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Molecular Mechanisms of Cell Death and Energy Metabolism in Apoptosis and Necrosis

This study explores the intricate molecular interactions involving RIP1, RIP3, and CYLD in programmed cell death (PCD) pathways. It examines the role of lipoxygenases and NADPH oxidase in regulating c-Jun kinases and the impact on energy metabolism through TNFR-1 signaling and ceramide production. The crosstalk between mitochondria, the nucleus, and the endoplasmic reticulum (ER) is highlighted, with a focus on reactive oxygen species (ROS), PARP activation, and the roles of various proteases such as cathepsins and calpains. The study provides insights on the interplay of apoptosis and necrosis.

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Molecular Mechanisms of Cell Death and Energy Metabolism in Apoptosis and Necrosis

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  1. RIP1, RIP3, CYLD, Lipoxygenases, NADPH Oxidase/c-Jun Kinases, Bmf, Energy metabolism TNFR-1/Ceramide Bcl-2 Bcl-2 Bcl-2 ? Mito Nucleus ? ER Crosstalk ? ROS, PARP, NAD+/ATP-depletion, AIF, Cathepsins, Calpains, EndoG, HtrA2/OMI ciPCD

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