PI3KÎ³ is a molecular switch that controls immune suppression.
Kaneda, Megan M; Messer, Karen S; Ralainirina, Natacha; Li, Hongying; Leem, Christopher J; Gorjestani, Sara; Woo, Gyunghwi; Nguyen, Abraham V; Figueiredo, Camila C; Foubert, Philippe; Schmid, Michael C; Pink, Melissa; Winkler, David G; Rausch, Matthew; Palombella, Vito J; Kutok, Jeffery; McGovern, Karen; Frazer, Kelly A; Wu, Xuefeng; Karin, Michael; Sasik, Roman; Cohen, Ezra E W; Varner, Judith A.
; 539(7629): 437-442, 2016 11 17.
Artigo em Inglês | MEDLINE | ID: mdl-27642729
Antigen Availability and DOCK2-Driven Motility Govern CD4<sup>+</sup> T Cell Interactions with Dendritic Cells In Vivo.
Different inhibition of GßÎ³-stimulated class IB phosphoinositide 3-kinase (PI3K) variants by a monoclonal antibody. Specific function of p101 as a GßÎ³-dependent regulator of PI3KÎ³ enzymatic activity.
Interaction of Ras with p110Î³ is required for thymic ß-selection in the mouse.
A class of highly selective inhibitors bind to an active state of PI3KÎ³.
Molecular determinants of PI3KÎ³-mediated activation downstream of G-protein-coupled receptors (GPCRs).
Integrating cardiac PIP3 and cAMP signaling through a PKA anchoring function of p110Î³.
p87 and p101 subunits are distinct regulators determining class IB phosphoinositide 3-kinase (PI3K) specificity.
PI3KÎ³ ablation does not promote diabetes in <i>db/db</i> mice, but improves insulin sensitivity and reduces pancreatic ß-cell apoptosis.
PI3KÎ³ activation is required for LPS-induced reactive oxygen species generation in respiratory epithelial cells.
p84 forms a negative regulatory complex with p110Î³ to control PI3KÎ³ signalling during cell migration.