Linked Life Data

21775687

Source:http://linkedlifedata.com/resource/pubmed/id/21775687

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-8-22
pubmed:abstractText
Type I NKT cells, or invariant NKT (iNKT) cells, express a semi-invariant TCR characterized by its unique V?14-J?18 usage (iV?14TCR). Upon interaction with glycolipid/CD1d complexes, the iV?14TCRs transduce signals that are essential for iNKT selection and maturation. However, it remains unclear how these signals are regulated and how important such regulations are during iNKT development. Diacylglycerol (DAG) is an essential second messenger downstream of the TCR that activates the protein kinase C-I?B kinase (IKK)?/?-NF-?B pathway, known to be crucial for iNKT development, as well as the RasGRP1-Ras-Erk1/2 pathway in T cells. DAG kinases play an important role in controlling intracellular DAG concentration and thereby negatively regulate DAG signaling. In this article, we report that simultaneous absence of DAG kinase ? and ? causes severe defects in iNKT development, coincident with enhanced IKK-NF-?B and Ras-Erk1/2 activation. Moreover, constitutive IKK? and Ras activities also result in iNKT developmental defects. Thus, DAG-mediated signaling is not only essential but also needs to be tightly regulated for proper iNKT cell development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
187
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2122-9
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Tight regulation of diacylglycerol-mediated signaling is critical for proper invariant NKT cell development.
pubmed:affiliation
Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural