http://purl.uniprot.org/citations/23250397 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/23250397 | http://www.w3.org/2000/01/rdf-schema#comment | "As a catalytically inactive homolog of caspase-8, a proapoptotic initiator caspase, c-FLIP blocks apoptosis by binding to and inhibiting caspase-8. The transcription factor nuclear factor κB (NF-κB) plays a pivotal role in maintaining the homeostasis of the intestine and the liver by preventing death receptor-induced apoptosis, and c-FLIP plays a role in the NF-κB-dependent protection of cells from death receptor signaling. Because c-Flip-deficient mice die in utero, we generated conditional c-Flip-deficient mice to investigate the contribution of c-FLIP to homeostasis of the intestine and the liver at developmental and postnatal stages. Intestinal epithelial cell (IEC)- or hepatocyte-specific deletion of c-Flip resulted in perinatal lethality as a result of the enhanced apoptosis and programmed necrosis of the IECs and the hepatocytes. Deficiency in the gene encoding tumor necrosis factor-α (TNF-α) receptor 1 (Tnfr1) partially rescued perinatal lethality and the development of colitis in IEC-specific c-Flip-deficient mice but did not rescue perinatal lethality in hepatocyte-specific c-Flip-deficient mice. Moreover, adult mice with interferon (IFN)-inducible deficiency in c-Flip died from hepatitis soon after depletion of c-FLIP. Pretreatment of IFN-inducible c-Flip-deficient mice with a mixture of neutralizing antibodies against TNF-α, Fas ligand (FasL), and TNF-related apoptosis-inducing ligand (TRAIL) prevented hepatitis. Together, these results suggest that c-FLIP controls the homeostasis of IECs and hepatocytes by preventing cell death induced by TNF-α, FasL, and TRAIL."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.org/dc/terms/identifier | "doi:10.1126/scisignal.2003558"xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Koike M."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Nakano H."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Okumura K."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Kurihara H."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Piao X."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Uchiyama Y."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Hara M."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "He Y.W."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Yagita H."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Schutz G."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Komazawa-Sakon S."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Nishina T."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Piao J.H."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Ohmuraya M."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Van Rooijen N."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/author | "Ehlken H."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/name | "Sci Signal"xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/pages | "ra93"xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/title | "c-FLIP maintains tissue homeostasis by preventing apoptosis and programmed necrosis."xsd:string |
http://purl.uniprot.org/citations/23250397 | http://purl.uniprot.org/core/volume | "5"xsd:string |
http://purl.uniprot.org/citations/23250397 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23250397 |