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Description
A1AT, 1-antitrypsin

& Chuang, Y.-C
Two things have to be mentioned: first, the tertiary structure of EL was never determined de novo, but deduced from modeling or molecular replacement, respectively [48, 54, 55]

By binding to p53, it induces nuclear exclusion, allowing p53 to translocate to the cytoplasm and mitochondria, subsequently activating the p53/BCL-2/Caspase-3 signaling pathway to execute selective apoptosis in senescent populations (Frontiers, 2025

Each trial involved placing the animal on a rotarod revolving at 5 rpm/min, then accelerating at 0.6 rpm/min
Both mechanisms ultimately result in the death of cancer cells [78]
