Send to

Choose Destination
Nat Commun. 2016 Apr 19;7:11389. doi: 10.1038/ncomms11389.

Aurora A drives early signalling and vesicle dynamics during T-cell activation.

Author information

Servicio de Inmunología, Hospital Universitario de la Princesa, Instituto Investigación Sanitaria Princesa (IIS-IP), Universidad Autónoma de Madrid, C/ Diego de León 62, Madrid 28006, Spain.
Cell-cell Communication Laboratory, Vascular Pathophysiology Area, Centro Nacional Investigaciones Cardiovasculares (CNIC), C/ Melchor Fdz Almagro 3, Madrid 28029, Spain.
Cell Division and Cancer Group, Centro Nacional de Investigaciones Oncológicas (CNIO), C/ Melchor Fdz Almagro 3, Madrid 28029, Spain.
Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, C/ Nicolás cabrera 1, Madrid 28049, Spain.
Laboratory of Cardiovascular Proteomics, Centro Nacional Investigaciones Cardiovasculares (CNIC), C/ Melchor Fdz Almagro 3, Madrid 28029, Spain.


Aurora A is a serine/threonine kinase that contributes to the progression of mitosis by inducing microtubule nucleation. Here we have identified an unexpected role for Aurora A kinase in antigen-driven T-cell activation. We find that Aurora A is phosphorylated at the immunological synapse (IS) during TCR-driven cell contact. Inhibition of Aurora A with pharmacological agents or genetic deletion in human or mouse T cells severely disrupts the dynamics of microtubules and CD3ζ-bearing vesicles at the IS. The absence of Aurora A activity also impairs the activation of early signalling molecules downstream of the TCR and the expression of IL-2, CD25 and CD69. Aurora A inhibition causes delocalized clustering of Lck at the IS and decreases phosphorylation levels of tyrosine kinase Lck, thus indicating Aurora A is required for maintaining Lck active. These findings implicate Aurora A in the propagation of the TCR activation signal.

[Indexed for MEDLINE]
Free PMC Article

Publication type, MeSH terms, Substances, Grant support

Publication type

MeSH terms


Grant support

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center