Michael‐Christopher Keogh

The paper shows that different binding modes to the nucleosome acidic patch lead to distinct cellular outcomes, with overexpression of Dot5 and camelid antibodies causing growth, DNA repair, and heterochromatin defects.

This study investigates how Legionella pneumophila's SET domain enzymes methylate histone H3K14, revealing structural mechanisms for substrate specificity and nucleosome engagement.

This study uses single-nucleus multiome sequencing and spatial transcriptomics to analyze liposarcoma subtypes, revealing distinct cellular states, immune features, and gene regulatory circuits.

This study investigates how the conserved SBD of EZH2 regulates PRC2 activity, showing its necessity for histone methylation and cancer cell proliferation.

This paper introduces Nuc-MS, a method to directly analyze chromatin reader-nucleosome interactions by disassembling complexes and identifying histone proteoforms involved in binding.

The paper provides a detailed CUT&RUN protocol for high-resolution epigenomic profiling, including best practices and controls for efficient target profiling.

The paper identifies H3 serine 28 phosphorylation as a mechanism driving chromatin derepression and immune cell fate transitions by disrupting repressive chromatin domains.

The paper investigates how nucleosome context influences chromatin reader binding preferences using biochemical and genomic approaches, revealing that multivalent engagement often has regulatory effects beyond simple additivity.

This study shows that the catalytic pocket of Clr4 (Suv39h) acts as a receptor for Cul4-dependent H3K14 ubiquitination, which regulates Clr4's methylation activity on H3K9.

This study shows PHRF1's PHD finger binds histone H3 N-terminal region, regulates transcription and RNA splicing, and is essential for DNA damage response.

The paper shows that the PBAF complex in melanoma facilitates REST occupancy at repressive chromatin, leading to upregulation of synaptic transcripts when ARID2 is mutated.

The paper identifies KDM4 demethylase inhibition as a therapeutic strategy for lymphoma and other cancers by rewiring heterochromatin and inducing DNA damage.

The paper identifies a critical binding interface in DNMT3A1 that facilitates DNA hypermethylation at Polycomb target genes by recognizing H2AK119Ub and the nucleosome acidic patch.

This study reveals that H2BK120ub blocks the nucleosome acidic patch, preventing protein binding, while H2AK119ub does not, highlighting distinct roles of these ubiquitinations in chromatin regulation.

The paper shows that histone reader domains interact with PTMs in a nucleosome-dependent manner, necessitating a refinement of the histone code concept to the nucleosome level.