Linked Life Data

20377744

Source:http://linkedlifedata.com/resource/pubmed/id/20377744

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-4-9
pubmed:abstractText
Activation of MAPK is negatively regulated by DUSP, which dephosphorylate the phosphothreonine and phosphotyrosine residues. We have identified a novel JNK-specific DUSP, DUSP16, from murine macrophages. Its involvement in T cells has not yet been defined. In the present study, we found expression of DUSP16 in thymocytes and activated T cells but not in naive T cells. To elucidate the roles of DUSP16 in T cells, transgenic mice expressing a dominant negative form of DUSP16 specifically in T cells were generated (dnDUSP16 Tg). JNK activity was selectively augmented in the thymocytes of these dnDUSP16 Tg mice. CD4 T cells in dnDUSP16 Tg mice showed normal levels of proliferation and IL-2 production after TCR triggering, while they produced increased IFN-gamma but reduced Th2 cytokines compared with wild type CD4 T cells. On the other hand CD8 T cells in dnDUSP16 Tg mice produced an increased amount of IL-2, which resulted in enhanced proliferation and IFN-gamma production. These results suggest that DUSP16 is an important regulator of JNK activity and effector functions of CD4 and CD8 T cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0385-5600
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
105-11
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Dual specificity phosphatase16 is a negative regulator of c-Jun NH2-terminal kinase activity in T cells.
pubmed:affiliation
Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Higashi-ku, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't