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Publication : Cutting edge: rho activation and actin polarization are dependent on plexin-A1 in dendritic cells.

First Author  Eun SY Year  2006
Journal  J Immunol Volume  177
Issue  7 Pages  4271-5
PubMed ID  16982860 Mgi Jnum  J:139332
Mgi Id  MGI:3807757 Doi  10.4049/jimmunol.177.7.4271
Citation  Eun SY, et al. (2006) Cutting edge: rho activation and actin polarization are dependent on plexin-A1 in dendritic cells. J Immunol 177(7):4271-5
abstractText  We recently identified expression of the semaphorin receptor, plexin-A1, in dendritic cells (DCs); however, its function in these cells remains to be elucidated. To investigate function and maximize physiological relevance, we devised a retroviral approach to ablate plexin-A1 gene expression using small hairpin RNA (shRNA) in primary bone marrow-derived DCs. We show that plexin-A1 localizes within the cytoplasm of immature DCs, becomes membrane-associated, and is enriched at the immune synapse in mature DCs. Reducing plexin-A1 expression with shRNA greatly reduced actin polarization as well as Rho activation without affecting Rac or Cdc42 activation. A Rho inhibitor, C3, also reduced actin polarization. These changes were accompanied by the near-ablation of T cell activation. We propose a mechanism of adaptive immune regulation in which plexin-A1 controls Rho activation and actin cytoskeletal rearrangements in DCs that is associated with enhanced DC-T cell interactions.
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