BSND

Chr 1AR

barttin CLCNK type accessory subunit beta

Also known as: BART, DFNB73

The protein encoded by this gene is an essential regulatory subunit for chloride channels in the kidney and inner ear, functioning as a chaperone that enables proper channel sorting and constitutive opening for basolateral chloride conductance. Mutations cause autosomal recessive Bartter syndrome type 4a with sensorineural deafness, affecting both renal salt wasting and hearing function. The gene shows very low constraint against loss-of-function variants (pLI ~0, LOEUF 1.78), consistent with recessive inheritance where heterozygous carriers are unaffected.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismARLOEUF 1.782 OMIM phenotypes
Clinical SummaryBSND
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Gene-Disease Validity (ClinGen)
Bartter disease type 4A · 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
55 unique Pathogenic / Likely Pathogenic· 132 VUS of 433 total submissions
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GeneReview available — BSND
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
1.78LOEUF
pLI 0.000
Z-score -0.60
OE 1.19 (0.781.78)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.07Z-score
OE missense 0.99 (0.881.11)
190 obs / 192.6 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE1.19 (0.781.78)
00.351.4
Missense OE0.99 (0.881.11)
00.61.4
Synonymous OE1.20
01.21.6
LoF obs/exp: 14 / 11.8Missense obs/exp: 190 / 192.6Syn Z: -1.42
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveBSND-related Bartter syndrome, type 4aLOFAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.6551th %ile
GOF
0.73top 25%
LOF
0.3842th %ile

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

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

ClinVar Variant Classifications

433 submitted variants in ClinVar

Classification Summary

Pathogenic27
Likely Pathogenic28
VUS132
Likely Benign196
Benign24
Conflicting25
27
Pathogenic
28
Likely Pathogenic
132
VUS
196
Likely Benign
24
Benign
25
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
12
4
11
0
27
Likely Pathogenic
18
5
5
0
28
VUS
7
111
11
3
132
Likely Benign
1
4
47
144
196
Benign
0
0
22
2
24
Conflicting
25
Total3812496149432

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

View in ClinVar →

Protein Context — Lollipop Plot

BSND · 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.

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Clinical Literature
Open Research Assistant →