Skip to main content
. Author manuscript; available in PMC: 2013 Aug 1.
Published in final edited form as: J Immunol. 2013 Mar 25;190(9):4508–4515. doi: 10.4049/jimmunol.1202923

FIGURE 6.

FIGURE 6

PDK1 peptides carrying Thr-513 to Ile or Asp mutations inhibit TCR-CD28-mediated NF-κB activation in mouse primary CD4+ T cells. A, Effect of PDK1 peptides on phosphorylation of PKCθ and IκBα degradation in mouse primary CD4+ T cells stimulated with anti-CD3 and anti-CD28 antibodies for 30 min. B, The effect of PDK1 peptide (PTD-PDK1-Thr-513-Ile or PTD-PDK1-Thr-513-Asp) on TCR-CD28-mediated NF-κB activation in mouse primary CD4+ T cells was analyzed by NF-κB reporter assay. The Renilla luciferase activity was used as a reference for normalization of gene expression in transiently transfected cells. C and D, The effect of PDK1 peptides on IL-2 production was analyzed by quantitative real-time PCR (C) or ELISA (D). Results: mean ± SD. Student’s t test: *, p < 0.05; **, p < 0.01. E, Schematic model of TCR-CD28-mediated NF-κB activation by PDK1 dimer formation. Thr-513 phosphorylation induces conversion of PDK1 kinase–PH domain binding into PDK1 PH–PH domain binding during T cell activation, which is required for TCR-CD28-mediated NF-κB activation.