Matches in UGent Biblio for { <https://biblio.ugent.be/publication/1089044#aggregation> ?p ?o. }
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- aggregation classification "A1".
- aggregation creator B582520.
- aggregation creator B582521.
- aggregation creator B582522.
- aggregation creator B582523.
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- aggregation date "2010".
- aggregation format "application/pdf".
- aggregation hasFormat 1089044.bibtex.
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- aggregation isPartOf urn:issn:0022-1767.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Oligodendrocyte-specific FADD deletion protects mice from autoimmune-mediated demyelination".
- aggregation abstract "Apoptosis of oligodendrocytes (ODCs), the myelin-producing glial cells in the CNS, plays a central role in demyelinating diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To investigate the mechanism behind ODC apoptosis in EAE, we made use of conditional knockout mice lacking the adaptor protein FADD specifically in ODCs (FADD(ODC-KO)). FADD mediates apoptosis by coupling death receptors with downstream caspase activation. In line with this, ODCs from FADD(ODC-KO) mice were completely resistant to death receptor-induced apoptosis in vitro. In the EAE model, FADD(ODC-KO) mice followed an ameliorated clinical disease course in comparison with control littermates. Lymphocyte and macrophage infiltration into the spinal cord parenchyma was significantly reduced, as was the extent of demyelination and proinflammatory gene expression. Collectively, our data show that FADD is critical for ODC apoptosis and the development of autoimmune demyelinating disease.".
- aggregation authorList BK934419.
- aggregation endPage "7653".
- aggregation issue "12".
- aggregation startPage "7646".
- aggregation volume "185".
- aggregation aggregates 2937640.
- aggregation isDescribedBy 1089044.
- aggregation similarTo jimmunol.1000930.
- aggregation similarTo LU-1089044.