ZNF536

Chr 19

zinc finger protein 536

This zinc finger transcriptional repressor negatively regulates neuronal differentiation by repressing retinoic acid-induced gene transcription and interrupting retinoic acid receptor binding to DNA response elements. Mutations cause neurodevelopmental disorder with or without anomalies of the brain, eye, or heart, inherited in an autosomal dominant pattern. The gene is highly constrained against loss-of-function variants, reflecting its critical role in normal neurodevelopment.

Summary from RefSeq, UniProt
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0
Active trials
8
Pubs (1 yr)
0
P/LP submissions
P/LP missense
LOEUF
LOF
Mechanism· predicted
Some data sources returned errors (1)

gnomad: TimeoutError: The operation was aborted due to timeout

Population Genetics & Constraint

Constraint data not available from gnomAD.

DN
0.2798th %ile
GOF
0.2198th %ile
LOF
0.86top 5%

The highest-scoring mechanism for this gene is loss-of-function (haploinsufficiency).

LOFprediction above median

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

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

ZNF536 · 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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