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Previously discussed, Gaucher’s Disease results from a dysfunctional autophagy-lysosome system, which is key in degrading misfolded proteins that contribute to nontypical and improper protein accumulation common in late onset neurodegenerative diseases (McNeill et al., 2014)
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Experimental studies have reported changes in transcriptional activity across multiple cell types, making GHK-Cu a useful tool for investigating how copper-associated signaling may influence broader regulatory networks
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