David J. Waxman

This study investigates the metabolic and gene expression effects of gain- and loss-of-function STAT5B variants in mice, revealing distinct impacts on lipid metabolism and hepatic sexual dimorphism.

The paper identifies GH-regulated sex-biased hepatocyte enhancers linked to liver metabolism and disease using HDI-STARR-seq and chromatin accessibility data.

This study uses single-nucleus multi-omics to identify sex-specific transcription factor motifs linked to chromatin accessibility and MASLD in mouse liver.

The paper introduces HDI-STARR-seq, a method for discovering condition-specific enhancers in mouse liver in vivo, identifying many enhancers linked to gene expression under different conditions.

This study investigates TCPOBOP-induced steatotic liver disease in mice, identifying primary and secondary gene responses linked to disease progression and potential biomarkers.

The paper shows that male-biased chromatin opening in liver is driven by pulsatile GH, with distinct epigenetic mechanisms compared to static DHS.

The paper identifies dysregulated lncRNAs in mouse liver disease using single-cell RNA-seq and links them to biological pathways and potential therapeutic targets.

This study uses single nucleus RNA sequencing to analyze sex-biased gene expression and zonation in mouse liver, revealing cell type-specific patterns and effects of GH and xenobiotic exposure.

This study shows that constitutively active STAT5b induces female-biased gene expression in male mouse liver, mimicking GH effects, but also causes histopathology at high doses.

The paper identifies cis regulators of sex-biased gene expression in mouse liver by comparing two strains and linking genetic variants to epigenetic and transcriptomic differences.

The paper characterizes transcript expression, maturation, and localization of lncRNAs in mouse liver, identifying novel sex-biased and TCPOBOP-responsive lncRNAs.

MAnorm2 is a tool for comparing ChIP-seq samples across groups, improving differential binding detection by accounting for within-group variability and outperforming existing methods.

This study identifies autosomal genetic factors that interact with growth hormone to regulate sex-specific gene expression in mouse liver, revealing over 200 instances of sex-specificity changes across strains.

The paper shows that PPARA upregulates Gm15441, which suppresses TXNIP and reduces NLRP3 inflammasome activation during metabolic stress.

The paper investigates how STAT5 regulates sex-dependent CpG methylation at distal regulatory elements in mouse liver, linking it to sex-biased gene expression.

The paper develops a mathematical model to explain immune recruitment and drug resistance in metronomic chemotherapy using a mouse glioma model and validates it across different drug regimens.

The paper investigates the role of EZH1 and EZH2 in sex-biased gene expression and liver disease susceptibility by analyzing chromatin modifications in male and female mice.

The paper identifies sex-biased lncRNAs in mouse liver that negatively correlate with opposite-sex protein-coding gene co-expression modules related to hypox responsiveness.

The paper identifies subTADs formed by CTCF and cohesin in mouse liver, showing they functionally resemble TADs and restrict enhancer-promoter interactions.