We have located links that may give you full text access.
Journal Article
Review
Role of phosphoinositide 3-kinase in innate immunity.
Biological & Pharmaceutical Bulletin 2007 September
Recent advances in our understanding of the molecular basis of mammalian host immune responses to microbial invasion suggest that the first line of defense against microbes is the recognition of pathogen-associated molecular patterns by Toll-like receptors (TLRs). Phosphoinositide 3-kinase (PI3K) is thought to participate in the TLR signaling pathway. The activation of PI3K is commonly observed after stimulation with various TLR ligands. The resultant activation of a serine-threonine protein kinase Akt leads to the phosphorylation of glycogen synthase kinase (GSK)-3beta, which is active in resting cells but is inactivated by phosphorylation. GSK-3beta has been linked to the regulation of a multitude of transcription factors, including NF-kappaB, AP-1, NF-AT, and CREB either negatively or positively. Thus, the altered activity of GSK-3beta causes diverse effects on cytokine expression. Generally, activation of PI3K results in the inhibition of proinflammatory events such as expression of IL-12 and TNF-alpha. Thus, PI3K is a negative regulator of TLR signaling. Among the members of the Class I PI3K family, p85/p110beta appears to be the subtype activated on TLR ligation, but the molecular basis for this specificity has yet to be elucidated.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app