Disrupted MAML1 Phase Separation Emerges as a New Mechanism Linking Notch Failure to Congenital Heart Disease

Highlights

MAML1, a core Notch transcriptional coactivator, is implicated as a candidate gene in congenital heart disease, particularly ventricular septal defect.

A patient-derived MAML1 Q401K variant reproduced septal and valvular phenotypes in knock-in mice and CRISPR-edited human heart organoids.

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