PRKACB

Chr 1ADSomatic

protein kinase cAMP-activated catalytic subunit beta

Also known as: CAFD2, PKA C-beta, PKACB

The protein is a catalytic subunit of cAMP-dependent protein kinase that mediates cAMP signaling to regulate cellular processes including proliferation, differentiation, cell cycle progression, and intracellular transport. Mutations cause cardioacrofacial dysplasia 2, which follows autosomal dominant inheritance with somatic mosaicism reported. The gene is moderately constrained against loss-of-function variants (LOEUF 0.479), and the condition affects cardiac and craniofacial development.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Cardioacrofacial dysplasia 2MIM #619143
ADSomatic
0
Active trials
27
Pubs (1 yr)
22
P/LP submissions
27%
P/LP missense
0.48
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryPRKACB
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.23) despite low pLI — interpret in context.
📋
ClinVar Variants
22 unique Pathogenic / Likely Pathogenic· 44 VUS of 100 total submissions
📖
GeneReview available — PRKACB
Authoritative clinical overview · Recommended first read
Open GeneReview ↗
Some data sources returned errors (1)

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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.48LOEUF
pLI 0.351
Z-score 3.35
OE 0.23 (0.120.48)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.80Z-score
OE missense 0.45 (0.370.53)
90 obs / 202.2 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.23 (0.120.48)
00.351.4
Missense OE0.45 (0.370.53)
00.61.4
Synonymous OE0.95
01.21.6
LoF obs/exp: 5 / 22.0Missense obs/exp: 90 / 202.2Syn Z: 0.35
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongPRKACB-related multiple congenital malformation syndromeOTHERAD
DN
0.75top 25%
GOF
0.73top 25%
LOF
0.4528th %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

100 submitted variants in ClinVar

Classification Summary

Pathogenic19
Likely Pathogenic3
VUS44
Likely Benign8
Benign1
Conflicting1
19
Pathogenic
3
Likely Pathogenic
44
VUS
8
Likely Benign
1
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
5
14
0
19
Likely Pathogenic
0
1
2
0
3
VUS
1
36
7
0
44
Likely Benign
0
2
4
2
8
Benign
0
0
1
0
1
Conflicting
1
Total14428276

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

View in ClinVar →

Protein Context — Lollipop Plot

PRKACB · protein map & ClinVar variants

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

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Targeting cholangiocarcinoma.
Mertens JC et al.·Biochim Biophys Acta Mol Basis Dis
2018Review
Carney complex: an update.
Correa R et al.·Eur J Endocrinol
2015Review
The molecular genetics of adrenal cushing.
Vaduva P et al.·Hormones (Athens)
2024Review
Top 5 results · since 2015Search PubMed ↗