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. |