| http://purl.uniprot.org/citations/25794705 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25794705 | http://www.w3.org/2000/01/rdf-schema#comment | "Fas-induced apoptosis is involved in diverse liver diseases. Herein, we investigated the effect of Mir155 deletion on Fas-induced liver injury. Wild-type (WT) mice and Mir155 knockout (KO) mice were i.p. administered with the anti-Fas antibody (Jo2) to determine animal survival and the extent of liver injury. After Jo2 injection, the Mir155 KO mice exhibited prolonged survival versus the WT mice (P < 0.01). The Mir155 KO mice showed lower alanine aminotransferase and aspartate aminotransferase levels, less liver tissue damage, fewer apoptotic hepatocytes, and lower liver tissue caspase 3/7, 8, and 9 activities compared with the WT mice, indicating that Mir155 deletion prevents Fas-induced hepatocyte apoptosis and liver injury. Hepatocytes isolated from Mir155 KO mice also showed resistance to Fas-induced apoptosis, in vitro. Higher protein level of myeloid cell leukemia-1 (Mcl-1) was also observed in Mir155 KO hepatocytes compared to WT hepatocytes. A miR-155 binding site was identified in the 3'-untranslated region of Mcl-1 mRNA; Mcl1 was identified as a direct target of miR-155 in hepatocytes. Consistently, pretreatment with a siRNA specific for Mcl1 reversed Mir155 deletion-mediated protection against Jo2-induced liver tissue damage. Finally, restoration of Mir155 expression in Mir155 KO mice abolished the protection against Fas-induced hepatocyte apoptosis. Taken together, these findings demonstrate that deletion of Mir155 prevents Fas-induced hepatocyte apoptosis and liver injury through the up-regulation of Mcl1."xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ajpath.2014.12.020"xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/author | "Han C."xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/author | "Chen W."xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/author | "Zhang J."xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/author | "Wu T."xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/author | "Song K."xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/name | "Am J Pathol"xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/pages | "1033-1044"xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/title | "Deletion of Mir155 prevents Fas-induced liver injury through up-regulation of Mcl-1."xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://purl.uniprot.org/core/volume | "185"xsd:string |
| http://purl.uniprot.org/citations/25794705 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25794705 |
| http://purl.uniprot.org/citations/25794705 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/25794705 |
| http://purl.uniprot.org/uniprot/#_P97287-mappedCitation-25794705 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/25794705 |
| http://purl.uniprot.org/uniprot/P97287 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/25794705 |