Hyuk‐Jin Cha

FateDriver prioritizes candidate regulators for specific cellular transitions using a weakly supervised dual-view graph neural network, outperforming existing methods in recovering known regulators.

The paper demonstrates that OSKM mRNA delivered via lipid nanoparticles induces liver progenitor-like cells, promoting tissue regeneration after acute liver injury.

This paper develops FATE, a mutation-agnostic base-editing platform that rescues HGPS phenotypes in neuromuscular organoids by disrupting the LMNA farnesylation motif.

This study identifies Mtf2 as an epigenetic barrier that maintains naive pluripotency by restricting trophectoderm competence in embryonic stem cells.

The paper identifies isoform 4 of RNF220 as the predominant and ubiquitously expressed variant in mice, essential for muscle differentiation.

The paper shows that glycogen depletion activates Ampk in naive ESCs, promoting their transition to a primed state by reducing fatty acid synthesis and altering pluripotency markers.

The paper identifies MSH2 and MSH6 as size-dependent determinants of prime editing efficiency in human embryonic stem cells, showing that their disruption significantly improves editing outcomes.

The paper establishes isogenic GNE myopathy disease models using base editors in hPSCs, showing mutation-specific hyposialylation and drug responses.

The paper identifies a nuclear receptor-enriched predictive signature for erastin-induced ferroptosis using gene expression analysis and pharmacogenomics datasets.

The paper develops a method to enrich genome-edited human pluripotent stem cells by inducing temporary drug resistance through SLC35F2 knockdown, achieving efficient selection in 3 weeks.