Cellular acidity, capacity for net acid extrusion, and expression of acid-base transporters in human breast carcinomas independently predict variation in proliferative activity, lymph node metastasis, and patient survival.
Cellular carbon accumulation systems are a fundamental prerequisite for biomineralization to stabilize pH and to supply inorganic carbon for CaCO3 precipitation under changing environmental conditions.
A multidisciplinary platform featured by patient-derived RPEs is established to study the disease-causing mechanisms of BEST1 mutations, and demonstrates gene-supplemented rescue of the mutation-caused deficiency in Ca2+-dependent Cl- current in human RPE.
HCO3–-sensitive regulation of endothelium-dependent vasorelaxation by receptor-type tyrosine-protein phosphatase RPTPγ provides a novel mechanism for acid-base-mediated coordination of cerebrovascular perfusion during increased local metabolism and for protection against ischemia.
NHE1-CaM complexes of multiple stoichiometries regulate cellular Ca2+-dependent NHE1 activity and can contribute to NHE1 dimerization, the latter shown by the NMR structure of CaM linking two NHE1 cytosolic tails.
Modifying membrane potential by an 'inhibitory' chloride conductance such as PSAM4-GlyR is inherently unstable because the normally low intracellular concentration of chloride is readily increased by influx of chloride.
ATF4, the master regulator of transcription during the Integrated Stress Response (ISR), causes global changes in cysteine sulfhydration of proteins and this event causes cellular metabolic reprogramming.
Physiological differentiation during symbiosis leads to division of labor between smaller and larger cells in an uncultured bacterial tubeworm symbiont population and results in remarkable metabolic diversity and complexity.