Ryan D. Sheldon

The paper shows that certain bacteria reduce microsporidia infection in C. elegans by altering host metabolism and producing inhibitory compounds.

This study shows that lipoic acid exists in two distinct cellular pools with different functions, and supplementation increases free LA without restoring mitochondrial function.

This study improves LC-MS metabolomics by reducing background ion burden from tributylamine, enhancing signal intensity and feature coverage across multiple biological samples.

The paper develops and applies complementary microflow HILIC and ion pair LC-MS methods to analyze single-cell metabolomics in a tuberculosis macrophage model, revealing infection-associated metabolic changes and a distinct bystander phenotype.

This paper introduces a nanoflow ion-pairing LC-MS method for ultra-low-input polar metabolomics and isotope tracing, showing improved sensitivity and retention for metabolites.

The paper identifies malonate as an endogenous intermediate supporting mitochondrial fatty acid synthesis and oxidative phosphorylation, showing ACC1-dependent synthesis from glucose.

This study presents cryo-EM structures of active H/ACA snoRNPs, revealing inter-protomer interactions and how mutations affect pseudouridine formation and ribosome biogenesis.

This study shows dietary restriction enhances CD8+ T cell ketolysis, improving mitochondrial function and anti-tumor immunity by reducing exhaustion.

This study identifies how sperm increase metabolic flux through aldolase to meet energy demands during capacitation, revealing conserved metabolic regulation mechanisms in mammalian cells.

This study identifies a non-canonical metabolic pathway in cancer cells that uses β-hydroxybutyrate for fatty acid synthesis, supporting tumor growth under lipid-limited conditions.

This study identifies glucose-dependent glycosphingolipid biosynthesis as essential for CD8+ T cell expansion and tumor control, independent of energy production.

This study identifies the KEAP1-NRF2 pathway as a driver of CD8 T cell exhaustion by regulating the prostacyclin receptor PTGIR.

The paper identifies a role for oocyte mitochondrial electron transport chain remodeling in linking maternal environment to offspring metabolism and survival.

This study shows that Mecr, a mitochondrial fatty acid synthesis gene, is critical for CD4+ T cell metabolism, function, and survival, with implications for inflammatory diseases and mitochondrial disorders.

This study uses metabolomics and 13C tracing to examine glucose allocation to membrane glycans in pancreatic cancer cell lines, revealing differences in glycan synthesis and metabolic pathways.

The paper shows lipid-starved cancer cells are more sensitive to ferroptosis due to increased PUFA trafficking into phospholipids, challenging the assumption that PUFA levels directly determine ferroptosis susceptibility.

The paper identifies group II p21-activated kinases as regulators of α-synucleinopathy by linking network vulnerability analysis to gene expression and pharmacological interventions.

This study identifies N1-APA, a noncanonical polyamine produced by bacteria, as a bioactive metabolite that antagonizes animal mitochondrial function and macrophage activation.

This study develops a single-embryo metabolomics method to analyze metabolic and transcriptional changes in early Drosophila embryos with high temporal resolution.

This study integrates metabolomics and RNAseq from the same liver samples to show that prior metabolite extraction does not harm RNAseq quality and reveals pyrimidine metabolism as a key pathway in acute viral infection.

This study shows that mitochondrial citrate metabolism and efflux regulate trophoblast differentiation through effects on histone acetylation and gene expression.

This paper describes a protocol to study T cell metabolism in vivo using isotopically labeled metabolites and mass spectrometry.