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Specifically, IL-5 priming led Siglec-8 cross-linking to cause a loss of mitochondrial membrane potential and production of ROS inside the eosinophil, which in turn drove the cell into apoptosis through a caspase-independent mechanism (183)

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Nadine the response was the opposite (Kogovsek et al., 2010), suggesting that host-dependent differential patterns of antioxidant induction could contribute to altered symptom severity in response to different PVY isolates

Interestingly, with the introduction of a S301A mutation containing consensus motifs for an N-linked glycosylation site in the variant region of CD44 (CD44v8-v10), CD44 variant isoforms failed to interact with xCT, thus underlining the importance of posttranslational modifications for CD44v9/membrane proteins interactions (Ishimoto et al., 2011)

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