ATXN2

Chr 12ADMulti

ataxin 2

Also known as: ATX2, SCA2, TNRC13

The ATXN2 protein localizes to the endoplasmic reticulum and plasma membrane where it regulates endocytosis, modulates mTOR signaling, and controls ribosomal translation and mitochondrial function. Pathogenic expansions of the polyglutamine tract (normally 14-31 residues) cause autosomal dominant spinocerebellar ataxia type 2 when expanded to 32-200 residues, while intermediate expansions increase susceptibility to amyotrophic lateral sclerosis. The pathogenic mechanism involves loss of normal protein function due to the expanded polyglutamine tract.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
MultiplemechanismAD/MultiLOEUF 0.333 OMIM phenotypes
Clinical SummaryATXN2
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Gene-Disease Validity (ClinGen)
spinocerebellar ataxia type 2 · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.85) — some intolerance to loss-of-function variants.
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ClinVar Variants
11 unique Pathogenic / Likely Pathogenic· 164 VUS of 251 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — ATXN2
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.33LOEUF
pLI 0.853
Z-score 5.48
OE 0.20 (0.130.33)
Highly constrained

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

Missense Constraint
2.35Z-score
OE missense 0.74 (0.680.80)
466 obs / 632.0 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.20 (0.130.33)
00.351.4
Missense OE0.74 (0.680.80)
00.61.4
Synonymous OE0.94
01.21.6
LoF obs/exp: 11 / 54.8Missense obs/exp: 466 / 632.0Syn Z: 0.68
DN
0.2997th %ile
GOF
0.2597th %ile
LOF
0.83top 5%

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 0.33
GOF1 literature citation

Literature Evidence

GOFSpinocerebellar ataxia type 2 (SCA2) is an autosomal dominant neurodegenerative disease caused by CAG repeat expansion in the ATXN2 gene.PMID:28525545

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

251 submitted variants in ClinVar

Classification Summary

Pathogenic9
Likely Pathogenic2
VUS164
Likely Benign30
Benign15
Conflicting5
9
Pathogenic
2
Likely Pathogenic
164
VUS
30
Likely Benign
15
Benign
5
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
1
8
0
9
Likely Pathogenic
1
1
0
0
2
VUS
1
107
55
1
164
Likely Benign
5
10
8
7
30
Benign
0
5
7
3
15
Conflicting
5
Total71247811225

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

View in ClinVar →

Protein Context — Lollipop Plot

ATXN2 · 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 →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗