Rui Zhao

This study identifies Eya3 in macrophages as a checkpoint for anti-tumor immunity in TNBC, showing that its depletion or inhibition enhances immune responses and reduces tumor growth.

The paper shows that U1-70K promotes exon definition by destabilizing U1-5' SS interactions, leading to exon skipping when depleted.

The paper identifies a core regulatory circuit in rhabdomyosarcoma and shows that targeting two co-activators synergistically inhibits tumor growth.

This study shows that U1C and Helix H of U1 snRNA are essential for branaplam's effect on weak 5 splice site recognition, while risdiplam requires additional factors for activity.

This study develops a small-molecule approach to reduce prion protein by modulating pre-mRNA splicing, achieving ~70% PrP reduction in cells and demonstrating synergistic effects with a Luc7L activator in mice.

The paper investigates the interaction between U1 snRNP and RNA polymerase II in yeast, finding that Prp40, not U1-70K, mediates this interaction, contrasting with the human system.

The paper identifies eIF3d and eIF3e as mediators of hypoxia-induced translational control and shows that small molecules can inhibit this process.

The paper determines cryo-EM structures of PP2A-B55 and Eya3 interaction, showing how a peptide inhibitor disrupts this interaction and affects Myc stability in TNBC.

This study identifies SASH1 as a regulator of melanocyte stem cell maintenance, showing that the S519N variant disrupts its function and links to pigmentation disorders.

The paper humanizes yeast U1 snRNP components to study 5 ss recognition, finding that U1C ZnF substitution causes splicing defects and mitochondrial dysfunction.

This study identifies CtBP1 and CtBP2 as drivers of inflammation in TBI and shows their inhibition reduces neuroinflammation and improves neurological outcomes in mice.