Kavitha S. Rao

The paper identifies Tbx5 as a gene critical for forming a compartment boundary in the interventricular septum, and shows its disruption leads to congenital heart defects.

This study shows that reduced TBX5 dosage disrupts atrial cardiomyocyte identity, leading to cellular and molecular changes associated with atrial diseases.

This study shows that reduced TBX5 dosage affects 3D chromatin organization in human cardiomyocytes, with cell-to-cell variation and partial protection by CTCF co-occupancy.

The paper models TBX5 haploinsufficiency in iPSC-derived cardiomyocytes to identify gene regulatory network imbalances linked to congenital heart disease.

This study shows that Brm deletion causes identity switches in cardiac mesoderm differentiation by altering chromatin accessibility and gene expression, revealing BRM's role in safeguarding developmental canalization.

The paper investigates the role of developmentally regulated cardiac lincRNAs in heart development and function, finding that their deletion does not cause severe cardiac phenotypes.