Jason W. Locasale

Metabolic shift to serine pathway induced by lipids confers oncogenic properties in non-transformed breast cells

The paper shows that lipid metabolism, specifically through OA, shifts metabolic pathways in breast cells, increasing SAM and 2-HG, which contribute to oncogenic properties and epigenetic changes.

Regulation of urea cycle by reversible high stoichiometry lysine succinylation

This study identifies high stoichiometry lysine succinylation sites in mouse liver, showing their functional role in urea cycle regulation and ammonia metabolism through SIRT5.

Quantification of metabolic activity from isotope tracing data using automated methodology

This study develops an automated method to quantify metabolic activity from isotope tracing data, revealing reprogrammed mitochondria-cytosol exchange cycles in tumor tissue.

Amino acid variability, tradeoffs and optimality in human diet

This study maps amino acid content in human diets, identifies health trade-offs, and constructs a Pareto front for optimal dietary protein intake.

Quantitative analysis of the physiological contributions of glucose to the TCA cycle

The paper quantitatively analyzes the physiological contributions of glucose to the TCA cycle using isotope-labeling data and metabolic flux analysis, showing glucose is the major nutrient source across tissues and conditions.

Evolved resistance to GAPDH inhibition results in loss of the Warburg Effect but retains a different state of glycolysis

This study evolves resistance to GAPDH inhibition and shows that cells lose the Warburg Effect but maintain a distinct glycolytic state with different metabolic dependencies.

Metabolic landscape of the tumor microenvironment

The paper develops a computational pipeline to analyze single-cell metabolic gene expression in human tumors, revealing higher metabolic activity and variation in malignant cells compared to bulk tumor studies.

NRF2-dependent metabolic reprogramming is required for tumor recurrence following oncogene inhibition

This study identifies NRF2-driven metabolic reprogramming as essential for breast cancer recurrence after oncogene inhibition and shows it can be targeted with glutaminase inhibitors.

Methionine metabolism influences the genomic architecture of H3K4me3 with the link to gene expression encoded in peak width

The paper shows that methionine metabolism affects H3K4me3 peak width, which encodes gene expression and cell identity, despite stable peak locations.

Environmental factors shape methionine metabolism in p16/MTAP deleted cells

This study shows that environmental factors like nutrition and tissue type have a greater impact on methionine metabolism in p16/MTAP deleted cells than the genetic deletion itself.

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer.

This study identifies metabolic adaptations in taxane-resistant triple-negative breast cancer cells that lead to epigenetic vulnerabilities, specifically through altered methionine metabolism and H3K27me3 redistribution.

Acetate is generated de novo from glucose metabolism in mammals and is coupled to central carbon metabolism

The paper shows that glucose metabolism generates acetate through two mechanisms and demonstrates its role in maintaining Ac-CoA pools and cell proliferation under specific metabolic conditions.