Mst1 Kinase Regulates the Actin-Bundling Protein L-Plastin To Promote T Cell Migration.
Ontology highlight
ABSTRACT: Exploring the mechanisms controlling lymphocyte trafficking is essential for understanding the function of the immune system and the pathophysiology of immunodeficiencies. The mammalian Ste20-like kinase 1 (Mst1) has been identified as a critical signaling mediator of T cell migration, and loss of Mst1 results in immunodeficiency disease. Although Mst1 is known to support T cell migration through induction of cell polarization and lamellipodial formation, the downstream effectors of Mst1 are incompletely defined. Mice deficient for the actin-bundling protein L-plastin (LPL) have phenotypes similar to mice lacking Mst1, including decreased T cell polarization, lamellipodial formation, and cell migration. We therefore asked whether LPL functions downstream of Mst1. The regulatory N-terminal
SUBMITTER: Xu X
PROVIDER: S-EPMC4992580 | biostudies-literature | 2016 Sep
REPOSITORIES: biostudies-literature
ACCESS DATA