Author

N. Mor

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Open access Aug 2026

Truncated ASXL3 Alters Chromatin Accessibility and Epigenetic Landscape in Bainbridge-Ropers Syndrome Suggesting a Gain-of-Function Etiology

The results support a dominant-negative mechanism for BRS causing truncating mutations, offering a compelling rationale for allele-specific ASO therapeutic strategy and new venues for treatment.

N. Mor, I. Shomer, S. Raviv et al. · medRxiv · 0 citations

Open access Jul 2026

ASXL3 truncating patient variants mediate transcriptional gain-of-function and are antisense oligonucleotide-responsive

ASXL3 patient truncations in neurodevelopmental condition Bainbridge-Ropers syndrome are shown to mediates gain-of-function (GOF) by escaping nonsense-mediated decay and Cullin 4-dependent degradation, resulting in aberrant protein accumulation, widespread transcriptional dysregulation, and altered chromatin accessibility.

Y. Nakamura, T. Nguyen, N. Mor et al. · medRxiv · 0 citations