David J. Gonzalez

The paper maps bacterial bile amidation by analyzing BSH transaminase activities and identifying BBAs in human samples.

The paper develops an optogenetic tool to rapidly inhibit autophagy and identifies nuclear pore complex proteins as autophagy substrates.

This study shows that knocking out PKA regulatory subunits RI and RII leads to distinct metabolic and phosphorylation changes, with RI KO increasing Tau phosphorylation linked to Alzheimer's disease.

This study identifies a link between ELMO1 and mitochondrial pathways in macrophages during Salmonella infection through proteome profiling and functional analysis.

The paper introduces mspms, an R package and graphical interface for analyzing MSP-MS data, validated using cathepsin substrate profiling.

This study uses APEX2 proximity labeling and mass spectrometry to uncover ligand-dependent CCR5 trafficking mechanisms, revealing distinct internalization and degradation pathways.

The paper identifies giant polyketide synthase genes in Prymnesium parvum that biosynthesize large polyether toxins, resolving a long-standing biosynthetic mystery.

This study shows that CCM lesions in mice cause behavioral impairments linked to neuroinflammation, affecting motor coordination and memory.

This study identifies a bacterial sialidase, NanH, in Bacteroides fragilis that mediates early gut colonization and resilience through host-derived glycans.

The paper identifies FBP1 as a nonenzymatic regulator that inhibits AKT activation to prevent insulin hyperresponsiveness and associated liver pathologies.

This study uses native E. coli as chassis to deliver transgenes, inducing persistent physiological changes in conventionally-raised hosts.

The paper estimates in vivo enzyme turnover numbers (kcats) in E. coli using metabolic specialist strains and shows their stability and predictive power over in vitro kcats.

This paper expands the interpretability of human metabolomes by using food-based annotations, increasing the fraction of molecular features understood 7-fold.

The paper shows EGFR is required for Wnt9a-Fzd9b signaling specificity in HSPC development, identifying key domains and phosphorylation events.