Scott B. Rothbart

This study identifies a feed-forward mechanism where UHRF1 reads and writes H3 mono-ubiquitination to maintain DNA methylation at CpG-sparse regions.

This study shows how bacterial effector RomA is regulated by host histone modifications, revealing a new layer of host-pathogen interaction through epigenetic crosstalk.

This paper identifies EZH1-dependent H3K27me1 as an adaptive chromatin barrier limiting DNMT inhibitor response in colorectal cancer and shows that dual EZH1/2 inhibition synergizes with DNMTi to enhance therapeutic efficacy.

This study shows UHRF1 ubiquitin ligase activity and DNMT1 ubiquitin reading activity are essential for maintaining low-density CpG methylation, and their disruption leads to hypomethylation and PMD formation in cancer.

This study investigates the association of HSV-1 genomes with H3K27me2 and PHF20L1 in fibroblasts, finding that H3K27me2 is linked to genome silencing and that this association is influenced by demethylase activity and transcriptional state.

This study identifies a mitotic chromatin-marking pathway that controls the asymmetric segregation of UV-induced DNA damage in human cells.

This paper introduces siQ-ChIP, a method to generate quantitative ChIP-seq data without spike-in normalization and shows how antibody specificity can be analyzed directly in ChIP-seq experiments.

This study shows ARID1A maintains repressive H3.3 chromatin through interactions with CHD4 and ZMYND8, suppressing genes involved in cell motility and epithelial-to-mesenchymal transition in endometriotic cells.

The paper introduces a quantitative framework for ChIP-seq analysis that avoids the need for spike-in reagents by leveraging competitive binding during the IP step and provides a visualization technique for richer data characterization.

The paper investigates mitotic bookmarking through histone modifications and nucleosome deposition patterns in human cells, showing that epigenomic landscapes and modified nucleosomes contribute to chromatin reestablishment after mitosis.

This study compares monoclonal and polyclonal antibodies for ChIP-seq of histone modifications, finding monoclonals perform similarly in most cases but show differences for H3K27ac.