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L187F

Category 3/4 — Most DruggablePathogenic/Likely pathogenicCytoplasmic · predictedEditorial
LeucinePhenylalanine at position 187 · N-terminal cytoplasmic domain (87-313) · WFS1 (Wolframin)

Leucine → Phenylalanine at position 187 in wolframin's N-terminal cytoplasmic domain. ClinVar Pathogenic/Likely pathogenic with broad clinical spectrum — Cataract 41, Wolfram-like syndrome, DFNA6. AlphaMissense 0.954, DynaMut2 ΔΔG -1.42 kcal/mol (destabilising). A conservative-looking substitution with substantial structural cost.

Interactive 3D Structure

Wild-type reference
Wild-type L187 — hydrogen bond to M183
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DynaMut2 mutant · L187F
Mutant F187 — hydrogen bond to N203 lost (3 contacts lost)
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Bond changes · DynaMut2 interaction analysis

3 lost2 gained14 preserved
Interaction typeWild-type partnerMutant partnerStatus
Hydrogen bondM183M183Preserved
Hydrogen bondY184Y184Preserved
Hydrogen bondL200Lost
Hydrogen bondN203N203Preserved
Polar contactM183M183Preserved
Polar contactY184Y184Preserved
Polar contactP189P189Preserved
Polar contactN203N203Preserved
Aromatic / πF247Gained
CarbonylY184Lost
Van der WaalsY184Y184Preserved
Van der WaalsL200Lost
HydrophobicM183M183Preserved
HydrophobicL200L200Preserved
HydrophobicN203Gained
HydrophobicV204V204Preserved
HydrophobicV207V207Preserved
HydrophobicL230L230Preserved
HydrophobicF247F247Preserved

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
-1.42kcal/mol
Destabilising — moderate
AlphaMissense
0.954
LPath
AlphaFold pLDDT
84
model confidence
Schema
Cat 3/4
Category 3/4 — Most Druggable

Clinical Evidence

ClinVar classificationPathogenic/Likely pathogenic
Review statuscriteria provided, multiple submitters, no conflicts
Associated conditionsCataract 41; Wolfram-like syndrome; Autosomal dominant nonsyndromic hearing loss 6 (DFNA6)
InheritanceAutosomal dominant pattern indicated by association with DFNA6 (WFS1-related hearing loss) and Wolfram-like syndrome.
Population frequency (gnomAD v4)Absent from gnomAD v4
cDNA changec.559C>T
ClinVar accessionVCV002193625
Last evaluated2024/04/16 00:00

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

Structural Context

Position 187 sits in wolframin's N-terminal cytoplasmic domain. The AlphaFold model places L187 within 5 Å of ASN188 (2.5 Å), LYS186 (2.5 Å), TYR184 (3.6 Å), MET183 (3.9 Å), and ASN203 (4.1 Å). The local environment is mixed — aromatic (Y184), polar (N188, N203), basic (K186), and hydrophobic (M183, L187 itself).

Replacing leucine with phenylalanine at this position is more disruptive than the chemistry pair suggests. Phenylalanine is roughly 50% larger by side-chain volume and introduces an aromatic ring where leucine had only branched aliphatic carbons. The local pocket — packed against TYR184 (3.6 Å) and MET183 (3.9 Å) — was sized for leucine. Adding a phenyl ring forces local rearrangement.

The |ΔΔG| of 1.42 kcal/mol reflects this volume mismatch. The fold absorbs the substitution but at meaningful energetic cost. The introduced aromatic ring also creates a new potential π-π stacking opportunity with TYR184 — but at a geometry not optimized for it in the wild-type fold, so this contact may or may not form productively.

The clinical breadth — Cataract 41, Wolfram-like syndrome, DFNA6 hearing loss — confirms severe functional consequence across multiple tissue contexts.

Amino-acid chemistry
Leucine (L) → Phenylalanine (F) — a medium-sized branched hydrophobic replaced by a larger aromatic hydrophobic. Volume increase plus π-electron system added.
Position in the protein
N-terminal cytoplasmic domain · position 187 sits in the cytosol-facing region of wolframin with good AlphaFold confidence (pLDDT 84).

Druggability Assessment

Category 3/4 — Most Druggable. |ΔΔG| = 1.42 kcal/mol — meaningful but below the Cat 2 threshold. AlphaMissense 0.954 + three documented clinical phenotypes confirm severe functional consequence.

The mechanism is volume mismatch in a cytoplasmic packing pocket (TYR184, MET183 environment). Therapeutic strategy: site-directed binders that occupy the disrupted packing region, or pharmacological chaperones biasing the fold toward the wild-type leucine geometry.

The clinical breadth (three phenotypes across both AD and tissue-specific presentations) makes this a high-value docking target.

Why this matters

L187F demonstrates that 'conservative' substitutions in chemistry tables can be structurally non-conservative — what looks like a small change in side-chain class (aliphatic to aromatic) becomes substantial when packed into a pocket that wasn't sized for the larger residue. The Atlas's neighbor analysis surfaces the specific contacts (TYR184, MET183) that the substitution perturbs, making the geometric target visible.
Therapeutic Strategy Handoff · prediction

Feed this card to Wolfram Intelligence

Download the L187F 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 L187F PDF card ↓Strategies are AI-generated predictions, not validated therapeutics.

UniProt Domain Annotation

Chain1890 · Wolframin
Region1321 · Interaction with ATP6V1A