KCNJ8

Chr 12

potassium inwardly rectifying channel subfamily J member 8

Also known as: KIR6.1, uKATP-1

The protein functions as an inward-rectifier potassium channel that allows potassium to flow preferentially into cells and is regulated by G-proteins and internal ATP. Mutations cause J-wave syndromes and have been associated with sudden infant death syndrome (SIDS), with inheritance patterns not clearly established from available data. This gene shows moderate constraint against loss-of-function variants (LOEUF 0.575) and has a dedicated GeneReviews entry reflecting its clinical importance.

Summary from RefSeq, UniProt
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Primary Disease Associations & Inheritance

UniProtSudden infant death syndrome
UniProtHypertrichotic osteochondrodysplasia
0
Active trials
10
Pubs (1 yr)
42
P/LP submissions
5%
P/LP missense
0.57
LOEUF
GOF
Mechanism· G2P
Clinical SummaryKCNJ8
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Gene-Disease Validity (ClinGen)
Brugada syndrome · ADDisputed

Disputed — evidence questions this relationship

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.22) despite low pLI — interpret in context.
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ClinVar Variants
42 unique Pathogenic / Likely Pathogenic· 157 VUS of 337 total submissions
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GeneReview available — KCNJ8
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Missense constrained — critical functional residues
LoF Constraint
0.57LOEUF
pLI 0.380
Z-score 2.64
OE 0.22 (0.100.57)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
3.45Z-score
OE missense 0.38 (0.320.45)
92 obs / 243.8 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.22 (0.100.57)
00.351.4
Missense OE0.38 (0.320.45)
00.61.4
Synonymous OE0.87
01.21.6
LoF obs/exp: 3 / 13.5Missense obs/exp: 92 / 243.8Syn Z: 0.96
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedKCNJ8-related Brugada syndromeOTHERAD
strongKCNJ8-related Cantu syndromeGOFAD
DN
0.7034th %ile
GOF
0.80top 10%
LOF
0.3842th %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 · 1 literature citation
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

GOFCantu syndrome is a rare genetic disorder caused by pathogenic variants in the ABCC9 and KCNJ8 genes, which result in gain of function of the SUR2 or Kir6.1 subunits of widely expressed KATP channels.PMID:31743099

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

337 submitted variants in ClinVar

Classification Summary

Pathogenic38
Likely Pathogenic4
VUS157
Likely Benign118
Benign12
Conflicting6
38
Pathogenic
4
Likely Pathogenic
157
VUS
118
Likely Benign
12
Benign
6
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
38
0
38
Likely Pathogenic
0
2
2
0
4
VUS
3
124
30
0
157
Likely Benign
0
3
9
106
118
Benign
0
0
8
4
12
Conflicting
6
Total312987110335

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

View in ClinVar →

Protein Context — Lollipop Plot

KCNJ8 · 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
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Key Publications
Landmark & review papers · by relevance
PubMed
Three-dimensional facial morphology in Cantú syndrome.
Roessler HI et al.·Am J Med Genet A
2020
Generalized hypertrichosis syndromes in Mexico.
Aguayo-Orozco TA et al.·Am J Med Genet C Semin Med Genet
2020
Molecular Pathways and Animal Models of Arrhythmias.
Stevens TL et al.·Adv Exp Med Biol
2024Functional
Top 5 results · since 2015Search PubMed ↗