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Publication : Caspase-6 and neurodegeneration.

First Author  Graham RK Year  2011
Journal  Trends Neurosci Volume  34
Issue  12 Pages  646-56
PubMed ID  22018804 Mgi Jnum  J:320401
Mgi Id  MGI:6874517 Doi  10.1016/j.tins.2011.09.001
Citation  Graham RK, et al. (2011) Caspase-6 and neurodegeneration. Trends Neurosci 34(12):646-56
abstractText  Caspases are cysteine-aspartic proteases that post-translationally modify their substrates through cleavage at specific sites, which causes either substrate inactivation or a gain of function through the generation of active fragments. Currently, each caspase is categorized as either an initiator of apoptosis or an end-stage executioner. Caspase-6 was originally identified as an executioner caspase owing to its role in cleavage of nuclear lamins. However, it has since been shown that caspase-6 cleaves caspases-2, 3 and 8. Furthermore, active caspase-6 is present in post mortem brains of Huntington and Alzheimer disease subjects that do not yet display apoptotic morphology, which suggests a function distinct from its well-validated executioner role. In this review, we discuss evidence to date regarding the role of caspase-6 in neurodegeneration. The findings suggest that selective inhibitors of caspase-6 may have therapeutic potential for various neurodegenerative disorders.
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