Working model.
- Soledad Matus (434944)
- Estefanía Lopez (434945)
- Vicente Valenzuela (434946)
- Melissa Nassif (434947)
- Claudio Hetz (159190)
Publication date
July 2013
DOIAbstract
<p>Accumulation of mutant SOD1 (SOD1<sup>mut</sup>) triggers ER stress engaging the UPR. Expression of ATF4 leads to the expression of genes involved in apoptosis induction including CHOP and BIM, in addition to genes operating in redox control. On a feedback loop, ER stress alters the redox status of the cell enhancing mutant SOD1 aggregation. ATF4 expression may attenuate SOD1 aggregation by controlling the expression of genes involved in redox buffering.</p
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