KLHL17

Chr 1

kelch like family member 17

Also known as: AF

The protein encoded by KLHL17 serves as a substrate-recognition component of cullin-RING E3 ubiquitin ligase complexes and contains domains that mediate dimerization and F-actin binding, functioning in actin-based neuronal processes. Mutations cause autosomal recessive neurodevelopmental disorders with intellectual disability and seizures. This gene is not highly constrained against loss-of-function variants.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
4
Pubs (1 yr)
129
P/LP submissions
1%
P/LP missense
1.26
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryKLHL17
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
122 unique Pathogenic / Likely Pathogenic· 190 VUS of 357 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.26LOEUF
pLI 0.000
Z-score 0.46
OE 0.91 (0.661.26)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.57Z-score
OE missense 1.08 (1.001.16)
467 obs / 433.5 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.91 (0.661.26)
00.351.4
Missense OE1.08 (1.001.16)
00.61.4
Synonymous OE1.79
01.21.6
LoF obs/exp: 26 / 28.7Missense obs/exp: 467 / 433.5Syn Z: -8.81
DN
0.7035th %ile
GOF
0.6834th %ile
LOF
0.4529th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction 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

357 submitted variants in ClinVar

Classification Summary

Pathogenic116
Likely Pathogenic6
VUS190
Likely Benign13
Benign11
Conflicting1
116
Pathogenic
6
Likely Pathogenic
190
VUS
13
Likely Benign
11
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
116
0
116
Likely Pathogenic
0
1
5
0
6
VUS
0
177
13
0
190
Likely Benign
1
3
4
5
13
Benign
1
0
6
4
11
Conflicting
1
Total21811449337

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

View in ClinVar →

Protein Context — Lollipop Plot

KLHL17 · 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
Open Research Assistant →