TARDBP

Chr 1AD

TAR DNA binding protein

Also known as: ALS10, TDP-43

The protein encoded by TARDBP is a transcriptional repressor that binds to chromosomally integrated TAR DNA to repress HIV-1 transcription and regulates alternative splicing of the CFTR gene. Mutations cause amyotrophic lateral sclerosis 10 with or without frontotemporal dementia and frontotemporal lobar degeneration through an autosomal dominant inheritance pattern. The pathogenic mechanism involves loss of function, as evidenced by the high constraint metrics indicating intolerance to loss-of-function variants.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
MultiplemechanismADLOEUF 0.282 OMIM phenotypes
Clinical SummaryTARDBP
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Gene-Disease Validity (ClinGen)
amyotrophic lateral sclerosis type 10 · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.99). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
63 unique Pathogenic / Likely Pathogenic· 209 VUS of 440 total submissions
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Clinical Trials
4 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — TARDBP
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.28LOEUF
pLI 0.985
Z-score 3.62
OE 0.06 (0.020.28)
Highly constrained

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

Missense Constraint
3.71Z-score
OE missense 0.32 (0.260.39)
74 obs / 233.5 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.06 (0.020.28)
00.351.4
Missense OE0.32 (0.260.39)
00.61.4
Synonymous OE1.10
01.21.6
LoF obs/exp: 1 / 17.2Missense obs/exp: 74 / 233.5Syn Z: -0.75
DN
0.4587th %ile
GOF
0.3689th %ile
LOF
0.75top 10%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to loss-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFprediction above median · LOEUF 0.28
GOF1 literature citation

Literature Evidence

GOFThese results suggest a toxic gain of function or dominant negative effect of mutant TDP-43.PMID:18309045

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

440 submitted variants in ClinVar

Classification Summary

Pathogenic39
Likely Pathogenic24
VUS209
Likely Benign108
Benign27
Conflicting15
39
Pathogenic
24
Likely Pathogenic
209
VUS
108
Likely Benign
27
Benign
15
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
9
30
0
39
Likely Pathogenic
1
15
8
0
24
VUS
8
131
67
3
209
Likely Benign
0
7
38
63
108
Benign
0
1
23
3
27
Conflicting
15
Total916316669422

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

View in ClinVar →

Protein Context — Lollipop Plot

TARDBP · 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 ↗