Proteolytic breakdown of cytoskeleton induces neurodegeneration during pathology of murine cerebral malaria.
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Summary
The results confirm that activation of multiple suicidal proteases, their cross talks and breakdown of the cytoskeletal proteins increase neuronal degeneration and lead to exacerbation of cerebral malaria pathology.
- Type
- article
- Published
- 2011-10-12
- Cited by
- 4
- References
- 55
- OpenAlex
- https://openalex.org/W2079396028
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:5536527
Keywords
Calpain, Proteases, Cytoskeleton, Neurodegeneration, Proteolysis
References
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- Implication of calpain in neuronal apoptosis
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- Oxidative stress in malaria parasite-infected erythrocytes: host-parasite interactions.
- Caspases cleave the amino-terminal calpain inhibitory unit of calpastatin during apoptosis in human Jurkat T cells.
- Ischemic neuronal death in the rat hippocampus: the calpain-calpastatin-caspase hypothesis.
- Cross-talk between Calpain and Caspase Proteolytic Systems During Neuronal Apoptosis*
- Extensive degradation of myelin basic protein isoforms by calpain following traumatic brain injury
- The cytotoxic T lymphocyte protease granzyme A cleaves and inactivates poly(adenosine 5'-diphosphate-ribose) polymerase-1.
- Distinct Mechanistic Roles of Calpain and Caspase Activation in Neurodegeneration as Revealed in Mice Overexpressing Their Specific Inhibitors*
- Differential PARP Cleavage: An Indication of Heterogeneous Forms of Cell Death and Involvement of Multiple Proteases in the Infarct of Focal Cerebral Ischemia in Rat
- Fas small interfering RNA reduces motoneuron death in amyotrophic lateral sclerosis mice
- A unified hypothesis for the genesis of cerebral malaria: sequestration, inflammation and hemostasis leading to microcirculatory dysfunction.
- Recent advances on neuronal caspases in development and neurodegeneration.
- Redox‐Dependent Apoptosis in Human Endothelial Cells after Adhesion of Plasmodium falciparum‐Infected Erythrocytes
- Calpain-dependent neurofilament breakdown in anoxic and ischemic rat central axons.
- Calpain and caspase: can you tell the difference?
Cited by
- Brain-derived neurotrophic factor and the course of experimental cerebral malaria.
- Host metabolic responses to Plasmodium falciparum infections evaluated by 1H NMR metabolomics.
- Dysregulation of LIMK‐1/cofilin‐1 pathway: A possible basis for alteration of neuronal morphology in experimental cerebral malaria
- Cytotoxic T Lymphocyte Granzyme-b mediates neuronal cell death during Plasmodium berghei ANKA induced experimental cerebral malaria.
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