title: Mousing around with caspases and IAPs.
abstract: In a paper in this issue of the Biochemical Journal that questions the role of c-IAP1 (cellular inhibitor of apoptosis 1) in inflammation, new results from the Duckett laboratory remind us of the importance of truly knowing the mice we depend on. It turns out that c-IAP1 is tightly linked to caspase 11 and cannot be segregated by recombination. This disturbing result implies that immune functions ascribed to c-IAP1 may be due to the caspase 11 mutation that is co-inherited with the locus.
authors.affiliation: Programs in Cell Death and Inflammation Research, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA. robert@sanfordburnham.org
authors.forename: Robert C
authors.initials: RC
authors.lastname: Rickert
authors.forename: Guy S
authors.initials: GS
authors.lastname: Salvesen
authors.forename: Carl F
authors.initials: CF
authors.lastname: Ware
mesh_terms: D000818:Animals; D020169:Caspases / Q000235:genetics*; D053471:Caspases, Initiator; D051034:Inhibitor of Apoptosis Proteins / Q000378:metabolism*; D009154:Mutation
chemical_list: D051034:Inhibitor of Apoptosis Proteins; C101136:Casp4 protein, mouse; D020169:Caspases; D053471:Caspases, Initiator