David Ernest James

This study identifies a renometabolic trade-off where increased urinary nutrient loss protects against obesity but increases vulnerability to acute kidney injury.

The paper uses personalized phosphoproteomics to show that mTORC1 regulates exercise-induced insulin sensitization in human skeletal muscle through a feedback pathway involving MKNK2 and eIF4G1.

This study shows that Rac1 deficiency in muscle reduces mitochondrial function and fatty acid metabolism, leading to muscle wasting and highlights potential therapeutic targets for age-related muscle decline.

Synteny prioritizes disease-relevant genes and identifies functionally important proteins using human genetic evidence.

This study identifies a genetic locus affecting insulin sensitivity in mice, showing that Defa26 modulates glucose homeostasis through microbiome interactions.

This study identifies SEC61B as a regulator of calcium flux and platelet hyperreactivity in diabetes by linking ER stress to increased SEC61B expression and calcium leak.

This study investigates the role of PKD in adipose tissue, revealing sex-dependent effects on metabolism through phosphoproteomics and a mouse model.

The paper identifies very long-chain ceramides in muscle as independently associated with insulin resistance, separate from adiposity effects, using genetic variation in mice.

eNODAL is a clustering method for nutriomics data that integrates experimental design with unsupervised learning to identify interpretable clusters of omics features affected by drug-diet interactions.

This study uses phosphoproteomics to show how genetic background and diet influence insulin signalling in muscle, revealing key regulators of insulin responsiveness and glycolysis in insulin resistance.

The paper identifies small molecules that reverse insulin resistance in mouse skeletal muscle by integrating systems genetics and chemical screening.

The paper identifies three genetic loci influencing mitochondrial proteins and heart hypertrophy in mice using proteomics and association mapping.

This study uses phosphoproteomics to show that insulin resistance involves rewired signaling networks and widespread dysregulation of GSK3 activity.

The paper compares proteomics profiles of subcutaneous and visceral adipose tissue in mice to identify depot-specific differences and responses to diet.

The paper identifies UFMylation as a negative regulator of skeletal muscle function through proteome-wide systems genetics in mice and validates it in a disease model.

The paper uses computational models and experiments to show mTORC1 activity depends biphasically on mTORC2 subunit Sin1 and highlights mLST8 as a therapeutic target in breast cancer.

The paper introduces hRUV, a hierarchical method to remove unwanted variation in large-scale metabolomics data, showing improved preservation of biological signals.

The paper identifies diet-responsive genes in Drosophila by analyzing genetic variation across diets and confirms their role in nutrient storage and utilization.

PhosR provides tools for processing and analyzing phosphoproteomic data, enabling data imputation, normalization, and functional analysis of kinase activity and signaling pathways.

The paper maps multi-omic changes during mouse pluripotency transition, showing phosphoproteome dynamics precede epigenome and transcriptome changes.