The mutation of Lys125 in connexin26 to glutamate, a carbamylation mimetic, pushes the equilibrium of the gap junction channel seen in cryo-EM towards a more closed conformation.

Exosomes from cancer-associated fibroblasts enhance the "Warburg effect" in tumors and contain de novo metabolites that can contribute to the entire compendia of central carbon metabolism within cancer cells.

A CO₂ receptor and a mechanism for the CO₂-mediated opening of gap junction hemichannels have been identified.

SDH-null cancer cells decrease mitochondrial complex I to drive rewired aspartate synthesis through reductive carboxylation and pyruvate carboxylase, supporting cell proliferation and tumor growth.

Isotope tracing into macromolecules enables functional analysis of metabolism in specific cell populations in tumors and provides insight into metabolic differences between cancer and stromal cells in their endogenous microenvironment.

A bacterial CO₂ concentrating mechanism enables Escherichia coli to fix CO₂ from ambient air into biomass.

Mitochondrial fatty acid synthesis is best known for producing lipoic acid, however, longer acyl chain products regulate mitochondrial electron transport chain assembly, oxidative TCA cycle metabolism, and skeletal myoblast differentiation.

Building on previous work (Meigh et al., 2013) we show that A88V, a mutation in connexin26 (Cx26) that causes Keratitis-Ichthyosis-Deafness (KID) syndrome in humans, is linked to a lack of sensitivity to CO₂ by Cx26 hemichannels.

Multi-omic analyses reveal a connection between the integrated stress response and the regulation of redox and amino acid metabolism when the TCA cycle is impaired.

In mice, but not in humans, the bone-derived hormone osteocalcin is O-glycosylated, a post-translational modification controlling its half-life in vivo.