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In our recent study, in addition to elucidating the pathogenic mechanism of FUS-associated ALS in both Drosophila and animal systems, we found that overexpression of GstO2, a Drosophila homolog of human GSTO1, reduces cytoplasmic FUS aggregates and attenuates neurodegenerative phenotypes, including mitochondrial dysfunction and neuronal toxicity 148

(2014) found that a relatively low risk for incidence of cardiovascular disease for those with a greater intake of ascorbic acid supplements

erinaceus alone resulted in only a slight decrease in SQSTM/p62 protein expression, but after the use of the AhR antagonist, the expression significantly increased

That said, this method may overlook important aspects of biological complexity, such as variations in protein expression