Jun Qi

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

This study shows that inhibiting KDM5A/B enhances antitumor innate immune responses and induces KSHV lytic reactivation in KSHV-positive B-cell lymphomas.

This study identifies TAK-418 as a histone demethylase inhibitor that rescues schizophrenia-like phenotypes in Setd1a-deficient mice by restoring H3K4me3 levels and gene expression.

This study identifies specific developmental epigenomic states that enable ZFTA-RELA-driven ependymoma formation and reveals how these states shape tumor progression.

This study identifies shifted mSWI/SNF subcomplex stoichiometry in DDEC/UEC cancers and shows that SMARCA4/2 inhibitors reduce tumor growth and synergize with chemotherapy.

The paper identifies HDAC1/2 inhibition as a method to promote colorectal cancer differentiation through H3K27ac gains, which can be reversed by blocking EP300.

The paper introduces a low-cost, flexible method for quantitative chromatin sequencing and enables cross-species epigenomic comparisons.

The paper shows that inhibiting bromodomain proteins like BRD4 reduces FGF15/19 expression, leading to hyperglycemia, and that overexpressing FGF19 can reverse these effects.

This study shows that BRD9 and ncBAF complexes maintain somatic cell identity and hinder reprogramming, with BRD9 inhibition increasing iPSC generation efficiency.

This study shows BRD4 promotes cardiac fibrosis by dynamically targeting chromatin and activating gene expression in fibroblasts, revealing a signaling pathway involved in heart failure.