PLCG2

Chr 16AD

phospholipase C gamma 2

Also known as: APLAID, FCAS3, PLC-IV, PLC-gamma-2

The encoded phospholipase C gamma 2 enzyme catalyzes the conversion of phosphatidylinositol 4,5-bisphosphate to the second messengers IP3 and diacylglycerol, which are crucial for transmitting signals from growth factor and immune system receptors across cell membranes. Mutations cause autoinflammation, antibody deficiency, and immune dysregulation syndrome as well as familial cold autoinflammatory syndrome 3, both inherited in an autosomal dominant pattern. This gene is highly constrained against loss-of-function mutations, indicating that protein function is essential for normal cellular processes.

OMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismADLOEUF 0.282 OMIM phenotypes
Clinical SummaryPLCG2
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
47 VUS of 100 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.28LOEUF
pLI 0.996
Z-score 6.87
OE 0.18 (0.120.28)
Highly constrained

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

Missense Constraint
0.82Z-score
OE missense 0.92 (0.860.98)
711 obs / 774.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.18 (0.120.28)
00.351.4
Missense OE0.92 (0.860.98)
00.61.4
Synonymous OE1.36
01.21.6
LoF obs/exp: 15 / 82.2Missense obs/exp: 711 / 774.8Syn Z: -5.04
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedPLCG2-related autoinflammation, antibody deficiency, and immune dysregulation syndromeOTHERAD
limitedPLCG2-related familial cold autoinflammatory syndromeLOFAD
DN
0.3991th %ile
GOF
0.5268th %ile
LOF
0.56top 25%

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.

LOFLOEUF 0.28
GOF1 literature citation

Literature Evidence

GOFGenomic deletions in PLCG2 cause gain of PLCg(2) function, leading to signaling abnormalities in multiple leukocyte subsets and a phenotype encompassing both excessive and deficient immune function.PMID:22236196

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

100 submitted variants in ClinVar

Classification Summary

VUS47
Likely Benign53
47
VUS
53
Likely Benign

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
3
38
6
0
47
Likely Benign
0
0
24
29
53
Benign
0
0
0
0
0
Total3383029100

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

View in ClinVar →

Protein Context — Lollipop Plot

PLCG2 · 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 ↗