pubmed-article:10510092 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10510092 | lifeskim:mentions | umls-concept:C0540654 | lld:lifeskim |
pubmed-article:10510092 | lifeskim:mentions | umls-concept:C1720947 | lld:lifeskim |
pubmed-article:10510092 | lifeskim:mentions | umls-concept:C0178874 | lld:lifeskim |
pubmed-article:10510092 | lifeskim:mentions | umls-concept:C1514762 | lld:lifeskim |
pubmed-article:10510092 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
pubmed-article:10510092 | lifeskim:mentions | umls-concept:C1999216 | lld:lifeskim |
pubmed-article:10510092 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
pubmed-article:10510092 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:10510092 | pubmed:dateCreated | 1999-11-4 | lld:pubmed |
pubmed-article:10510092 | pubmed:abstractText | Death receptor-mediated apoptosis can be modulated by several antiapoptotic proteins, such as the FLICE (FADD [Fas-associated death domain]-like IL-1beta-converting enzyme)-inhibitory proteins (FLIPs). The FLIP family includes both cellular and viral members. The Kaposi's sarcoma-associated herpesvirus protein (KSHV)-FLIP is expressed by human herpesvirus 8 (HHV-8), which is associated with malignancies such as Kaposi's sarcoma and certain lymphomas. In this paper, we demonstrate that KSHV-FLIP protects cells from Fas-mediated apoptosis by inhibiting caspase activation and permits clonal growth in the presence of death stimuli in vitro. Furthermore, we show that KSHV-FLIP can act as a tumor progression factor by promoting tumor establishment and growth in vivo. When injected into immunocompetent recipient mouse strains, murine B lymphoma cells (A20) transduced with KSHV-FLIP rapidly develop into aggressive tumors showing a high rate of survival and growth. The tumor-progressive activity of KSHV-FLIP is mediated by prevention of death receptor-induced apoptosis triggered by conventional T cells. Consequently, inhibitors of death receptor signaling can be regarded as a new class of tumor progression factors, and HHV-8-associated tumors may represent naturally occurring examples of the tumorigenic effect of such inhibitors. | lld:pubmed |
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pubmed-article:10510092 | pubmed:language | eng | lld:pubmed |
pubmed-article:10510092 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10510092 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:10510092 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10510092 | pubmed:month | Oct | lld:pubmed |
pubmed-article:10510092 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:10510092 | pubmed:author | pubmed-author:BiberfeldPP | lld:pubmed |
pubmed-article:10510092 | pubmed:author | pubmed-author:BogerFF | lld:pubmed |
pubmed-article:10510092 | pubmed:author | pubmed-author:GrandienAA | lld:pubmed |
pubmed-article:10510092 | pubmed:author | pubmed-author:CatrinaA IAI | lld:pubmed |
pubmed-article:10510092 | pubmed:author | pubmed-author:DjerbiMM | lld:pubmed |
pubmed-article:10510092 | pubmed:author | pubmed-author:ScrepantiVV | lld:pubmed |
pubmed-article:10510092 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10510092 | pubmed:day | 4 | lld:pubmed |
pubmed-article:10510092 | pubmed:volume | 190 | lld:pubmed |
pubmed-article:10510092 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10510092 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10510092 | pubmed:pagination | 1025-32 | lld:pubmed |
pubmed-article:10510092 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:10510092 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10510092 | pubmed:articleTitle | The inhibitor of death receptor signaling, FLICE-inhibitory protein defines a new class of tumor progression factors. | lld:pubmed |
pubmed-article:10510092 | pubmed:affiliation | Department of Immunology, Wenner-Gren Institute, University of Stockholm, S-10691 Stockholm, Sweden. | lld:pubmed |
pubmed-article:10510092 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10510092 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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