Rochelle L. Tiedemann

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

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.

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.