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• W2000207919 startingPage "94" @default.
• W2000207919 abstract "In multiple sclerosis (MS) and its widely accepted animal model, experimental autoimmune encephalomyelitis (EAE), the failure of autoreactive immune cells to undergo apoptosis is thought to contribute to CNS tissue damage and disease progression. Promoting apoptosis of myelin-reactive immune cells in diseases such as MS, may delay disease progression and decrease the frequency and severity of relapses. X-linked inhibitor of apoptosis (XIAP) is a potent anti-apoptotic protein that inhibits intrinsic, extrinsic, and c-Jun amino-terminal kinase mediated apoptosis and was the only member of the inhibitor of apoptosis (IAP) family upregulated in whole blood from EAE mice. Similar increases in XIAP were also observed in both peripheral and encephalitogenic T lymphocytes. Increased XIAP expression in T cells within areas of demyelination in the CNS suggests that XIAP may be enhancing cell survival and thereby contributing to disease pathology." @default.
• W2000207919 created "2016-06-24" @default.
• W2000207919 creator A5012819778 @default.
• W2000207919 creator A5016431105 @default.
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• W2000207919 date "2008-01-01" @default.
• W2000207919 modified "2023-10-05" @default.
• W2000207919 title "Inhibitor of apoptosis protein (IAP) profiling in experimental autoimmune encephalomyelitis (EAE) implicates increased XIAP in T lymphocytes" @default.
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• W2000207919 doi "https://doi.org/10.1016/j.jneuroim.2007.10.022" @default.
• W2000207919 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18055022" @default.
• W2000207919 hasPublicationYear "2008" @default.
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