PHKG2

Chr 16AR

phosphorylase kinase catalytic subunit gamma 2

Also known as: GSD9C

The phosphorylase kinase gamma regulatory subunit catalyzes the phosphorylation and activation of glycogen phosphorylase, which is essential for glycogen breakdown in the liver. Biallelic mutations cause glycogen storage disease type IXc, characterized by hepatomegaly and growth retardation typically presenting in infancy or early childhood with autosomal recessive inheritance. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.657), primarily affecting hepatic glycogen metabolism.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismARLOEUF 0.661 OMIM phenotype
Clinical SummaryPHKG2
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Gene-Disease Validity (ClinGen)
glycogen storage disease IXc · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
37 unique Pathogenic / Likely Pathogenic· 129 VUS of 329 total submissions
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GeneReview available — PHKG2
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.66LOEUF
pLI 0.004
Z-score 2.76
OE 0.36 (0.210.66)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.45Z-score
OE missense 0.92 (0.821.03)
228 obs / 247.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.36 (0.210.66)
00.351.4
Missense OE0.92 (0.821.03)
00.61.4
Synonymous OE1.15
01.21.6
LoF obs/exp: 8 / 22.0Missense obs/exp: 228 / 247.9Syn Z: -1.13
DN
0.7132th %ile
GOF
0.82top 10%
LOF
0.2678th %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

329 submitted variants in ClinVar

Classification Summary

Pathogenic26
Likely Pathogenic11
VUS129
Likely Benign119
Benign5
Conflicting10
26
Pathogenic
11
Likely Pathogenic
129
VUS
119
Likely Benign
5
Benign
10
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
15
5
6
0
26
Likely Pathogenic
7
4
0
0
11
VUS
3
116
10
0
129
Likely Benign
0
9
40
70
119
Benign
0
1
3
1
5
Conflicting
10
Total251355971300

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

View in ClinVar →

Protein Context — Lollipop Plot

PHKG2 · 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 →