PRKACA

Chr 19AD

protein kinase cAMP-activated catalytic subunit alpha

Also known as: CAFD1, PKACA, PPNAD4

This gene encodes a catalytic subunit of protein kinase A, which phosphorylates numerous substrates in the cytoplasm and nucleus to regulate cellular processes including differentiation, proliferation, and apoptosis. Mutations cause cardioacrofacial dysplasia 1 and ACTH-independent adrenal Cushing syndrome, with autosomal dominant inheritance. The gene is highly constrained against loss-of-function variation (pLI 0.97), indicating that such mutations are likely pathogenic.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

Cardioacrofacial dysplasia 1MIM #619142
AD
Cushing syndrome, ACTH-independent adrenal, somaticMIM #615830
UniProtPrimary pigmented nodular adrenocortical disease 4
0
Active trials
72
Pubs (1 yr)
23
P/LP submissions
13%
P/LP missense
0.32
LOEUF· LoF intol.
Multiple*
Mechanism· predicted
Clinical SummaryPRKACA
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.97). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
15 unique Pathogenic / Likely Pathogenic· 43 VUS of 93 total submissions
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GeneReview available — PRKACA
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.32LOEUF
pLI 0.971
Z-score 3.71
OE 0.10 (0.040.32)
Highly constrained

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

Missense Constraint
2.97Z-score
OE missense 0.43 (0.360.51)
92 obs / 214.5 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.10 (0.040.32)
00.351.4
Missense OE0.43 (0.360.51)
00.61.4
Synonymous OE1.03
01.21.6
LoF obs/exp: 2 / 19.8Missense obs/exp: 92 / 214.5Syn Z: -0.22
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongPRKACA-related multiple congenital malformation syndromeOTHERAD
DN
0.7132th %ile
GOF
0.73top 25%
LOF
0.59top 25%

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function, loss-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 · 1 literature citation
LOFLOEUF 0.32
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

GOFOne in three CPAs carries a recurrent gain-of-function mutation (L206R) in the PRKACA gene, encoding the catalytic subunit of PKA.PMID:27445978

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

93 submitted variants in ClinVar

Classification Summary

Pathogenic12
Likely Pathogenic3
VUS43
Likely Benign17
Benign3
Conflicting1
12
Pathogenic
3
Likely Pathogenic
43
VUS
17
Likely Benign
3
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
12
0
12
Likely Pathogenic
0
2
1
0
3
VUS
0
39
3
1
43
Likely Benign
0
1
4
12
17
Benign
0
1
0
2
3
Conflicting
1
Total043201579

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

View in ClinVar →

Protein Context — Lollipop Plot

PRKACA · 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.

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Clinical Literature
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