NDLI: Transition from heterotypic to homotypic PDK1 homodimerization is essential for TCR-mediated NF-κB activation.

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Transition from heterotypic to homotypic PDK1 homodimerization is essential for TCR-mediated NF-κB activation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hayden, Matthew S. Park, Sung-Gyoo Kang, Jung-Ah Park, Daeho Ghosh, Sankar Jeong, Sang Phil
Description	Author Affiliation: Kang JA ( School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, Republic of Korea.)
Abstract	Strong NF-κB activation requires ligation of both the CD28 coreceptor and TCR. Phosphoinositide-dependent kinase 1 (PDK1) acts as a scaffold by binding both protein kinase CÎ¸ (PKCÎ¸) and CARMA1, and is therefore essential for signaling to NF-κB. In this article, we demonstrate the importance of PDK1 Thr(513) phosphorylation in regulating the intermolecular organization of PDK1 homodimers. Thr(513) is directly involved in heterotypic PDK1 homodimer formation, in which binding is mediated through the pleckstrin homology (PH) and kinase domains. Upon activation, phosphorylated Thr(513) instead mediates homotypic intermolecular binding through the PH domains. Consequently, cell-permeable peptides with a Thr(513) to Ile derivative (protein transduction domain [PTD]-PDK1-Thr(513)-Ile) bound the kinase domain, whereas a Thr(513)-to-Asp peptide (PTD-PDK1-Thr(513)-Asp) bound the PH domain. PTD-PDK1-Thr(513)-Ile blocked binding between PDK1 and PKCÎ¸, phosphorylation of PKCÎ¸ Thr(538), and activation of both NF-κB and AKT. In contrast, PTD-PDK1- Thr(513)-Asp selectively inhibited binding between PDK1 and CARMA1, and blocked TCR/CD28-induced NF-κB activation. Therefore, Thr(513) phosphorylation regulates a critical intermolecular switch governing PDK1 homodimer structure and the capacity to interact with downstream signaling pathway components. Given the pleiotropic functions of PDK1, these data may open the door to the development of immunosuppressive therapies that selectively target the PDK1 to NF-κB pathway in T cell activation.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202923
Journal	The Journal of Immunology
Issue Number	9
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Nf-kappa B Immunology Metabolism Protein-serine-threonine Kinases Receptors, Antigen, T-cell 3-phosphoinositide-dependent Protein Kinases Animals Antigens, Cd28 Blood Proteins Card Signaling Adaptor Proteins Cell Line Cell Line, Tumor Dimerization Guanylate Cyclase Hek293 Cells Interleukin-2 Isoenzymes Jurkat Cells Lymphocyte Activation Mice Mice, Inbred C57bl Phosphoproteins Phosphorylation Protein Kinase C Proto-oncogene Proteins C-akt Signal Transduction Threonine Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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