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International Journal of Zoological Research
  Year: 2006 | Volume: 2 | Issue: 3 | Page No.: 226-241
DOI: 10.3923/ijzr.2006.226.241
Peroxiredoxins and Neurodegeneration
R.G. Ahmed, Yuan Ye Ma and S.H. Lee

Peroxiredoxins (Prxs) are a family of novel antioxidant proteins that are found in a variety of species and participate in a number of vital biological processes such as proliferation, differentiation, response to oxidative stress and intracellular signaling. It has been proposed that they might participate in these cellular processes by playing a role in eliminating or regulating the intracellular concentration of peroxides produced during metabolism as well as in the signaling cascades of growth factors and cytokines. Mammalian cells express six isoforms of Prx (Prx I to VI), which are classified into three subgroups (typical 2-Cys, atypical 2-Cys and 1-Cys) based on the number and position of cysteine (Cys) residues that participate in catalysis and on amino acid sequences and the immunological reactivity. Members of the typical 2-Cys subgroup include Prx I through Prx IV and contain an additional conserved cysteine in the carboxyl-terminal region, whereas Prx V and Prx VI, members of the atypical 2-Cys and 1-Cys subgroups, respectively, do not contain this second conserved Cys. On the other hand, Prxs activity can be regulated by phosphorylation and proteolysis processes in addition to overoxidation. Taken together, this study suggest that the generation of the oxidative stress which caused neurodegeneration may couple with produced Prxs and the reverse is true. However, this argument is still unclear on account of the difficulties of the direct observation of the reactive oxygen species due to their biological lifetime is short. Thus, experiments will be required to solve these problems and to comprehend the actual role of Prxs in neurodegeneration.
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How to cite this article:

R.G. Ahmed, Yuan Ye Ma and S.H. Lee , 2006. Peroxiredoxins and Neurodegeneration. International Journal of Zoological Research, 2: 226-241.

DOI: 10.3923/ijzr.2006.226.241








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