Cytotoxicity associated with APOL1 renal-risk variants occurs through its plasma-membrane localization, where aberrant channel activity drives a sustained sodium and calcium influx leading to cell swelling and eventually cell death.
Calcium-driven protein changes, causing glycogenolysis, poor synthesis, and diminished content of glycogen, along with diminished glucose transporters, lead to hyperglycemia in patients prone to calcium leaks from intracellular muscle stores.
Sex-inclusive research practices have increased in many biological disciplines over the past decade, yet critical sex-based analyses and reporting have remained stagnant in most of these disciplines.
The metabolic rate of mice is disproportionately affected by the site of experimentation, affecting the phenotypic interpretation of genetically modified strains.
Mitochondrial electron transport chain dysfunction triggers the integrated stress response due to an asparagine deficiency downstream of impaired NADH oxidation in proliferating myoblasts, but not in differentiated myotubes.
The interaction between activated αIIbβ3 on platelets and SLC44A2 on circulating neutrophils facilitates neutrophil capture and drives flow-dependent NETosis.
