KLF18 encodes a transcription factor that binds to specific DNA sequences to regulate gene expression by RNA polymerase II. Currently, no established human diseases have been definitively linked to mutations in this gene. The clinical significance of KLF18 variants in pediatric neurological conditions remains to be determined.

OMIMResearchSummary from RefSeq
Multiplemechanism
Some data sources returned errors (1)

gnomad: Error: Gene not found

Population Genetics & Constraint

Constraint data not available from gnomAD.

DN
0.7229th %ile
GOF
0.7028th %ile
LOF
0.4331th %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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

KLF18 · 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
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Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
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Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
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