83%4,597 / 6,0621775~1 in 1
Remaining individuals71.94%44,955 / 62,48616232~1 in 1
European (non-Finnish)67.81%800,094 / 1,179,894271400~1 in 1
Finnish60.34%37,887 / 62,78611517~1 in 1
Amish56.83%516 / 908140~1 in 1

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.

Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the S855= card below and upload it to Wolfram Intelligence to generate therapeutic-strategy proposals matched to this Silent synonymous variant and its domain context.

Full Variant Card

S855= — WFS1 Molecular Atlas Card

Variant type: Synonymous (silent) Codon: position 855 (Serine, S) — amino acid unchanged Domain context: C-terminal ER-lumenal (calcium binding, calmodulin, chaperone)


Schema category: Silent — Silent — no amino-acid change

No amino-acid change (S855 is unchanged): the codon is altered but the protein sequence is identical to wild-type. No structural, stability or AlphaMissense effect applies. Synonymous variants are typically benign unless they affect splicing or regulatory elements; this one is not adjacent to an exon boundary.


Clinical evidence

Inheritance and scope

Benign — for WFS1-related spectrum (unresolved mode) (dominant or recessive); Nonsyndromic hearing loss (DFNA6/14/38) (autosomal dominant, OMIM 600965)

ClinVar classifies this variant as Benign for WFS1-related spectrum (unresolved mode) (dominant or recessive); Nonsyndromic hearing loss (DFNA6/14/38) (autosomal dominant, OMIM 600965). 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
  • Review status: criteria provided, multiple submitters, no conflicts
  • Associated conditions: WFS1-Related Spectrum Disorders; Autosomal dominant nonsyndromic hearing loss 6
  • cDNA change: c.2565A>G
  • ClinVar accession: VCV000045456
  • Last evaluated: 2026/02/04 00:00
  • Submissions: 1

Card generated by wolfram-atlas-batch (synonymous pipeline) on 2026-06-08T02:56:47.019706Z. WFS1: UniProt O76024, AlphaFold v6. Synonymous variants carry no protein-structural effect.