Nicholas Alexander Graham

This study shows that disrupting the SYNGAP1 PDZ ligand motif speeds up differentiation of human iPSC-derived GABAergic neurons, revealing its role in neuronal maturation.

The paper uses LC-MS proteomics to identify PRMT-1 substrates and quantify proteome changes in C. elegans prmt-1 and prmt-5 knockout mutants.

The paper integrates computational metabolic modeling with experimental validation to identify hexokinase as a therapeutic target in colorectal cancer by analyzing CAF-conditioned tumor organoids.

This paper introduces DMEA, a method that improves drug repurposing by grouping drugs with shared mechanisms of action, enhancing prioritization and reducing off-target effects.

This paper develops a kinetic and data-driven model of pancreatic β-cell metabolism to understand its role in glucose-stimulated insulin secretion and predict therapeutic interventions.

This study investigates tumor-stromal metabolic interactions in colorectal cancer by integrating constraint-based models with metabolomics data, revealing how cancer-associated fibroblasts reprogram tumor cell metabolism.

The paper identifies a proteomic signature of senescence in primary human mammary epithelial cells using mass spectrometry-based proteomics and integrates it with transcriptomic data.

The paper develops a single-nuclei RNA sequencing approach to study MECP2 dysfunction in Rett Syndrome, identifying aberrant gene expression and a role for POU2F1/OCT1 in stress response.

This paper introduces DGSEA, a method to compare the relative enrichment of two gene sets, showing it outperforms GSEA in capturing metabolic shifts and identifying novel dependencies in cancer cell lines.

The paper shows that AKT, but not MYC, causes cell death in oxidative conditions by increasing reactive oxygen species, revealing a metabolic vulnerability in cancer cells.

The paper investigates how the SynGAP-1 PBM regulates NMDA receptor signaling and cognitive function in mice, finding that disrupting the PBM leads to synaptic and cognitive impairments.

The paper identifies L-cystine reduction as a metabolic vulnerability in cancer cells under glucose deprivation and proposes co-targeting GLUT1 and glutathione synthesis as a therapeutic strategy.

The paper develops a combined chemical and immunoaffinity approach to profile protein methylation, identifying novel PRMT1 targets and revealing dynamic interactions between methyltransferases.

This study shows that inhibiting nucleotide synthesis induces replicative senescence in human mammary epithelial cells by blocking metabolic flux into nucleotide pathways.

The paper develops a computational model to explain site-specific phosphorylation kinetics of CARs using phospho-proteomic data and mechanistic modeling.