Sven Heinz

The paper introduces a novel dual-spike-in normalization method for ChIP-seq, demonstrating its ability to clarify the relationship between RNA polymerase II activity and histone modifications.

This study maps transcription initiation in mouse astrocytes to define how inflammatory signals drive cell-type-specific gene regulation and links enhancer activity to human disease risk.

This study shows that AIBP deficiency in mice leads to increased foam cell inflammation and atherosclerosis through enhanced inflammaraft expression and lipid accumulation.

Prod&PQ-seq detects and quantifies protein-protein interactions and protein abundance across different cellular conditions, showing changes in PRC2 interactions with EZH2 inhibition and H3 variants.

The paper introduces spa-ChIP-seq, an automated ChIP-seq protocol, showing it achieves comparable signal-to-noise ratios to manual methods and identifies sensitivity of weak signals to antibody-to-cell-number ratio changes.

This study shows that DOT1L regulates specific gene networks in cardiac development and cell cycle withdrawal through H3K79me2 modifications.