Shao‐En Ong

This study identifies NUAK1 substrates in neurons and shows that NUAK1 phosphorylation of PSD3 regulates ARF6 activation and dendritic spine maturation, linking NUAK1 to autism risk.

The paper introduces ORCA, a method to isolate mitochondria associated with specific organelles, revealing distinct proteomes and functional roles at organelle contact sites.

This study identifies NUAK1 as a critical host factor for Plasmodium falciparum infection and shows that NUAK1 inhibitors block parasite growth.

This paper introduces an improved chemoproteomics method for mapping kinase PPI networks, showing it identifies more interactions and predicts drug targets in neuroblastoma models.

This study shows that mitochondrial calcium signaling regulates branched-chain amino acid catabolism and the urea cycle in fibrolamellar carcinoma through transcriptional control of metabolic genes.

The paper uses O-MAP to study a cardiac-specific RNA factory around TTN RNA, revealing its chromatin interactions, RNA composition, and role of RBM20 in gene regulation.

The paper introduces O-MAP, a method for discovering RNA-interacting proteins, transcripts, and genomic loci in situ with high precision and without genetic manipulation.

The paper identifies TAOK1 as a plasma membrane remodeling kinase and shows how mutations in it cause neurodevelopmental disorders by disrupting its membrane association and function.

The paper introduces a water droplet-in-oil digestion method for single-cell proteomics that improves protein and peptide recovery and enables quantification of 462 proteins from 100 cells.

The paper identifies 14-3-3 proteins as interactors of phosphorylated Septin 7 that regulate dendritic spine formation and stability.

The paper shows that mutations in PKAc cause displacement from AKAP signaling islands, leading to distinct pathogenic signaling pathways in Cushing's syndrome.

The paper introduces a PAR photoaffinity probe to identify PAR-binding proteins, revealing novel binders and demonstrating length-selective PAR binding.