Source:http://linkedlifedata.com/resource/pubmed/id/16680006
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2006-5-8
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pubmed:abstractText |
The phosphoinositide 3-kinases (PI3Ks) are a conserved family of signal transduction enzymes that are involved in regulating cellular activation, inflammatory responses, chemotaxis, and apoptosis. We have discovered that a carbohydrate ligand, glucan, will stimulate the endogenous PI3K/Akt signaling pathway. This article reviews the current data on the role of the PI3K/Akt signaling pathway as a negative feedback mechanism or compensatory regulator of septic and inflammatory responses. Of greater importance, the data reviewed in this article suggest that modulation of the PI3K/Akt signaling pathway can reduce the morbidity and mortality associated with septic and I/R injury. Thus, manipulation of the endogenous PI3K/Akt signaling pathway may represent a new and novel therapeutic approach to management of important diseases.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Glucans,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/TLR4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1073-2322
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
432-9
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:16680006-Animals,
pubmed-meshheading:16680006-Cytokines,
pubmed-meshheading:16680006-Glucans,
pubmed-meshheading:16680006-Humans,
pubmed-meshheading:16680006-Immunity, Innate,
pubmed-meshheading:16680006-Inflammation,
pubmed-meshheading:16680006-Models, Biological,
pubmed-meshheading:16680006-Myocardium,
pubmed-meshheading:16680006-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:16680006-Reperfusion Injury,
pubmed-meshheading:16680006-Sepsis,
pubmed-meshheading:16680006-Signal Transduction,
pubmed-meshheading:16680006-Time Factors,
pubmed-meshheading:16680006-Toll-Like Receptor 4
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pubmed:year |
2006
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pubmed:articleTitle |
Modulation of the phosphoinositide 3-kinase signaling pathway alters host response to sepsis, inflammation, and ischemia/reperfusion injury.
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pubmed:affiliation |
Department of Surgery, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA. williamd@estu.edu
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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