The polarity protein Par1b/EMK/MARK2 regulates T cell receptor-induced microtubule-organizing center polarization.

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.
Mesh Terms:
14-3-3 Proteins, Antigen Presentation, B-Lymphocytes, Cell Line, Tumor, Cell Polarity, Humans, Immunological Synapses, Jurkat Cells, Microtubule-Organizing Center, Phosphorylation, Protein Transport, Protein-Serine-Threonine Kinases, Receptors, Antigen, T-Cell, Signal Transduction
J. Immunol.
Date: Jul. 15, 2009
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