In conclusion, our silent mutant rescue system has determined that translation and cell viability are regulated in distinct manners by LAMR and that the extraribosomal functions of LAMR are required for maintaining cell viability.
In all, the viability/morphology results from our FACS analysis are consistent with the rescue of phenotypic effects we observed by microscopy, and indicate that the C-terminal residues of LAMR are required for maintaining cell viability.
Maintaining cell viability is a major challenge associated with transplanting cells into ischemic myocardium to restore function.
BCL-W maintains cell viability by preventing mitochondrial membrane depolarization and caspase activation [6].
It has been proposed that TRP-2 may maintain cell viability by controlling the intracellular concentration of 5,6-dihydroxyndole, a toxic intermediate of melanin biosynthesis [42].
Autophagy is upregulated during periods of stress and maintains cell viability by enabling basic biomolecule and energy recycling.
The ability of SGT1 mutants to maintain cell viability was assessed by curing for pRS316-SGT1 by incubating the transformants on drop-out media without leucine, but containing uracil (25 mg/l) and 5-FOA (0.1%).
Overall, these results suggest that DMOG, or DFO, or serum starvation induces autophagy in epithelial and neuronal cells that maintain cell viability perhaps by inhibiting apoptotic-mediated cell death.
Hypercapnic acidosis decreased 24-h stretch-induced interleukin-8 secretion (a, b), preserved membrane integrity as assessed by epithelial LDH leakage (c, d), and maintained cell viability (e, f) in human bronchial epithelial cells and BEAS-2B cells, respectively.
