PYCARD

Chr 16

PYD and CARD domain containing

Also known as: ASC, CARD5, TMS, TMS-1, TMS1

The protein functions as a key adapter in inflammasome assembly and caspase-mediated apoptosis, mediating innate immune responses and inflammatory signaling pathways. Mutations cause autoinflammatory disorders with autosomal recessive inheritance, typically presenting with early-onset recurrent fever, skin rash, and arthritis. The gene shows low constraint to loss-of-function variants (pLI 0.0002, LOEUF 1.9), consistent with recessive inheritance patterns.

ResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 1.90
Clinical SummaryPYCARD
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
10 unique Pathogenic / Likely Pathogenic· 20 VUS of 39 total submissions
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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available
Some data sources returned errors (1)

omim: Error: OMIM fetch failed: 429

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.90LOEUF
pLI 0.000
Z-score -0.44
OE 1.24 (0.611.90)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.40Z-score
OE missense 0.89 (0.761.05)
103 obs / 115.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE1.24 (0.611.90)
00.351.4
Missense OE0.89 (0.761.05)
00.61.4
Synonymous OE1.13
01.21.6
LoF obs/exp: 5 / 4.0Missense obs/exp: 103 / 115.2Syn Z: -0.74
DN
0.7326th %ile
GOF
0.76top 25%
LOF
0.1697th %ile

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

GOFprediction above median
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.

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

ClinVar Variant Classifications

39 submitted variants in ClinVar

Classification Summary

Pathogenic9
Likely Pathogenic1
VUS20
Likely Benign1
Benign1
9
Pathogenic
1
Likely Pathogenic
20
VUS
1
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
9
0
9
Likely Pathogenic
0
0
1
0
1
VUS
0
13
7
0
20
Likely Benign
0
0
0
1
1
Benign
0
0
0
1
1
Total01317232

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

View in ClinVar →

Protein Context — Lollipop Plot

PYCARD · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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