| pubmed-article:10623660 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0205042 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0178324 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0178539 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0540654 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:10623660 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:10623660 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:10623660 | pubmed:dateCreated | 2000-2-8 | lld:pubmed |
| pubmed-article:10623660 | pubmed:abstractText | We previously isolated MACH-related inducer of toxicity (MRIT), a homolog of caspase 8. MRIT, also known as c-FLICE-inhibitory protein (c-FLIP), is an enzymatically inactive homolog of caspase 8 with homology to viral FLIP (v-FLIP). Because of this homology and resemblance to dominant negative proteins, c-FLIP is widely believed to be an antagonist to the death receptor-initiated apoptotic pathways that use caspase 8. We generated a polyclonal antibody, MAG1, and show that this antibody specifically recognizes two splice forms, long form (c-FLIPL) and short form (c-FLIPS). By in situ hybridization and immunohistochemistry, we demonstrate that c-FLIP is expressed in endothelial cells, macrophages, and smooth muscle cells (SMCs) both in human coronary arteries and in cultured cells. In an uninjured rat carotid arteries, c-FLIP protein is abundant in the vascular media. After balloon angioplasty, c-FLIP protein is rapidly down-regulated in medial SMCs for 2 weeks and regains expression by 4 weeks. In contrast, the neointima is strongly immunoreactive to c-FLIP from day 7 after the initial injury and remains strongly immunoreactive until 4 to 6 weeks. Similarly there is strong c-FLIP immunoreactivity in SMCs from nonatherosclerotic diffuse intimal thickening and in the overlying endothelial cells. In contrast, c-FLIP immunoreactivity is uneven and often absent in SMCs within the atherosclerotic plaque. Double labeling with c-FLIP antibody and terminal deoxynucleotidyltransferase-mediated UDP end labeling (TUNEL) in the injured rat common carotid artery show that TUNEL-positive cells in the first 2 days after injury lack detectable c-FLIP, suggested a role for caspase 8 in this form of death. In contrast, there is no correlation of c-FLIP with the spontaneous elevation in death of intima seen at 7 days after injury. For human atherosclerotic plaques, the majority of TUNEL-positive cells lack detectable c-FLIP. The expression pattern of c-FLIP and the relation between c-FLIP and TUNEL suggest a role for c-FLIP- and caspase 8-driven death in control of viability of the cells of the atherosclerotic intima. | lld:pubmed |
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| pubmed-article:10623660 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10623660 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10623660 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10623660 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10623660 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:10623660 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:10623660 | pubmed:author | pubmed-author:ImanishiTT | lld:pubmed |
| pubmed-article:10623660 | pubmed:author | pubmed-author:SchwartzS MSM | lld:pubmed |
| pubmed-article:10623660 | pubmed:author | pubmed-author:McBrideJJ | lld:pubmed |
| pubmed-article:10623660 | pubmed:author | pubmed-author:KIMS BSB | lld:pubmed |
| pubmed-article:10623660 | pubmed:author | pubmed-author:O'BrienK DKD | lld:pubmed |
| pubmed-article:10623660 | pubmed:author | pubmed-author:ORRS FSF | lld:pubmed |
| pubmed-article:10623660 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10623660 | pubmed:volume | 156 | lld:pubmed |
| pubmed-article:10623660 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10623660 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10623660 | pubmed:pagination | 125-37 | lld:pubmed |
| pubmed-article:10623660 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10623660 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10623660 | pubmed:articleTitle | Expression of cellular FLICE-inhibitory protein in human coronary arteries and in a rat vascular injury model. | lld:pubmed |
| pubmed-article:10623660 | pubmed:affiliation | Departments of Pathology, Medicine (Cardiology), and Molecular Biotechnology, University of Washington, Seattle, Washington 98195, USA. | lld:pubmed |
| pubmed-article:10623660 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10623660 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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