KCNJ1

Chr 11AR

potassium inwardly rectifying channel subfamily J member 1

Also known as: KIR1.1, ROMK, ROMK1

This gene encodes an inward-rectifier potassium channel that is activated by internal ATP and plays a major role in renal potassium homeostasis by allowing potassium to flow preferentially into cells. Mutations cause Bartter syndrome type 2, an autosomal recessive disorder characterized by antenatal onset of salt wasting, hypokalemic alkalosis, hypercalciuria, and low blood pressure. The gene is not highly constrained against loss-of-function variants (pLI = 0.00004), consistent with its recessive inheritance pattern.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

Bartter syndrome, type 2MIM #241200
AR
UniProtBartter syndrome 2, antenatal
0
Active trials
10
Pubs (1 yr)
105
P/LP submissions
37%
P/LP missense
1.28
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryKCNJ1
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Gene-Disease Validity (ClinGen)
Bartter disease type 2 · 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.
📋
ClinVar Variants
75 unique Pathogenic / Likely Pathogenic· 126 VUS of 300 total submissions
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GeneReview available — KCNJ1
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
1.28LOEUF
pLI 0.000
Z-score 0.89
OE 0.71 (0.421.28)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.28Z-score
OE missense 1.05 (0.941.18)
229 obs / 217.5 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.71 (0.421.28)
00.351.4
Missense OE1.05 (0.941.18)
00.61.4
Synonymous OE0.97
01.21.6
LoF obs/exp: 8 / 11.2Missense obs/exp: 229 / 217.5Syn Z: 0.23
DN
0.81top 10%
GOF
0.82top 10%
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
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

300 submitted variants in ClinVar

Classification Summary

Pathogenic34
Likely Pathogenic41
VUS126
Likely Benign87
Benign3
Conflicting8
34
Pathogenic
41
Likely Pathogenic
126
VUS
87
Likely Benign
3
Benign
8
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
11
3
20
0
34
Likely Pathogenic
9
25
7
0
41
VUS
1
112
11
2
126
Likely Benign
0
1
14
72
87
Benign
0
0
3
0
3
Conflicting
8
Total211415574299

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

View in ClinVar →

Protein Context — Lollipop Plot

KCNJ1 · 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
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