| pubmed-article:11777967 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11777967 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:11777967 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:11777967 | lifeskim:mentions | umls-concept:C0439064 | lld:lifeskim |
| pubmed-article:11777967 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:11777967 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11777967 | pubmed:dateCreated | 2002-1-4 | lld:pubmed |
| pubmed-article:11777967 | pubmed:abstractText | TWEAK, a recently identified member of the TNF family, is expressed on IFN-gamma-stimulated monocytes and induces cell death in certain tumor cell lines. In this study, we characterized the TWEAK-induced cell death in several tumor cell lines that exhibited distinct features. Although the TWEAK-induced cell death in Kym-1 cells was indirectly mediated by TNF-alpha and was inhibited by cycloheximide, the TWEAK-induced cell death in HSC3 cells or IFN-gamma-treated HT-29 cells was not inhibited by anti-TNF-alpha mAb or cycloheximide, suggesting a direct triggering of cell death via TWEAK receptor in the latter cell lines. The TWEAK-induced apoptosis in HSC3 cells and IFN-gamma-treated HT-29 cells was associated with caspase-8 and caspase-3 activation. Although a pan-caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, inhibited the TWEAK-induced cell death in HSC3 cells, it rather sensitized HT-29 cells to TWEAK-induced cell death by necrosis. This necrosis was abrogated by lysosomal proteinase inhibitors, particularly a cathepsin B inhibitor, [L-3-trans-(propylcarbamoyl)oxirane-2-carbonyl]-L-isoleucyl-L-proline methyl ester. During the process of TWEAK-induced necrosis, cathepsin B was released from lysosome to cytosol. Although DR3 has been reported to be a receptor for TWEAK, all TWEAK-sensitive tumor cell lines used in this study did not express DR3 at either protein or mRNA level, but did bind CD8-TWEAK specifically. These results indicated that TWEAK could induce multiple pathways of cell death, including both caspase-dependent apoptosis and cathepsin B-dependent necrosis, in a cell type-specific manner via TWEAK receptor(s) distinct from DR3. | lld:pubmed |
| pubmed-article:11777967 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11777967 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:11777967 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11777967 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:11777967 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:YagitaHideoH | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:NakayamaMasaf... | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:IshidohKazumi... | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:KayagakiNobuh... | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:KojimaYukoY | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:YamaguchiNori... | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:NakanoHiroyas... | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:KominamiEikiE | lld:pubmed |
| pubmed-article:11777967 | pubmed:author | pubmed-author:OkumuraKoK | lld:pubmed |
| pubmed-article:11777967 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11777967 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11777967 | pubmed:volume | 168 | lld:pubmed |
| pubmed-article:11777967 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11777967 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11777967 | pubmed:pagination | 734-43 | lld:pubmed |
| pubmed-article:11777967 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11777967 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11777967 | pubmed:articleTitle | Multiple pathways of TWEAK-induced cell death. | lld:pubmed |
| pubmed-article:11777967 | pubmed:affiliation | Department of Immunology, Allergy Research Center, Division of Pathology, Central Laboratory of Medical Sciences, Juntendo University School of Medicine, Tokyo, Japan. | lld:pubmed |
| pubmed-article:11777967 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11777967 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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