In conclusion, we suggest that lipid raft components can exert their regulatory activity in apoptosis execution at three different levels: (1) in the DISC formation at the plasma membrane; (2) in the intracellular redistribution at cytoplasmic organelles, and, (3) in the structural and functional mitochondrial modifications associated with apoptosis execution.
Some authors have proposed that mitochondrial modifications or redox imbalance are the origin for Ca2+ signal disfunction [ 14; 24].
Interestingly, overexpression of the gene can decrease methylglyoxal-induced mitochondrial protein modifications and increase lifespan (Morcos et al., 2008).
Overall, these initial studies demonstrate that respiratory exposure to high concentrations of mostly agglomerated SWCNTs provokes not only pulmonary toxicity but vascular effects related to mitochondrial oxidative modifications and accelerated atheroma formation.
In most cases, fertility restoration is attained through nuclear-encoded Rf-gene-dependent mitochondrial RNA modification and concurrent reduction of the CMS-associated protein.
This dataset excludes mitochondrial variants, as SuRFR has been trained on nuclear, not mitochondrial, variants and relies heavily on functional data that are not applicable to mitochondrial variants (most notably, histone modifications and DNase HS data).
Mice carrying a heterozygous deletion of Sod2 (Sod2 +/-) are viable but show increased oxidative stress, increased nuclear and mitochondrial DNA modifications, impaired mitochondria function, and increased apoptosis rates [ 9- 13].
It also totally or partially prevented the aging-related detrimental changes observed in mitochondrial membrane unsaturation, protein oxidative modifications, and immune and behavioral functions, without changing longevity.
In the present study, decreased SOD2 protein levels and activity significantly increased mitochondrial damage, protein modification, and oil red-O staining areas in apoE−/ −, SOD2+/− mice.
However, due to the comparably low cellular abundance of mitochondrial tRNAs the study of their modifications and modification pathways lags far behind that of cytoplasmic or bacterial tRNAs.
