Cassandra J. Wong

This study identifies PRMT1 as a replisome-associated methyltransferase that suppresses ssDNA gap formation by methylating MCM4, thereby maintaining fork integrity during DNA replication.

This study investigates how BLBS-causing H3.3 mutations affect H3K36 methylation and effector protein binding, revealing molecular similarities across mutations.

This study integrates spatial proteomics and genomics in PDAC to identify tumour-immune-stroma interactions and their genomic associations, showing multi-omics models improve patient survival prediction.

The paper investigates how multiple FGFR1 mutations affect tumorigenic mechanisms in glioneuronal tumors by analyzing their interactomes and functional impacts.

The paper identifies RAD54L2 as a regulator of recombination by showing its interaction with the BTRR complex and its role in suppressing sister chromatid exchanges.

The paper determines the high-resolution structure of V-ATPase in native synaptic vesicles using cryo-EM, revealing interactions with cholesterol and synaptophysin.

The paper compares noDE and DDA/DIA methods for protein-protein interaction detection, finding noDE provides better sensitivity and identifies more high confident interactors.

Profiling 192 subcellular markers by proximity-dependent biotinylation (BioID) in human HEK 293 cells maps 4,145 proteins across 32 compartments via 35,902 interactions, available with analysis tools at humancellmap.org.

Proximity-dependent biotinylation of 27 SARS-CoV-2 proteins in A549 cells maps 7810 virus-host proximity interactions across 2242 host proteins, including membrane-associated partners missed by affinity purification.

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

The paper introduces BFG-GI to map DNA damage-dependent genetic interactions in yeast by combining party mating and barcode fusion genetics, revealing new condition-specific interactions.

This paper develops a deep mutational scanning framework to map functional missense variants in human genes and applies it to four proteins, identifying pathogenic variants and showing scalability to disease genes.