Yiwen Zhu

The paper identifies hidden enhancers in mouse embryos that are not detected by conventional chromatin profiling methods, highlighting a significant gap in enhancer discovery.

The paper maps the mutagenic sensitivity of human enhancers in vivo by systematically mutating enhancer sequences and using predictive modeling to identify critical nucleotides.

The paper identifies 14,000 human craniofacial enhancers across developmental stages and shows 56% are conserved in mice, providing cell type- and stage-specific activity profiles.

The paper investigates how childhood adversity during sensitive periods affects DNA methylation in genes regulating developmental plasticity using a gene set-based approach.

This study shows that SETD2 deficiency promotes renal fibrosis by activating the TGF-β/Smad signaling pathway in VHL-deficient mice.

The paper uses single-cell RNA sequencing to systematically phenotype mouse genetic models, identifying molecular and cellular changes across multiple mutants and wildtypes.

This study shows that changes in socioeconomic environment during childhood affect DNA methylation at age 7, with middle childhood being a sensitive period for socioeconomic adversity's impact.

The paper assesses how changes in data versions and analytic methods affect the reproducibility of epigenome-wide association study results using the ALSPAC cohort.

This review examines the association between socioeconomic position (SEP) and DNA methylation across the life course, finding that early-life SEP and persistent low SEP strongly influence DNAm patterns.

The paper examines how genetic pathways regulating sensitive periods and socioeconomic disadvantage interact to influence depression risk using genome-wide data and developmental gene expression patterns.

This study shows that deleting TAD boundaries in mice often causes molecular or developmental phenotypes, highlighting their importance for genome function.

The paper identifies BAF complex subunit dynamics during cardiac differentiation, showing how BAF60c and BAF170 regulate gene expression programs in cardiac precursors and cardiomyocytes.