Amygdala astrocytes play a critical role in mediating the effects of stress during infancy on neuronal excitability, synaptic plasticity, and memory.

Differentiation of the pathogenic bacterium, Chlamydia trachomatis, from its non-infectious to infectious form is linked to the redox state of the organism.

Genome-wide CRISPRi screens and proteome profiling of lysosomes link lipid dysregulation to ESCRT disruption and proteostasis defect.

CysM and CysK2 play complementary and overlapping roles in Mtb's adaptation to environmental stress that are crucial for survival.

To investigate why bats are long-lived and cancer-resistant, multi-omic data from bat and human cells was analyzed using computational flux modeling, suggesting dysregulation of succinate-fumarate dynamics and an ischemic-like basal metabolism in bat cells.

PPM1D-mutant leukemia cells exhibit a dysregulated redox landscape, a diminished response to oxidative stress, and rely on SOD1 for their survival.

Mitochondrial functional and structural defects caused by PARL deficiency lead to arrested spermatogenesis and germ cell ferroptosis.

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.

Genetic or pharmacological suppression of lipid peroxidation pathway protects skeletal muscle from disuse-induced atrophy and weakness in young and old mice.