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P2X7 Mediates Superoxide Production in Primary Microglia and Is Up-regulated in a Transgenic Mouse Model of Alzheimer's Disease*
TLDR
Both ATP and BzATP stimulated microglia-induced cortical cell death indicating this pathway may contribute to neurodegeneration and P2X7 receptor was specifically up-regulated around β-amyloid plaques in a mouse model of Alzheimer's disease. Expand
Caspase-mediated fragmentation of calpain inhibitor protein calpastatin during apoptosis.
TLDR
It is reported that the endogenous calpain inhibitor calpastatin is fragmented by caspase(s) to various extents during early apoptosis in two cell types and proposed that the proteolysis of calpastatins might have yet unidentified effects on the cross-talk between the two protease systems. Expand
Regional calpain and caspase‐3 proteolysis of α‐spectrin after traumatic brain injury
TLDR
Distinct regional and temporal patterns of calpain/caspase-3 processing of α-spectrin were observed in brain regions ipsilateral to the site of injury after TBI, including large increases of 145 kDa calpain-mediated SBDP in cortex (up to 30-fold), and enduring increases ( up to 2 weeks) of 145KDa SBDPIn hippocampus and thalamus. Expand
Simultaneous Degradation of αII- and βII-Spectrin by Caspase 3 (CPP32) in Apoptotic Cells*
TLDR
It is postulate that in concert with calpain, caspase rapidly targets critical sites in both αII- and βII-spectrin and thereby initiates a rapid dissolution of the spectrin-actin cortical cytoskeleton with apoptosis. Expand
Simultaneous Degradation of αII- and βII-Spectrin by Caspase 3 (CPP32) in Apoptotic Cells*
The degradation of αII- and βII-spectrin during apoptosis in cultured human neuroblastoma SH-SY5Y cells was investigated. Immunofluorescent staining showed that the collapse of the cortical spectrinExpand
Mechanisms of calpain proteolysis following traumatic brain injury: implications for pathology and therapy: implications for pathology and therapy: a review and update.
TLDR
New evidence indicating that overactivation of calpains plays a major role in the neurodegenerative cascade following TBI in vivo is reviewed, and an overview from in vivo and in vitro models of CNS injuries suggesting that administration of calpain inhibitors during the initial 24-h period following injury can attenuate injury-induced derangements of neuronal structure and function is presented. Expand
A calpain inhibitor attenuates cortical cytoskeletal protein loss after experimental traumatic brain injury in the rat
TLDR
Western blot data indicate that calpain inhibitors could represent a viable strategy for preserving the cytoskeletal structure of injured neurons after experimental traumatic brain injury in vivo. Expand
Mechanisms of Calpain Proteolysis Following Traumatic Brain Injury: Implications for Pathology and Therapy: A Review and Update
TLDR
New evidence indicating that overactivation of calpains plays a major role in the neurodegenerative cascade following TBI in vivo is reviewed, suggesting that administration of calpain inhibitors during the initial 24-h period following injury can attenuate injury-induced derangements of neuronal structure and function. Expand
mu-calpain activation and calpain-mediated cytoskeletal proteolysis following traumatic brain injury.
TLDR
The results indicate that rapid and persistent mu-calpain activation plays an important role in cortical neuronal degeneration aftertraumatic brain injury and suggest that specific inhibitors of calpain could be potential therapeutic agents for the treatment of traumatic brain injury in vivo. Expand
Immunohistochemical study of calpain-mediated breakdown products to alpha-spectrin following controlled cortical impact injury in the rat.
TLDR
The appearance of calpain-mediated BDPs at sites distal to the contusion site and in the hippocampus also suggests that calpain activation may precede and/or occur in the absence of extensive morphopathological changes. Expand
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