ANKRD26

Chr 10AD

ankyrin repeat domain 26

Also known as: THC2, bA145E8.1

The protein contains ankyrin repeats that mediate protein-protein interactions and regulates adipogenesis and feeding behavior. Mutations cause autosomal dominant thrombocytopenia-2, a bleeding disorder characterized by reduced platelet counts. This gene is not highly constrained against loss-of-function variants and has an established GeneReviews entry for clinical guidance.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Thrombocytopenia 2MIM #188000
AD
1
Active trials
19
Pubs (1 yr)
0
P/LP submissions
P/LP missense
0.73
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryANKRD26
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Gene-Disease Validity (ClinGen)
thrombocytopenia 2 · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
326 VUS of 500 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
📖
GeneReview available — ANKRD26
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.73LOEUF
pLI 0.000
Z-score 3.68
OE 0.58 (0.470.73)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
-0.40Z-score
OE missense 1.04 (0.981.10)
855 obs / 823.1 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.58 (0.470.73)
00.351.4
Missense OE1.04 (0.981.10)
00.61.4
Synonymous OE0.99
01.21.6
LoF obs/exp: 53 / 90.9Missense obs/exp: 855 / 823.1Syn Z: 0.16
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongANKRD26-related thrombocytopeniaOTHERAD
DN
0.82top 10%
GOF
0.6638th %ile
LOF
0.2190th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). The Badonyi & Marsh model scores dominant-negative highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports gain-of-function. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median · 1 literature citation
DNprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Literature Evidence

GOFTaken together, these data suggest that THC2 is more likely to be due to a gain of function effect rather than a haploinsufficiency of ANKRD26.PMID:21211618

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

500 submitted variants in ClinVar

Classification Summary

VUS326
Likely Benign152
Benign1
Conflicting4
326
VUS
152
Likely Benign
1
Benign
4
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
0
0
0
Likely Pathogenic
0
0
0
0
0
VUS
11
295
19
1
326
Likely Benign
0
11
19
122
152
Benign
0
0
1
0
1
Conflicting
4
Total1130639123483

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

View in ClinVar →

Protein Context — Lollipop Plot

ANKRD26 · protein map & ClinVar variants

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

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