http://purl.uniprot.org/citations/22461627 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/22461627 | http://www.w3.org/2000/01/rdf-schema#comment | "Naturally occurring Foxp3(+)CD4(+)CD25(+) T regulatory cell (nTreg)-mediated suppression of lung allergic responses is abrogated following ligation of glucocorticoid-induced tumor necrosis receptor (GITR) family-related protein. In vitro stimulation of nTregs with GITR ligand increased phosphorylation of c-Jun N-terminal kinase (JNK) but not extracellular signal-regulated protein kinase (ERK) or p38 MAPK. SP600125, a known JNK inhibitor, prevented GITR-mediated phosphorylation of JNK. Activation of JNK was associated with increases in the upstream mitogen-activated protein kinase kinase 7 (MKK7) and the downstream transcription factor NF-κβ. Phosphorylated c-Jun (p-c-Jun), indicative of the activation of JNK, was detected in the immunoprecipitates of nTregs from wild-type but not JNK- or GITR-deficient mice. Treatment with an inhibitor of JNK phosphorylation resulted in complete reversal of all GITR-induced changes in nTreg phenotype and function, with full restoration of suppression of in vivo lung allergic responses and in vitro proliferation of activated CD4(+)CD25(-) T cells. Thus, regulation of JNK phosphorylation plays a central role in T regulatory cell function with therapeutic implications for the treatment of asthma and autoimmune diseases."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m111.316943"xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/author | "Okamoto M."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/author | "Takeda K."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/author | "Ohnishi H."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/author | "Gelfand E.W."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/author | "Domenico J."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/author | "Joetham A."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/author | "Dakhama A."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/author | "Schedel M."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/pages | "17100-17108"xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/title | "Loss of T regulatory cell suppression following signaling through glucocorticoid-induced tumor necrosis receptor (GITR) is dependent on c-Jun N-terminal kinase activation."xsd:string |
http://purl.uniprot.org/citations/22461627 | http://purl.uniprot.org/core/volume | "287"xsd:string |
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