FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration

Amyloid-β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNFα from neuronal protection to death

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FAIM-L Is an IAP-Binding Protein That Inhibits XIAP Ubiquitinylation and Protects from Fas-Induced Apoptosis

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The Novel Caspase-3 Substrate Gap43 is Involved in AMPA Receptor Endocytosis and Long-Term Depression

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XIAP Regulates Caspase Activity in Degenerating Axons

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A Caspase Cascade Regulating Developmental Axon Degeneration

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The Ubiquitin Ligase XIAP Recruits LUBAC for NOD2 Signaling in Inflammation and Innate Immunity

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Caspase-3 Activation via Mitochondria Is Required for Long-Term Depression and AMPA Receptor Internalization

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The Death Receptor Antagonist FLIP-L Interacts with Trk and Is Necessary for Neurite Outgrowth Induced by Neurotrophins

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