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  4. Membrane repair induced HDAC6-independent autophagy and aggresome formation
 
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Membrane repair induced HDAC6-independent autophagy and aggresome formation

Date Issued
2009
Date
2009
Author(s)
Weng, Yu-Ting
URI
http://ntur.lib.ntu.edu.tw//handle/246246/178900
Abstract
Transient plasma membrane disruptions commonly occur in cells that experience mechanical stress or external force. From what we have known, disruption of the plasma membrane would lead to the exposure of the cell interior to the external oxidizing environment and change the oxidation state of proteins in cells. These oxidized proteins would become extensively aggregated or cross-linked and attach to the disrupted plasma membrane. Furthermore, extracellular Ca2+ would enter cells, promoting vesicle fusion and exocytosis to form membrane patches that prevent cell contents from spilling out of cells. Afterward, damaged cells proceed to endocytosis and the formation of endosomes that promote the replacement of wound areas in plasma membrane. Protein aggregates, membrane patches, and endosomes that occur during plasma membrane disruption might cause cell stress. At present, it remains unclear how protein aggregates, membrane patches, and endosomes are eliminated in cells after membrane damage.ere, the results suggest that membrane damage at 4 hour after magnetic beads rolling is able to induce autophagy. By blocking autophagy with 3-methyladenine (3-MA), cell viability decreased after beads rolling. These results imply that autophagy participates in membrane repair. Moreover, we found that polyubiquitination and HDAC6 were not involved in the autophagic process following membrane damage and repair. Since ubiquitination plays a minimal role, autophagy, an alternative pathway caused by beads rolling, might help to eliminate protein aggregates, membrane patches and endosomes.
Subjects
autophagy
membrane repair
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