Showing papers by "Dan Lindholm published in 2004"
TL;DR: Caspase inhibition by overexpression of XIAP prevented caspase-9 and caspases-3 activation but not cell death, presumably because of increased casp enzyme-independent cell death.
Abstract: One hemisphere of postnatal day 8 (P8) rats or P10 mice was irradiated with a single dose of 4–12 Gy, and animals were killed from 2 h to 8 weeks after irradiation (IR). In the subventricular zone (SVZ) and the granular cell layer (GCL) of the dentate gyrus, harboring neural and other progenitor cells, nitrosylation and p53 peaked 2–12 h after IR, followed by markers for active caspase-3, apoptosis-inducing factor and TUNEL (6–24 h). Ki67-positive (proliferating) cells had disappeared by 12 h and partly reappeared by 7 days post-IR. The SVZ and GCL areas decreased approximately 50% 7 days after IR. The development of white matter was hampered, resulting in 50–70% less myelin basic protein staining. Pretreatment with erythropoietin did not confer protection against IR. Caspase inhibition by overexpression of XIAP prevented caspase-9 and caspase-3 activation but not cell death, presumably because of increased caspase-independent cell death.
120 citations
TL;DR: The results indicate that oxidative and ER induced stress causing caspase-12 activation are involved in neuronal death and disease progression in ALS.
116 citations
TL;DR: Findings provide the first evidence that increased XIAP levels protect the neonatal brain against HI, and XIAP was colocalized with XAF-1, Smac, and HtrA2 in injured neurons after hypoxia-ischemia.
102 citations
TL;DR: The ubiquitin proteasome system contributes to the pathophysiology of neurodegenerative diseases and it is also a major determinant of synaptic protein degradation and activity.
Abstract: The ubiquitin proteasome system (UPS) contributes to the pathophysiology of neurodegenerative diseases, and it is also a major determinant of synaptic protein degradation and activity. Recent studies in rodents and in the fruit fly Drosophila have shown that the activity of the UPS is involved in axonal degeneration. Increased knowledge of the UPS in synaptic and axonal reactions may provide novel drug targets for treatments of neuronal injuries and neurodegenerative disorders.
69 citations
TL;DR: The elucidation of the physiological functions of mitochondrial proteins may lead to new insights into the role of these organelles in cell degeneration and to identification of novel drug targets for the prevention and treatment of different diseases.
42 citations
TL;DR: It has been shown in neurons that cell differentiation is accompanied by a decrease in Apaf-1 and the activity of the apoptosome with an increased ability of the inhibitor of apoptosis proteins (IAPs) to sustain survival.
Abstract: The molecular mechanisms by which differentiated cells combat cell death and injury have remained unclear. In the current issue, it has been shown in neurons that cell differentiation is accompanied by a decrease in Apaf-1 and the activity of the apoptosome with an increased ability of the inhibitor of apoptosis proteins (IAPs) to sustain survival (Wright et al., 2004). These results, together with earlier ones, deepen our understanding of how cell death and the apoptosome are regulated during differentiation and in tumor cells.
28 citations
TL;DR: Treatment with low concentrations of NMDA upregulates the neuroprotective molecule, X-chromosome-linked inhibitor of apoptosis protein (XIAP) in cultured hippocampal neurons at the post-transcriptional level and induces an anti-apoptotic program in hippocampusal neurons that involves mitochondria and alterations of the levels of caspase-3 and XIAP.
19 citations