Protein carbonylation, cellular dysfunction, and disease progression

Protein carbonylation, cellular dysfunction, and disease progression

Carbonylation of proteins is an irreversible oxidative damage, often leading to a loss of protein function, which is considered a widespread indicator of severe oxidative damage and disease-derived protein dysfunction. Whereas moderately carbonylated proteins are degraded by the proteasomal system, heavily carbonylated proteins tend to form high-molecular-weight aggregates that are resistant to...

Protein carbonylation.

Protein carbonylation is a type of protein oxidation that can be promoted by reactive oxygen species. It usually refers to a process that forms reactive ketones or aldehydes that can be reacted by 2,4-dinitrophenylhydrazine (DNPH) to form hydrazones. Direct oxidation of side chains of lysine, arginine, proline, and threonine residues, among other amino acids, in the ‘‘primary protein carbonylat...

Redox proteomics: from protein modifications to cellular dysfunction and disease.

Reactive oxygen and nitrogen species (ROS and RNS, respectively) are part of any aerobic lifestyle/metabolism: low (i.e., subtoxic) concentrations of selected ROS and RNS are continuously produced inside and outside the cell by a number of pathways, either accidentally or purposefully. In all eukaryotic cells, the mitochondrial electronic transport chain is the main endogenous source during cel...

Rab11 in Disease Progression

Membrane/ protein trafficking in the secretory/ biosynthetic and endocytic pathways is mediated by vesicles. Vesicle trafficking in eukaryotes is regulated by a class of small monomeric GTPases the Rab protein family. Rab proteins represent the largest branch of the Ras superfamily GTPases, and have been concerned in a variety of intracellular vesicle trafficking and different intracellular sig...

Quantification of protein carbonylation