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A distinctive feature of the stress response in multicellular eukaryotes is programmed cell death, or apoptosis, which eliminates damaged cells.
Selection acts on mitochondria through the autophagy process, which eliminates damaged and old organelles (mitophagy, see Youle and Van Der Bliek 2012).
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Because many cancer treatments cause DNA damage, apoptosis is thought to be the major mechanism eliminating damaged oocytes.
When cells experience irreversible ER stress, this pathway eliminates damaged cells by apoptosis.
Mitophagy is a form of autophagy that specifically eliminates damaged mitochondria.
The induction of autophagy is seen in adult and neonatal mouse striatum and cortex after hypoxic-ischemic injury,, and oxidative stress following cerebral hypoxia-ischemia may induce autophagy, which initially aborts apoptosis by eliminating damaged mitochondria and preventing necrosis via catabolic energy production.
DNA damage response reactions include removal of damaged DNA and restoration of the continuity of the DNA structure; activation of a DNA damage checkpoint, which arrests cell cycle progression in order to allow repair and transmission of damaged or incompletely replicated chromosomes; or apoptosis, which eliminates seriously damaged cells.
Autophagy is an evolutionarily conserved intracellular process which plays an important role in eliminating damaged organelles and long-live proteins for maintenance of cellular homestasis (Mizushima, 2009).
DNA damage by ionizing irradiation (IR) triggers rapid activation of DNA-damage checkpoint response, resulting in either cell-cycle arrest that allows DNA repair or induction of apoptosis, which eliminates seriously damaged or deregulated cells [ 1].
Under normal conditions, apoptosis is a protective mechanism which eliminates old, useless, and damaged cells.
The assembly of SWNTs is carried out in a sealed microchannel which eliminates the potential damage of the nanosensors during the bonding process.
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