The DST protein is a cytoskeletal linker that integrates intermediate filaments, actin, and microtubule networks, anchoring intermediate filaments to the actin cytoskeleton in neural and muscle cells and keratin filaments to hemidesmosomes in epithelial cells. Autosomal recessive mutations cause congenital myopathy with contractures, lethal congenital contracture syndrome, hereditary sensory and autonomic neuropathy type VI, and epidermolysis bullosa simplex with skin blistering. This gene is highly constrained against loss-of-function variants, reflecting its critical role in maintaining cytoskeletal integrity across multiple tissue types including skin, muscle, and peripheral nerves.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismARLOEUF 0.184 OMIM phenotypes
Clinical SummaryDST
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Gene-Disease Validity (ClinGen)
hereditary sensory and autonomic neuropathy type 6 · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
23 unique Pathogenic / Likely Pathogenic· 113 VUS of 200 total submissions
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Clinical Trials
5 active or recruiting trials — potential therapeutic options may be available
Some data sources returned errors (1)

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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.18LOEUF
pLI 1.000
Z-score 13.32
OE 0.14 (0.100.18)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
2.22Z-score
OE missense 0.88 (0.840.91)
2223 obs / 2537.8 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.14 (0.100.18)
00.351.4
Missense OE0.88 (0.840.91)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 38 / 277.4Missense obs/exp: 2223 / 2537.8Syn Z: 0.43
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedDST-related neuropathy, hereditary sensory and autonomicOTHERAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
1.00top 5%
GOF
1.00top 5%
LOF
0.2970th %ile

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

200 submitted variants in ClinVar

Classification Summary

Pathogenic19
Likely Pathogenic4
VUS113
Likely Benign61
Benign2
Conflicting1
19
Pathogenic
4
Likely Pathogenic
113
VUS
61
Likely Benign
2
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
16
0
3
0
19
Likely Pathogenic
4
0
0
0
4
VUS
1
92
8
12
113
Likely Benign
0
3
11
47
61
Benign
0
0
2
0
2
Conflicting
1
Total21952459200

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

DST · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗