Linked Life Data

20473789

Source:http://linkedlifedata.com/resource/pubmed/id/20473789

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-10-15
pubmed:abstractText
PI3Ks play important roles in the signaling pathways used by a wide variety of cell surface receptors on neutrophils. Class IB PI3K plays a major role in the initial generation of PtdIns(3,4,5)P? by Gi-coupled G-protein coupled receptors (GPCRs) (e.g., receptors for fMLP, C5a, LTB?). Class IA PI3Ks generate PtdIns(3,4,5)P? downstream of receptors which directly or indirectly couple to protein tyrosine kinases such as integrins, Fc?Rs, cytokine receptors, and GPCRs. The PtdIns(3,4,5)P? made by Class I PI3Ks regulates the activity of several different effector proteins, many of which are plasma membrane GEFs or GAPs for small GTPases. Class III PI3K generates PtdIns(3)P in the phagosome membrane and plays an important role in efficient assembly of the NADPH oxidase at this location. Much still remains to be discovered about the molecular details that govern activation of PI3Ks and the mechanisms by which these enzymes regulate complex cellular processes, such as neutrophil spreading, chemotaxis, phagocytosis, and killing of pathogens. However, it is clear from recent use of transgenic mouse models and isoform-selective PI3K inhibitors that these pathways are important in regulating neutrophil recruitment to sites of infection and damage in vivo. Thus, PI3K pathways may present novel opportunities for selective inhibition in some inflammatory pathologies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0070-217X
pubmed:author
pubmed:issnType
Print
pubmed:volume
346
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
183-202
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
PI3K signaling in neutrophils.
pubmed:affiliation
The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK. Philip.hawkins@bbsrc.ac.uk
pubmed:publicationType
Journal Article, Review