| pubmed-article:11717445 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11717445 | lifeskim:mentions | umls-concept:C0758959 | lld:lifeskim |
| pubmed-article:11717445 | lifeskim:mentions | umls-concept:C0010656 | lld:lifeskim |
| pubmed-article:11717445 | lifeskim:mentions | umls-concept:C1720947 | lld:lifeskim |
| pubmed-article:11717445 | lifeskim:mentions | umls-concept:C1514762 | lld:lifeskim |
| pubmed-article:11717445 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:11717445 | pubmed:issue | 24 | lld:pubmed |
| pubmed-article:11717445 | pubmed:dateCreated | 2001-11-21 | lld:pubmed |
| pubmed-article:11717445 | pubmed:abstractText | A role for caspase-10, previously implicated in the autoimmune lymphoproliferative syndrome, in death receptor signaling has not been directly shown. Here we show that caspase-10 can function independently of caspase-8 in initiating Fas- and tumor necrosis factor-related apoptosis-inducing ligand-receptor-mediated apoptosis. Moreover, Fas crosslinking in primary human T cells leads to the recruitment and activation of caspase-10. Fluorescent resonance energy transfer analysis indicates that the death-effector domains of caspase-8 and -10 both interact with the death-effector domain of FADD. Nonetheless, we find that caspase-8 and -10 may have different apoptosis substrates and therefore potentially distinct roles in death receptor signaling or other cellular processes. | lld:pubmed |
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| pubmed-article:11717445 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11717445 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11717445 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11717445 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11717445 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:11717445 | pubmed:author | pubmed-author:WangJJ | lld:pubmed |
| pubmed-article:11717445 | pubmed:author | pubmed-author:VEALJ RJR | lld:pubmed |
| pubmed-article:11717445 | pubmed:author | pubmed-author:SpencerD MDM | lld:pubmed |
| pubmed-article:11717445 | pubmed:author | pubmed-author:ChowH YHY | lld:pubmed |
| pubmed-article:11717445 | pubmed:author | pubmed-author:LenardoM JMJ | lld:pubmed |
| pubmed-article:11717445 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11717445 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:11717445 | pubmed:volume | 98 | lld:pubmed |
| pubmed-article:11717445 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11717445 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11717445 | pubmed:pagination | 13884-8 | lld:pubmed |
| pubmed-article:11717445 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:11717445 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11717445 | pubmed:articleTitle | Caspase-10 is an initiator caspase in death receptor signaling. | lld:pubmed |
| pubmed-article:11717445 | pubmed:affiliation | Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11N311, 10 Center Drive, MSC 1892, Bethesda, MD 20892, USA. | lld:pubmed |
| pubmed-article:11717445 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11717445 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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