Journal
APOPTOSIS
Volume 9, Issue 2, Pages 111-121Publisher
SPRINGER
DOI: 10.1023/B:APPT.0000018793.10779.dc
Keywords
apoptosis; axon guidance; caspase; ischemic tolerance; neural plasticity; neuroprotection; preconditioning; proteasome; review
Categories
Funding
- NICHD NIH HHS [P30HD15052, P30 HD015052] Funding Source: Medline
- NINDS NIH HHS [R01 NS050396-01, R01 NS050396] Funding Source: Medline
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Caspases are a family of cysteine proteases that are expressed as inactive zymogens and undergo proteolytic maturation in a sequential manner in which initiator caspases cleave and activate the effector caspases 3, 6 and 7. Effector caspases cleave structural proteins, signaling molecules, DNA repair enzymes and proteins which inhibit apoptosis. Activation of effector, or executioner, caspases has historically been viewed as a terminal event in the process of programmed cell death. Emerging evidence now suggests a broader role for activated caspases in cellular maturation, differentiation and other non-lethal events. The importance of activated caspases in normal cell development and signaling has recently been extended to the CNS where these proteases have been shown to contribute to axon guidance, synaptic plasticity and neuroprotection. This review will focus on the adaptive roles activated caspases in maintaining viability, the mechanisms by which caspases are held in check so as not produce apoptotic cell death and the ramifications of these observations in the treatment of neurological disorders.
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