| pubmed-article:16737533 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16737533 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:16737533 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:16737533 | lifeskim:mentions | umls-concept:C0059386 | lld:lifeskim |
| pubmed-article:16737533 | lifeskim:mentions | umls-concept:C0870071 | lld:lifeskim |
| pubmed-article:16737533 | pubmed:dateCreated | 2006-7-10 | lld:pubmed |
| pubmed-article:16737533 | pubmed:abstractText | The lack of detailed understanding of the mechanism of action of many biowarfare agents poses an immediate challenge to biodefense efforts. Many potential bioweapons have been shown to affect the cellular pathways controlling apoptosis 1234. For example, pathogen-produced exotoxins such as Staphylococcal Enterotoxin B (SEB) and Anthrax Lethal Factor (LF) have been shown to disrupt the Fas-mediated apoptotic pathway 24. To evaluate how these agents affect these pathways it is first necessary to understand the dynamics of a normally functioning apoptosis network. This can then serve as a baseline against which a pathogen perturbed system can be compared. Such comparisons can expose both the proteins most susceptible to alteration by the agent as well as the most critical reaction rates to better instill control on a biological network. | lld:pubmed |
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| pubmed-article:16737533 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16737533 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16737533 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16737533 | pubmed:issn | 1471-2180 | lld:pubmed |
| pubmed-article:16737533 | pubmed:author | pubmed-author:JettMartiM | lld:pubmed |
| pubmed-article:16737533 | pubmed:author | pubmed-author:FeidlerJordan... | lld:pubmed |
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| pubmed-article:16737533 | pubmed:author | pubmed-author:HammamiehRash... | lld:pubmed |
| pubmed-article:16737533 | pubmed:author | pubmed-author:ChangWenling... | lld:pubmed |
| pubmed-article:16737533 | pubmed:author | pubmed-author:HiggsBrandon... | lld:pubmed |
| pubmed-article:16737533 | pubmed:author | pubmed-author:SmithHaley... | lld:pubmed |
| pubmed-article:16737533 | pubmed:author | pubmed-author:PetersOlivia... | lld:pubmed |
| pubmed-article:16737533 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:16737533 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:16737533 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16737533 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16737533 | pubmed:pagination | 48 | lld:pubmed |
| pubmed-article:16737533 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:16737533 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16737533 | pubmed:articleTitle | Modeling the effects of a Staphylococcal Enterotoxin B (SEB) on the apoptosis pathway. | lld:pubmed |
| pubmed-article:16737533 | pubmed:affiliation | Emerging Technologies Office, The MITRE Corporation, McLean, VA, USA. bhiggs@mitre.org | lld:pubmed |
| pubmed-article:16737533 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16737533 | pubmed:publicationType | Comparative Study | lld:pubmed |
