Tat leads to neuronal death by activating calcium release from IP3-sensitive intracellular pools, causing endolysosomal dysfunction and dendritic impairments, which ultimately contribute to spatial memory impairment and premature brain aging [154,155,156,157,158]
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Previous studies have highlighted the important role played by hepatocyte gap junctions (GJs) with regard to increasing the severity of APAP-induced liver toxicity
Unexpected responses may indicate degradation products with different biological activities