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T337I

Category 3/4 — Most DruggableLikely pathogenicTransmembrane · predictedEditorial
ThreonineIsoleucine at position 337 · Connecting loop · WFS1 (Wolframin)

Threonine → Isoleucine at position 337 in a connecting loop. ClinVar Likely pathogenic for Wolfram syndrome 1. AlphaMissense 0.865, DynaMut2 ΔΔG -0.48 kcal/mol (destabilising). pLDDT 65 borderline.

Interactive 3D Structure

Wild-type reference
Wild-type T337 — hydrogen bond to N335
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DynaMut2 mutant · T337I
Mutant I337 — hydrogen bond to F340 lost (2 contacts lost)
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Bond changes · DynaMut2 interaction analysis

2 lost2 gained7 preserved
Interaction typeWild-type partnerMutant partnerStatus
Hydrogen bondN335N335Preserved
Hydrogen bondF340F340Preserved
Hydrogen bondF341F341Preserved
Polar contactN335N335Preserved
Polar contactD339D339Preserved
Polar contactF340F340Preserved
Polar contactF341F341Preserved
Van der WaalsN335Gained
Van der WaalsF340Lost
Van der WaalsF341Lost
HydrophobicD339Gained

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
-0.48kcal/mol
Destabilising — mild
AlphaMissense
0.865
LPath
AlphaFold pLDDT
65
model confidence
Schema
Cat 3/4
Category 3/4 — Most Druggable
ΔΔG confidence: Low confidence · Transmembrane
  • transmembrane position; predictor benchmarked on soluble proteins
  • pLDDT 65.12 below 70

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.

The underlying AlphaFold model has pLDDT below 70 at this position, so the structure the stability calculation was run on is itself uncertain.

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

Clinical Evidence

ClinVar classificationLikely pathogenic
Review statuscriteria provided, multiple submitters, no conflicts
Associated conditionsWolfram syndrome 1
InheritanceWolfram syndrome 1 (AR) documented.
Population frequency (gnomAD v4)Absent from gnomAD v4
cDNA changec.1010C>T
ClinVar accessionVCV002203515
Last evaluated2025/08/26 00:00

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

Classified for2★ documented assertion

ClinVar classifies this variant as Likely pathogenic for Wolfram syndrome (classic) (autosomal recessive, OMIM 222300). Classic Wolfram syndrome is recessive: a single copy does not produce it, and this classification says nothing about a carrier's own risk.

  • 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)
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 337 sits in a connecting loop near TM2. The AlphaFold model places T337 within 5 Å of ILE338 (2.4 Å), LEU336 (2.5 Å), ASN335 (4.1 Å), ASP339 (4.2 Å), and PHE340 (4.4 Å). The local environment is mixed polar-hydrophobic.

The wild-type threonine's hydroxyl likely H-bonds with the nearby N335 or D339. Replacing it with isoleucine eliminates the H-bonding capacity. The fold absorbs the substitution (|ΔΔG| 0.48), but the local H-bond network reorganizes.

AlphaMissense 0.865 + Wolfram 1 confirm pathogenic consequence. The mechanism is loss of T337's H-bonding role in the loop's polar network. pLDDT 65 is borderline; structural details deserve wet-lab confirmation.

Amino-acid chemistry
Threonine (T) → Isoleucine (I) — small polar hydroxyl replaced by branched aliphatic hydrophobic. Loss of H-bonding.
Position in the protein
Connecting loop · position 337 in a borderline-confidence region (pLDDT 65).

Druggability Assessment

Category 3/4 — Most Druggable (pLDDT caveat). |ΔΔG| = 0.48 — fold survives. AlphaMissense 0.865 + Wolfram 1 confirm pathogenic consequence. pLDDT 65 borderline.

Mechanism is loss of T337 H-bonding role. Therapeutic strategy: site-directed at the connecting loop polar network.

Why this matters

T337I is another threonine-to-isoleucine variant in the Atlas (with T361I). The class of T→I substitutions, removing H-bonding capacity, recurs at multiple positions and is consistently pathogenic.
Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the T337I 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 T337I PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.

UniProt Domain Annotation

Chain1890 · Wolframin