PRKAR1B

Chr 7AD

protein kinase cAMP-dependent type I regulatory subunit beta

Also known as: MASNS, PRKAR1

The protein encoded by this gene is a regulatory subunit of cyclic AMP-dependent protein kinase A (PKA), which is involved in the signaling pathway of the second messenger cAMP. Two regulatory and two catalytic subunits form the PKA holoenzyme, disbands after cAMP binding. The holoenzyme is involved in many cellular events, including ion transport, metabolism, and transcription. Several transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Aug 2015]

GeneReviewsOMIMResearchGenerating clinical summary…
MultiplemechanismADLOEUF 0.541 OMIM phenotype
Clinical SummaryPRKAR1B
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.26) despite low pLI — interpret in context.
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ClinVar Variants
21 unique Pathogenic / Likely Pathogenic· 207 VUS of 388 total submissions
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GeneReview available — PRKAR1B
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint?
0.54LOEUF
pLI 0.179
Z-score 3.05
OE 0.26 (0.130.54)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint?
2.08Z-score
OE missense 0.64 (0.560.73)
171 obs / 266.6 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios?
LoF OE?0.26 (0.130.54)
00.351.4
Missense OE?0.64 (0.560.73)
00.61.4
Synonymous OE?1.07
01.21.6
LoF obs/exp: 5 / 19.5Missense obs/exp: 171 / 266.6Syn Z: -0.62
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
moderatePRKAR1B-related developmental disorderOTHERAD

This gene — mechanism propensity

DN
0.7229th %ile
GOF
0.6931th %ile
LOF
0.3454th %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

388 submitted variants in ClinVar

Classification Summary

Pathogenic16
Likely Pathogenic5
VUS207
Likely Benign115
Benign20
Conflicting8
16
Pathogenic
5
Likely Pathogenic
207
VUS
115
Likely Benign
20
Benign
8
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
13
1
2
0
16
Likely Pathogenic
2
3
0
0
5
VUS
6
194
6
1
207
Likely Benign
0
5
14
96
115
Benign
0
1
10
9
20
Conflicting
8
Total2120432106371

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

View in ClinVar →

42 pathogenic / likely-pathogenic (of 57) ClinVar copy-number / structural variants overlap PRKAR1B — these span large chromosomal regions, not the gene specifically, and are excluded from the counts above. Explore in CNV tools →

Protein Context — Lollipop Plot

PRKAR1B · 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 →