title: The polarity protein Par1b/EMK/MARK2 regulates T cell receptor-induced microtubule-organizing center polarization.
abstract: Engagement of a T cell to an APC induces the formation of an immunological synapse as well as reorientation of the microtubule-organizing center (MTOC) toward the APC. How signals emanating from the TCR induce MTOC polarization is not known. One group of proteins known to play a critical role in asymmetric cell division and cell polarization is the partitioning defective (Par) family of proteins. In this study we found that Par1b, a member of the Par family of proteins, was inducibly phosphorylated following TCR stimulation. This phosphorylation resulted in 14-3-3 protein binding and caused the relocalization of Par1b from the membrane into the cytoplasm. Because a dominant-negative form of Par1b blocked TCR-induced MTOC polarization, our data suggest that Par1b functions in the establishment of T cell polarity following engagement to an APC.
authors: Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110, USA.
authors: Joseph
authors: J
authors: Lin
authors: Kirk K
authors: KK
authors: Hou
authors: Helen
authors: H
authors: Piwnica-Worms
authors: Andrey S
authors: AS
authors: Shaw
mesh_terms: D048948:14-3-3 Proteins / Q000378:metabolism; D017951:Antigen Presentation; D001402:B-Lymphocytes / Q000276:immunology; D045744:Cell Line, Tumor; D016764:Cell Polarity; D006801:Humans; D054992:Immunological Synapses; D019169:Jurkat Cells; D022101:Microtubule-Organizing Center / Q000502:physiology*; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism / Q000502:physiology*; D021381:Protein Transport; D011948:Receptors, Antigen, T-Cell / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D048948:14-3-3 Proteins; D011948:Receptors, Antigen, T-Cell; C094670:MARK2 protein, human; D017346:Protein Serine-Threonine Kinases