Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Jan:75:100657.
doi: 10.1016/j.jbior.2019.100657. Epub 2019 Sep 28.

Class I phosphoinositide 3-kinase (PI3K) regulatory subunits and their roles in signaling and disease

Affiliations
Review

Class I phosphoinositide 3-kinase (PI3K) regulatory subunits and their roles in signaling and disease

Manoj K Rathinaswamy et al. Adv Biol Regul. 2020 Jan.

Abstract

The Class I phosphoinositide 3-kinases (PI3Ks) are a group of heterodimeric lipid kinases that regulate crucial cellular processes including proliferation, survival, growth, and metabolism. The diversity in functions controlled by the various catalytic isoforms (p110α, p110β, p110δ, and p110γ) depends on their abilities to be activated by distinct stimuli such as receptor tyrosine kinases (RTKs), G-protein coupled receptors (GPCRs), and the Ras family of small G-proteins. A major factor determining the ability of each p110 enzyme to be activated is the presence of regulatory binding partners. Given the overwhelming evidence for the involvement of PI3Ks in diseases such as cancer, inflammation, immunodeficiency and diabetes, an understanding of how these regulatory proteins influence PI3K function is essential. This article highlights research deciphering the role of regulatory subunits in PI3K signaling and their involvement in human disease.

Keywords: PI3K; PIK3CA; PIK3R1; Phosphoinositide 3-kinase; p110; p85.

PubMed Disclaimer

Conflict of interest statement

Declaration of competing interest The authors declare that they have no conflict of interest with the publication of this manuscript.

Publication types

MeSH terms

Substances

LinkOut - more resources