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Published on: March 20, 2016
The polarity protein Par1b/EMK/MARK2 regulates T cell receptor-induced microtubule-organizing center polarization
Joseph Lin1, Kirk K Hou, Helen Piwnica-Worms
1Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110, USA.
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.
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