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M518K

Category 3/4 — Most DruggableConflictingTransmembrane · predictedEditorial
MethionineLysine at position 518 · Connecting loop · WFS1 (Wolframin)

Methionine → Lysine at position 518 in a connecting loop. ClinVar Conflicting including optic neuropathy. AlphaMissense 0.925, ΔΔG -0.64 (destabilising). Same position as M518I (Atlas card).

Interactive 3D Structure

Wild-type reference
Wild-type M518 — hydrogen bond to L521
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DynaMut2 mutant · M518K
Mutant K518 — hydrogen bond to L521 lost (4 contacts lost)
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Bond changes · DynaMut2 interaction analysis

4 lost4 gained8 preserved
Interaction typeWild-type partnerMutant partnerStatus
Hydrogen bondL514L514Preserved
Hydrogen bondF515F515Preserved
Hydrogen bondL521L521Preserved
Hydrogen bondG526Gained
Polar contactL514L514Preserved
Polar contactF515F515Preserved
Polar contactL521L521Preserved
Van der WaalsA458Gained
Van der WaalsL514Gained
Van der WaalsL521Gained
HydrophobicY454Lost
HydrophobicT455T455Preserved
HydrophobicA458Lost
HydrophobicL514Lost
HydrophobicF515Lost
HydrophobicY534Y534Preserved

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
-0.64kcal/mol
Destabilising — mild
AlphaMissense
0.925
LPath
AlphaFold pLDDT
84
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 classificationConflicting classifications of pathogenicity
Review statuscriteria provided, conflicting classifications
Associated conditionsOptic neuropathy
InheritanceOptic neuropathy documented.
Population frequency (gnomAD v4)Ultra-rare · AF 0.0013%
cDNA changec.1553T>A
ClinVar accessionVCV001320487
Last evaluated2025/08/01 00:00

Observed at very low frequency in gnomAD.

Classified for1★ unverified submission

ClinVar classifies this variant as Conflicting classifications of pathogenicity for Optic atrophy / optic neuropathy (autosomal dominant). These are dominant WFS1-related disorders and are clinically distinct from classic recessive Wolfram syndrome. This classification is not a statement about Wolfram syndrome severity.

  • Optic atrophy / optic neuropathyautosomal dominantsubmitted as: Optic neuropathy
  • 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 0.0013% · 19 / 1,460,046 alleles
Homozygotes
0
Highest-frequency population
South Asian · AF 0.021%

Highest in South Asian: AF 0.021% (18 of 86,258 alleles), 16.0x the global figure. The global AF describes the general population, not the at-risk group.

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 Asian0.021%18 / 86,2580~1 in 2400
Remaining individuals · under-sampled0.0017%1 / 60,3840

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 518 same neighbors as M518I: ALA519 (2.5 Å), ARG517 (2.5 Å — adjacent existing arginine), PHE515 (3.7 Å), LEU514 (3.8 Å), LEU521 (3.9 Å).

M518K is the second substitution at position 518. Unlike M518I (conservative hydrophobic-to-hydrophobic), M518K introduces a charged residue. The new K518 amine adjacent to existing R517 creates a two-basic cluster where wild-type had M518's sulfur chemistry.

The |ΔΔG| of 0.64 is larger than M518I's 0.29 — the charge introduction has greater structural cost than conservative volume change. AlphaMissense 0.925 + optic neuropathy confirm severe consequence.

Amino-acid chemistry
Methionine (M) → Lysine (K) — flexible sulfur-containing hydrophobic replaced by long positively-charged amine. Charge introduction into a hydrophobic loop position.
Position in the protein
Connecting loop · position 518 (pLDDT 84). Same position as M518I.

Druggability Assessment

Category 3/4 — Most Druggable. |ΔΔG| = 0.64 — fold survives. AlphaMissense 0.925 + optic neuropathy confirm severe consequence.

Mechanism: charge introduction into the M518 hydrophobic environment, creating a two-basic cluster with R517. Therapeutic: same M518 microregion as M518I.

Why this matters

M518K + M518I at same position — both pathogenic but through different mechanisms (charge introduction vs lost methionine chemistry).
Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the M518K 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 M518K PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.

UniProt Domain Annotation

Chain1890 · Wolframin