CLEC12A

Chr 12

C-type lectin domain family 12 member A

Also known as: CD371, CLL-1, CLL1, DCAL-2, MICL, hKLRL1

The protein functions as a myeloid inhibitory C-type lectin receptor that negatively regulates immune cell activation by recognizing various ligands including neutrophil extracellular traps, urate crystals, and pathogen-associated molecules. Mutations in CLEC12A cause autosomal recessive autoinflammatory disease with immunodeficiency, typically presenting in infancy with recurrent infections and inflammatory manifestations. The gene shows low constraint against loss-of-function variants (LOEUF 1.43), consistent with recessive inheritance requiring biallelic mutations for disease manifestation.

Summary from RefSeq, UniProt
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2
Active trials
18
Pubs (1 yr)
36
P/LP submissions
0%
P/LP missense
1.43
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryCLEC12A
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
36 unique Pathogenic / Likely Pathogenic· 86 VUS of 142 total submissions
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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.43LOEUF
pLI 0.000
Z-score 0.44
OE 0.87 (0.541.43)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.22Z-score
OE missense 1.05 (0.921.21)
141 obs / 133.9 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.87 (0.541.43)
00.351.4
Missense OE1.05 (0.921.21)
00.61.4
Synonymous OE1.04
01.21.6
LoF obs/exp: 11 / 12.7Missense obs/exp: 141 / 133.9Syn Z: -0.23
DN
0.85top 5%
GOF
0.72top 25%
LOF
0.1598th %ile

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

DNprediction above median
GOFprediction 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.

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

ClinVar Variant Classifications

142 submitted variants in ClinVar

Classification Summary

Pathogenic34
Likely Pathogenic2
VUS86
Likely Benign11
34
Pathogenic
2
Likely Pathogenic
86
VUS
11
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
34
0
34
Likely Pathogenic
0
0
2
0
2
VUS
0
81
5
0
86
Likely Benign
0
11
0
0
11
Benign
0
0
0
0
0
Total092410133

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

View in ClinVar →

Protein Context — Lollipop Plot

CLEC12A · protein map & ClinVar variants

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

Clinical Literature
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