| http://purl.uniprot.org/citations/12438448 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12438448 | http://www.w3.org/2000/01/rdf-schema#comment | "T cell-mediated fulminant hepatitis is a life-threatening event for which the underlying mechanism is not fully understood. Injection of concanavalin A (Con A) into mice recapitulates the histological and pathological sequelae of T cell-mediated hepatitis. In this model, both signal transducer and activator of transcription factor 1 (STAT1) and STAT3 are activated in the liver. Disruption of the STAT1 gene by way of genetic knockout attenuates liver injury, suppresses CD4(+) and NK T cell activation, and downregulates expression of proapoptotic interferon regulatory factor-1 protein and suppressor of cytokine signaling-1 (SOCS1), but enhances STAT3 activation and STAT3-controlled antiapoptotic signals. Studies from IFN-gamma-deficient mice indicate that IFN-gamma not only is the major cytokine responsible for STAT1 activation but also partially accounts for STAT3 activation. Moreover, downregulation of STAT3 activation in IL-6-deficient mice is associated with decreased STAT3-controlled antiapoptotic signals and expression of SOCS3, but upregulation of STAT1 activation and STAT1-induced proapoptotic signals and exacerbation of liver injury. Taken together, these findings suggest that STAT1 plays a harmful role in Con A-mediated hepatitis by activation of CD4(+) and NK T cells and directly inducing hepatocyte death, whereas STAT3 protects against liver injury by suppression of IFN-gamma signaling and induction of antiapoptotic protein Bcl-X(L). STAT1 and STAT3 in hepatocytes also negatively regulate one another through the induction of SOCS."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.org/dc/terms/identifier | "doi:10.1172/jci15841"xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/author | "Gao B."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/author | "Tian Z."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/author | "Hong F."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/author | "Kim W.H."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/author | "Radaeva S."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/author | "Nguyen V.A."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/author | "Jaruga B."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/author | "El-Assal O.N."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/name | "J Clin Invest"xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/pages | "1503-1513"xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/title | "Opposing roles of STAT1 and STAT3 in T cell-mediated hepatitis: regulation by SOCS."xsd:string |
| http://purl.uniprot.org/citations/12438448 | http://purl.uniprot.org/core/volume | "110"xsd:string |
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