Xin-Xin I. Zeng

The paper identifies ribosomal protein genes as contributors to hypoplastic left heart syndrome through functional analysis across multiple model systems.

The paper investigates how a COG4 mutation causes SWS by disrupting non-canonical Wnt signaling in zebrafish and fibroblasts, leading to developmental defects.

The paper identifies LRP2 as a novel genetic driver of hypoplastic left heart syndrome using whole genome sequencing and multi-model systems.

This study identifies fstl1b as critical for cardiac development in zebrafish, showing its role in regulating sarcomere structure and contractility through modulation of BMP signaling.

This study shows that differentiated zebrafish muscle cells can be reprogrammed into endoderm-like cells in vivo through Sox32 and Oct4 co-expression, challenging previous assumptions about lineage restriction.