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CD28 — PI3

Text-mined interactions from Literome

Shin et al., Mol Immunol 1999 : These results suggest that CD28 signaling leading to the c-jun promoter involves acidic sphingomyelinase, but not PI3-kinase , to activate factors binding to the MEF2 and ATF sites
Rudd et al., Immunol Rev 2003 : Our recent work has demonstrated that CD28 can activate the lipid kinase phosphatidylinositol 3-kinase (PI-3K) and can cooperate with adapters Vav and SLP-76 to influence the induction of interleukin (IL)-2 and IL-4 transcription in the absence of TCR ligation
Parry et al., Mol Cell Biol 2005 : In contrast, PD-1 signaling inhibits Akt phosphorylation by preventing CD28 mediated activation of phosphatidylinositol 3-kinase (PI3K)
Yao et al., Nature communications 2013 : Meanwhile, cAMP mediated suppression of T-cell receptor signalling is overcome by simultaneous activation of PI3-kinase through EP2/EP4 and/or CD28
Truitt et al., J Exp Med 1994 (Mast-Cell Sarcoma) : Here we demonstrate that stimulation of CD28 , either by B7, its natural ligand, or by the anti-CD28 monoclonal antibody 9.3, induces an association between CD28 and phosphatidylinositol 3-kinase (PI3-K) in Jurkat T cells, raising the possibility that an interaction with PI3-K contributes to CD28 mediated signaling
Hutchcroft et al., Proc Natl Acad Sci U S A 1995 (Leukemia, T-Cell) : We conclude that PI3 kinase activity may not be required for CD28 dependent IL-2 production from Jurkat T cells in the presence of PMA
Truitt et al., J Immunol 1995 (Second Messenger Systems) : Stimulation of CD28 induces its association with phosphatidylinositol 3'-kinase (PI3-K) , raising the possibility that PI3-K plays a critical role in CD28 signaling
Lu et al., Eur J Immunol 1995 : CD28 stimulation causes both protein-tyrosine kinase and phosphatidylinositol3-kinase (PI3-K) activation, suggesting a possible role for these enzyme activities in CD28 co-signal transduction
Teng et al., Tissue Antigens 1996 : These results imply that in this system phosphorylation of tyrosine 173 and hence activation of PI3-kinase is not required for CD28 induced IL-2 secretion
Reif et al., Curr Biol 1997 : Phosphoinositide 3-kinase ( PI 3-kinase ) is activated by a diverse set of receptors that determine T-cell function, including the T-cell antigen receptor ( TCR ), the costimulatory receptor CD28 , and negative regulators of T-cell activation such as CTLA-4
Parry et al., Biochem J 1997 : PI 3-kinase exhibits dual specificity as both a lipid kinase and a protein serine kinase, and site-specific mutagenesis of the Tyr173 residue in the CD28 cytoplasmic tail, which abolishes CD28 coupling to PI 3-kinase [ Pages, Ragueneau, Rottapel, Truneh, Nunes, Imbert and Olive ( 1994 ) Nature ( London ) 369, 327-329 ], also prevents ligation stimulated phosphorylation of CD28 ... However, the two PI 3-kinase inhibitors wortmannin and LY294002 had no effect on phosphorylation of CD28 after ligation by B7.1
Lu et al., J Immunol 1998 : Ligation of the TCR or CD28 induces activation of phosphatidylinositol 3-kinase (PI3K) , the TEC family protein tyrosine kinase, EMT/ITK/TSK ( EMT ), and the SRC family tyrosine kinase, LCK