Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-6-1
pubmed:abstractText
Natural killer (NK) cells use multiple mechanisms to defend against viral infections, and different stimuli can activate these antiviral effects. When engaged, receptors for innate cytokines produced during infections and for ligands on target cells can both induce NK cell cytotoxicity and the production of cytokines. These stimuli use different classes of intracellular signaling pathways to elicit the overlapping responses. What is the advantage of using different roads to the same ends? One answer might be in the nature of the alternative regulatory pathways that are in place to control the respective stimuli. A model of flexibility in accessing NK cell function, in the context of negative regulation of particular intracellular signaling pathways, is proposed here.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1471-4906
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
252-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Keeping NK cells in highly regulated antiviral warfare.
pubmed:affiliation
Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural