Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
50
|
pubmed:dateCreated |
1998-1-15
|
pubmed:abstractText |
The CD5 receptor on T lymphocytes is involved in T cell activation and T-B cell interactions. In the present study, we have characterized the signaling pathways induced by anti-CD5 stimulation in human T lymphocytes. In T lymphocytes, anti-CD5 co-stimulation enhances the phytohemagglutinin/anti-CD28-induced interleukin-2 (IL-2) mRNA accumulation 1.6-fold and IL-2 protein secretion 2. 2-fold, whereby the up-regulation is mediated at both the transcriptional and post-transcriptional level. The CD5 signaling pathway up-regulates the IL-2 gene expression by increasing the DNA binding and transactivation activity of activator protein 1 but affects none of the other transcription factors like nuclear factor of activated T cells, nuclear factor kappaB, Oct, and CD28-responsive complex/nuclear factor of mitogen-activated T cells involved in the regulation of the IL-2 promoter activity. The CD5-induced increase of the activator protein 1 activity is mediated through the activation of calcium/calmodulin-dependent (CaM) kinase type IV, and is independent of the activation of mitogen-activated protein kinases Jun N-terminal kinase, extracellular signal-regulated kinase, and p38/Mpk2, and calcium/calmodul-independent kinase type II. The expression of a dominant negative mutant of CaM kinase IV in T lymphocytes transfected with an IL-2 promoter-driven reporter construct completely abrogates the response to CD5 stimulation, indicating that CaM kinase IV is essential to the CD5 signaling pathway. In addition, it is demonstrated that calcium/calmodulin-dependent kinase type IV is also involved in the stabilization of the IL-2 transcripts, which is observed after co-stimulation of phytohemagglutinin/anti-CD28 activated T lymphocytes with anti-CD5.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-(5-Isoquinolinesulfonyl)-2-Methylp...,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD5,
http://linkedlifedata.com/resource/pubmed/chemical/CAMK4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Calmodulin-Dependent...,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Calmodulin-Dependent...,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/KN 62,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0021-9258
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
12
|
pubmed:volume |
272
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
31809-20
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:9395527-1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine,
pubmed-meshheading:9395527-Antigens, CD5,
pubmed-meshheading:9395527-Binding Sites,
pubmed-meshheading:9395527-Calcium-Calmodulin-Dependent Protein Kinase Type 4,
pubmed-meshheading:9395527-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:9395527-Enzyme Inhibitors,
pubmed-meshheading:9395527-Gene Expression,
pubmed-meshheading:9395527-Humans,
pubmed-meshheading:9395527-Interleukin-2,
pubmed-meshheading:9395527-Promoter Regions, Genetic,
pubmed-meshheading:9395527-RNA, Messenger,
pubmed-meshheading:9395527-Signal Transduction,
pubmed-meshheading:9395527-T-Lymphocytes,
pubmed-meshheading:9395527-Transcription Factor AP-1,
pubmed-meshheading:9395527-Transcriptional Activation
|
pubmed:year |
1997
|
pubmed:articleTitle |
The Ca2+/calmodulin-dependent kinase type IV is involved in the CD5-mediated signaling pathway in human T lymphocytes.
|
pubmed:affiliation |
Division of Hematology, Department of Internal Medicine, University of Groningen, 9713 GZ Groningen, The Netherlands.
|
pubmed:publicationType |
Journal Article,
In Vitro
|