Proteomics for the identification of specifically oxidized proteins in brain: Technology and application to the study of neurodegenerative disorders

被引:42
作者
Butterfield, DA
Castegna, A
机构
[1] Univ Kentucky, Dept Chem, Ctr Membrane Sci, Lexington, KY 40506 USA
[2] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40506 USA
关键词
proteomics; Alzheimer's disease; oxidized proteins; neurodegeneration;
D O I
10.1007/s00726-003-0027-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Proteomics offers the opportunity elucidate the complex protein interactions of cellular systems by studying the products of genes, i.e., proteins, and their structure, function and localization. The purpose of proteomics is to explain the information contained in the genome sequences in order to provide clues on cellular events, especially related to disease. Our proteomic approach has made possible the identification of specifically oxidized proteins in Alzheimer's disease (AD) brain, providing for the first time evidence on how oxidative stress plays a crucial role in AD-related neurodegeneration. This represents an example of the use of proteomics to solve biological problems related to disease. The field, which is still in its infancy, represents a very promising way to elucidate mechanism of disease at a protein level. However, the techniques that support its development present several limitations and require introduction of new tools and innovation in order to achieve a fast, reliable and sensitive method to understand normal biological processes and their regulation as well as these cellular properties in disease.
引用
收藏
页码:419 / 425
页数:7
相关论文
共 31 条
[1]   A post-genomic challenge: learning to read patterns of protein synthesis [J].
Abbott, A .
NATURE, 1999, 402 (6763) :715-720
[2]   Mass spectrometry in proteomics [J].
Aebersold, R ;
Goodlett, DR .
CHEMICAL REVIEWS, 2001, 101 (02) :269-295
[3]   Oxidative modification of creatine kinase BB in Alzheimer's disease brain [J].
Aksenov, M ;
Aksenova, M ;
Butterfield, DA ;
Markesbery, WR .
JOURNAL OF NEUROCHEMISTRY, 2000, 74 (06) :2520-2527
[4]   A comparison of selected mRNA and protein abundances in human liver [J].
Anderson, L ;
Seilhamer, J .
ELECTROPHORESIS, 1997, 18 (3-4) :533-537
[5]   Oxidative damage and tyrosine nitration from peroxynitrite [J].
Beckman, JS .
CHEMICAL RESEARCH IN TOXICOLOGY, 1996, 9 (05) :836-844
[6]   Oxidation of (carboxyalkyl)thiopropionic acid derivatives by hydroxyl radicals.: Mechanisms and kinetics of competitive inter- and intramolecular formation of σ- and σ*-type sulfuranyl radicals [J].
Bobrowski, K ;
Pogocki, D ;
Schöneich, C .
JOURNAL OF PHYSICAL CHEMISTRY A, 1998, 102 (51) :10512-10521
[7]  
Butterfield D.A., 1997, ADV CELL AGING GERON, V2, P161
[8]  
Butterfield DA, 2002, NEUROBIOL AGING, V23, P655
[9]   Evidence of oxidative damage in Alzheimer's disease brain:: central role for amyloid β-peptide [J].
Butterfield, DA ;
Drake, J ;
Pocernich, C ;
Castegna, A .
TRENDS IN MOLECULAR MEDICINE, 2001, 7 (12) :548-554
[10]   Lipid peroxidation and protein oxidation in Alzheimer's disease brain:: Potential causes and consequences involving amyloid β-peptide-associated free radical oxidative stress [J].
Butterfield, DA ;
Lauderback, CM .
FREE RADICAL BIOLOGY AND MEDICINE, 2002, 32 (11) :1050-1060