Yong‐Dong Wang

This study identifies tissue-specific proteomic changes in a Drosophila SCA17 model, showing polyglutamine-expanded TBP affects pathways beyond transcription.

This study identifies co-targeting of MCL-1 and ETC complex I as a synergistic therapy for high-risk AML, showing improved viability reduction and survival in preclinical models.

This study tests antisense oligonucleotides targeting Hnrnph2 in a mouse model, showing reduced Hnrnph2 levels, increased Hnrnph1, and improved phenotypes like seizures and motor function.

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

The paper shows glucose starvation impairs ER-to-Golgi trafficking, reducing surface proteins like E-cadherin and promoting metastasis through AMPK and ULK1 signaling.

This study identifies a point mutation in SRRM2 as a risk factor for ALS, showing it disrupts protein interactions and dysregulates synapse-related genes.

This study identifies an arachidonic acid binding pocket in SMO that modulates SHH signaling, revealing context-specific allostery crucial for cardiopulmonary development.

This study shows that somatic mtDNA mutations affect metabolic plasticity in leukemia development, with heterozygous mutations supporting NMyc-driven leukemia while homozygous mutations impair it.

This study develops chemical probes to label and enrich histone monoaminylation, revealing its enrichment in cancer tissues and its role in chromatin architecture regulation.

The paper develops a patient-derived cortical organoid model of UBA5-associated encephalopathy, identifies neurodevelopmental defects, and highlights potential therapeutic strategies.

This study shows CDK6 promotes oRG expansion and neocortical folding in mice, ferrets, and human cerebral organoids, with its function independent of kinase activity and disrupted by microcephaly-causing mutations.

This paper creates a mouse model of HNRNPH2-related neurodevelopmental disorder, showing similar symptoms to humans and revealing genetic compensation mechanisms.

The paper identifies differentially methylated regions in myeloid differentiation, showing genetic and developmental influences on methylome dynamics.