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Protein Aggregation and Multiple Organelle Damage After Brain Ischemia

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Translational Stroke Research

Abstract

Protein aggregation leads to a broad range of conformational diseases. Protein folding during synthesis and assembly to subcellular structures require cooperation of several sophisticated ATP-dependent cellular systems including protein chaperoning, protein trafficking, protein assembling, as well as protein degradation. Emerging evidence strongly suggests that brain ischemia leads to dysfunction of these ATP-dependent protein assembly and quality control systems, resulting in protein misfolding, ubiquitination, and aggregation during the postischemic phase. Misfolded proteins are aggregated with subcellular organelles and eventually damage these organelles, leading to multiple organelle failure and delayed neuronal death after brain ischemia. In this chapter, we will first review the provenance and history of protein aggregation in the brain ischemic field and then update latest concept and mechanisms of protein aggregation and multiple organelle damage after brain ischemia.

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Abbreviations

EPTA:

Ethanolic phosphotungstic acid

Ubi-proteins:

Ubiquitin-conjugated proteins

DG:

Dentate gyrus

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Correspondence to Bingren Hu PhD .

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Liu, C.H., Zhang, F., Krisrian, T., Polster, B., Fiskum, G.M., Hu, B. (2012). Protein Aggregation and Multiple Organelle Damage After Brain Ischemia. In: Lapchak, P., Zhang, J. (eds) Translational Stroke Research. Springer Series in Translational Stroke Research. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-9530-8_5

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