KCNJ11

Chr 11ADAR

potassium inwardly rectifying channel subfamily J member 11

Also known as: BIR, HHF2, IKATP, KIR6.2, MODY13, PHHI, PNDM2, TNDM3

This protein forms an inward-rectifying potassium channel that associates with the sulfonylurea receptor to regulate insulin secretion in pancreatic beta cells. Mutations cause a spectrum of glucose homeostasis disorders including familial hyperinsulinemic hypoglycemia (autosomal recessive), transient and permanent neonatal diabetes mellitus, and maturity-onset diabetes of the young type 13 (autosomal dominant), with some forms of permanent neonatal diabetes presenting with neurologic features. Disease predominantly results from gain-of-function effects that disrupt normal channel regulation and insulin secretion control.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
MultiplemechanismAD/ARLOEUF 1.214 OMIM phenotypes
Clinical SummaryKCNJ11
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Gene-Disease Validity (ClinGen)
monogenic diabetes · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

2 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.01) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
76 unique Pathogenic / Likely Pathogenic· 208 VUS of 477 total submissions
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Clinical Trials
3 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — KCNJ11
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
1.21LOEUF
pLI 0.011
Z-score 1.20
OE 0.53 (0.261.21)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
1.65Z-score
OE missense 0.71 (0.630.81)
186 obs / 260.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.53 (0.261.21)
00.351.4
Missense OE0.71 (0.630.81)
00.61.4
Synonymous OE0.90
01.21.6
LoF obs/exp: 4 / 7.5Missense obs/exp: 186 / 260.9Syn Z: 0.81
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveKCNJ11-related familial hyperinsulinismLOFAR
definitiveKCNJ11-related diabetes mellitus, transient neonatalGOFAD
DN
0.81top 10%
GOF
0.87top 5%
LOF
0.2288th %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 · 1 literature citation

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

DNAbnormalities of pancreatic islets by targeted expression of a dominant-negative KATP channelPMID:9342346
GOFActivating or gain of function mutations of KATP channel genes namely KCNJ11 and ABCC8 are most predominant cause of permanent neonatal diabetes mellitus (PNDM).PMID:32893419

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

ClinVar Variant Classifications

477 submitted variants in ClinVar

Classification Summary

Pathogenic30
Likely Pathogenic46
VUS208
Likely Benign104
Benign9
Conflicting74
30
Pathogenic
46
Likely Pathogenic
208
VUS
104
Likely Benign
9
Benign
74
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
9
12
9
0
30
Likely Pathogenic
19
26
1
0
46
VUS
0
176
23
9
208
Likely Benign
0
6
1
97
104
Benign
0
7
1
1
9
Conflicting
74
Total2822735107471

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

View in ClinVar →

Protein Context — Lollipop Plot

KCNJ11 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗