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There were no significant alterations in telomeres or cellular protection markers before treatment onset

For instance, the dysregulation of Cu transport ATPase A (ATP7A), ceruloplasmin (CP), superoxide dismutase 3 (SOD3), and other Cu proteins in pancreatic -cells may lead to intracellular Cu accumulation, triggering increased ROS generation and causing pancreatic islet damage, ultimately resulting in DM (59)

Cellular models as tools for the study of the role of alpha-synuclein in Parkinsons disease

Similarly, deletion of the Ca 2+ sensor STIM1 leads to spontaneous activation of the STING-TBK1-IRF3 pathway, which results in type I IFN-mediated ER stress (130)

Treatment with GGC (200 M) provided significant protection from exposure to oligomeric A 40