PHKA1

Chr XXLR

phosphorylase kinase regulatory subunit alpha 1

Also known as: PHKA

The PHKA1 gene encodes the alpha subunit of phosphorylase kinase, which catalyzes phosphorylation of substrates including troponin I and regulates glycogen breakdown in skeletal muscle. Mutations cause X-linked recessive muscle glycogenosis (glycogen storage disease type 9D), presenting as muscle weakness and exercise intolerance. This gene is highly constrained against loss-of-function variants (LOEUF 0.547), indicating that such mutations are likely pathogenic.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismXLRLOEUF 0.551 OMIM phenotype
Clinical SummaryPHKA1
🧬
Gene-Disease Validity (ClinGen)
glycogen storage disease IXd · XLDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📖
GeneReview available — PHKA1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.55LOEUF
pLI 0.000
Z-score 4.33
OE 0.38 (0.270.55)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.88Z-score
OE missense 0.76 (0.690.83)
363 obs / 478.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.38 (0.270.55)
00.351.4
Missense OE0.76 (0.690.83)
00.61.4
Synonymous OE1.05
01.21.6
LoF obs/exp: 22 / 57.4Missense obs/exp: 363 / 478.8Syn Z: -0.55
DN
0.6455th %ile
GOF
0.7125th %ile
LOF
0.3358th %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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

PHKA1 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →