Spectrin and calpain: a 'target' and a 'sniper' in the pathology of neuronal cells.
It is well documented that activation of calpain, a calcium-sensitive cysteine protease, marks the pathology of naturally and experimentally occurring neurodegenerative conditions. Calpain-mediated proteolysis of major membrane-skeletal protein, alphaII-spectrin, results in the appearance of two unique and highly stable breakdown products, which is an early event in neural cell pathology. This review focuses on spectrin degradation by calpain within neurons induced by diverse conditions, emphasizing a current picture of multi-pattern neuronal death and a recent success in the development of spectrin-based biomarkers. The issue is presented in the context of the major structural and functional properties of the two proteins.
Czogalla
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Institute of Biochemistry and Molecular Biology, University of Wrocław, ul. Przybyszewskiego 63/77, 51-148, Wrocław, Poland.
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D000375:Aging; D000595:Amino Acid Sequence; D001930:Brain Injuries / Q000201:enzymology* / Q000473:pathology; D002545:Brain Ischemia / Q000201:enzymology* / Q000473:pathology; D002154:Calpain / Q000378:metabolism*; D016923:Cell Death; D006801:Humans; D008969:Molecular Sequence Data; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D017470:Receptors, Glutamate / Q000187:drug effects; D013049:Spectrin / Q000378:metabolism*; D014118:Toxins, Biological / Q000494:pharmacology
D017470:Receptors, Glutamate; D014118:Toxins, Biological; D013049:Spectrin; D002154:Calpain