Histone methylation patterns may differ depending on the enzymatic source of the methyl donor S-adenosylmethionine, suggesting the biological effects of low SAM may affect methylation targets in different ways, depending on the synthase producing it.

Genome-scale integration of transposon mutagenesis with a redox biosensor identified a hypothetical transcription factor- Rv0158 required to calibrate the growth, cytoplasmic redox potential, and respiration of Mycobacterium tuberculosis in response to metabolic switching from glucose to fatty acids.

Antigen receptor control of methionine transport is critical to co-ordinate protein synthesis and the production of methyl donors for nucleotide and protein methylations which are required for T cell differentiation.

A unique, widely distributed gut bacterial enzyme selectively metabolizes plant-derived cardiac glycoside drugs.

A network of the gut chemical landscape predicts microbe-mediated biotransformation of foods and drugs and supports the generation of mechanistic hypotheses of microbiome metabolic phenotypes that shape human biology.

A gaseous signaling molecule hydrogen sulfide stimulates mitochondrial bioenergetics, maintains glutathione redox poise, and suppresses ROS to subvert viral rebound in latently infected CD4⁺ T cells from HIV subjects.

Hippocampal metabolomic analyses following episodic learning at different ages revealed a critical role for neuronal glutathione reductase activity in long-term infantile memory formation.

Metabolic activity of the methionine/S-adenosylmethionine cycle is sensed and transcriptionally regulated by a nuclear hormone receptor in Caenorhabditis elegans in order to maintain metabolic homeostasis in a tightly controlled regime.

Computational reaction representations and profile hidden Markov model searches of metagenomics databases can be harnessed to accurately predict bacterial species and enzyme sequences responsible for biotransformations in the human gut microbiome.

Interplay between AML and stromal cells can initiate a mechanism involving gap junctions where ROS is transferred from cancer cells to stromal cells which then produce acetate which can in return be absorbed/utilised by the cancer cells.