Katherine Chan

The paper develops a method to quantify genetic interactions from CRISPR-Cas9 screens and identifies systematic variations in screen data.

The paper constructs a genome-scale genetic interaction network from 4 million double mutants in HAP1 cells, revealing conserved genetic network principles across species and uncovering novel gene functions and cancer dependencies.

This study identifies functional relationships between TSC22D, WNK, and NRBP gene families in macromolecular crowding sensing and cell volume regulation across metazoans.

The paper presents a scalable CRISPR-Cas9 platform for chemical-genetic screens of DNA damage-inducing compounds, identifying enriched modes-of-action and revealing late ICL repair pathway responses.

The paper shows that N-terminal acetylation by NatC protects proteins from degradation, enhancing longevity and motility, and that UBR4-KCMF1 targets unacetylated N-terminal Met followed by hydrophobic residues.

The paper identifies three types of chromatin boundaries that regulate cohesin traffic, which guides enhancer-promoter interactions and affects gene regulation.

The paper identifies ACE2 as the only common host dependency for SARS-CoV-2 across multiple cell lines, while other host factors are cell line specific.

The paper introduces FLEX, a pipeline for benchmarking CRISPR screen data, and identifies a dominant mitochondria-associated signal in genome-wide screens.

This study maps genetic interactions in FASN-deficient cells to identify genes involved in lipid uptake and metabolic adaptation.