Feng Cai

This study uses metabolomics to analyze 474 subjects with inborn errors of metabolism, identifying genotype-specific metabolic alterations and providing diagnostic tools and a database of metabolomic features.

This study identifies GAA accumulation in gliomas as a driver of neuronal activity and tumor growth, linking cancer metabolism to neuroscience through GABAA receptor activation.

This study identifies UFMylation of PDH as a regulator of mitochondrial metabolism, showing it enhances pyruvate oxidation and TCA cycle activity.

This study shows that L-2HG accumulation due to L2HGDH deficiency impairs neuronal differentiation by epigenetically activating MYC, leading to stem cell self-renewal and reduced neuron formation.

This study identifies NUDT5 as a regulator of purine metabolism and thiopurine sensitivity by interacting with PPAT, independent of its known enzymatic activity.

This paper introduces HTz-GlcNAc, a tool for real-time tracking of glycoconjugates and secretome mapping in live cells.

This study shows mutant IDH reprograms neural progenitor cell fate by silencing Gsx2, promoting gliomagenesis through lineage switching.

This study identifies glycosaminoglycan-mediated lipoprotein uptake as a mechanism by which cancer cells resist ferroptosis and lipid oxidative stress.

This study identifies hyper-glycosylation as a driver of Alzheimer's disease through metabolic analysis and interventions, showing its impact on cognitive decline and mortality.

The paper introduces a web application for exploring metabolomics data from plasma and fibroblasts of patients with inborn errors of metabolism, enabling analysis of metabolic deviations and relationships.

This study maps the mouse brain metabolome using targeted metabolomics, creating detailed maps of 79 metabolites at high resolution.