pubmed-article:15163405 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15163405 | lifeskim:mentions | umls-concept:C0020962 | lld:lifeskim |
pubmed-article:15163405 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
pubmed-article:15163405 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
pubmed-article:15163405 | lifeskim:mentions | umls-concept:C0010656 | lld:lifeskim |
pubmed-article:15163405 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
pubmed-article:15163405 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:15163405 | pubmed:dateCreated | 2004-5-27 | lld:pubmed |
pubmed-article:15163405 | pubmed:abstractText | Caspases not only play an essential role during apoptotic cell death, but a subfamily of them-the inflammatory caspases-are associated with immune responses to microbial pathogens. Activation of inflammatory caspases, such as caspase-1 and caspase-5, occurs upon assembly of an intracellular complex, designated the inflammasome. This results in the cleavage and activation of the proinflammatory cytokines IL-1beta and IL-18. Mutations in one of the scaffold proteins of the inflammasome, NALP3/Cryopyrin, are associated with autoinflammatory disorders underscoring the importance of regulating inflammatory caspase activation. | lld:pubmed |
pubmed-article:15163405 | pubmed:language | eng | lld:pubmed |
pubmed-article:15163405 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15163405 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15163405 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15163405 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15163405 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15163405 | pubmed:month | May | lld:pubmed |
pubmed-article:15163405 | pubmed:issn | 0092-8674 | lld:pubmed |
pubmed-article:15163405 | pubmed:author | pubmed-author:TschoppJürgJ | lld:pubmed |
pubmed-article:15163405 | pubmed:author | pubmed-author:MartinonFabio... | lld:pubmed |
pubmed-article:15163405 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15163405 | pubmed:day | 28 | lld:pubmed |
pubmed-article:15163405 | pubmed:volume | 117 | lld:pubmed |
pubmed-article:15163405 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15163405 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15163405 | pubmed:pagination | 561-74 | lld:pubmed |
pubmed-article:15163405 | pubmed:dateRevised | 2005-11-16 | lld:pubmed |
pubmed-article:15163405 | pubmed:meshHeading | pubmed-meshheading:15163405... | lld:pubmed |
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pubmed-article:15163405 | pubmed:meshHeading | pubmed-meshheading:15163405... | lld:pubmed |
pubmed-article:15163405 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15163405 | pubmed:articleTitle | Inflammatory caspases: linking an intracellular innate immune system to autoinflammatory diseases. | lld:pubmed |
pubmed-article:15163405 | pubmed:affiliation | Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, CH-1066 Epalinges, Switzerland. | lld:pubmed |
pubmed-article:15163405 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15163405 | pubmed:publicationType | Review | lld:pubmed |
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