David C.S. Huang

This paper identifies the structural basis of PU.1-BAF interaction and shows small molecules can disrupt it, offering a new therapeutic strategy for cancer.

This study shows that CLL cells rapidly adapt to venetoclax by upregulating pro-survival proteins and cytokines, suggesting combination therapies targeting these pathways could improve treatment outcomes.

This study identifies fibrillarin as a repressor of the γ-globin gene and shows its dual role in activating BCL11A and repressing γ-globin expression, offering a potential therapeutic target for β-hemoglobinopathies.

This study identifies key residues in the BAK:VDAC2 interaction, showing that disrupting this interaction can inhibit or promote apoptosis depending on the context.

The paper introduces scRaCH-seq, a method for single-cell long-read sequencing that improves detection of isoform usage and mutations in targeted genes, demonstrating its application in CLL samples.

The paper develops FLT-seq and FLAMES to characterize full-length isoforms in single cells of human and mouse, identifying thousands of unannotated isoforms and linking them to functional modules and drug resistance mutations.

This study identifies two parallel pathways regulated by WAPL and telomere deprotection that lead to mitotic death in replication stressed human cells.