Faculty Collaboration Database

Tyrosine kinases EnAbling adaptor molecules for chemokine-induced Rap1 activation in T cells. Sci Signal 2012 Jul 31;5(235):pe33

Date

08/03/2012

Pubmed ID

22855504

Pubmed Central ID

PMC4307919

DOI

10.1126/scisignal.2003383

Scopus ID

2-s2.0-84864554527   3 Citations

Abstract

Chemokines regulate T cell trafficking into secondary lymphoid organs and migration across endothelial cells in response to inflammatory signals. The small guanosine triphosphatase Rap1 is a critical regulator of chemokine signaling in T cells, but how chemokines activate Rap1 has been unclear. A study showed that Abl family tyrosine kinases were essential for chemokine-induced Rap1 activation, T cell polarization, and migration. Abl family kinases promoted Rap1 activation by phosphorylating the adaptor protein human enhancer of filamentation 1 (HEF1), thus establishing a critical Abl-HEF1-Rap1 signaling axis for chemokine-induced T cell migration.

Author List

Malherbe LP, Wang D

Author

Demin Wang PhD Assistant Professor in the Microbiology and Immunology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adaptor Proteins, Signal Transducing
Cell Movement
Chemokines
Humans
Lymphocyte Activation
Models, Immunological
Phosphoproteins
Phosphorylation
Protein-Tyrosine Kinases
Signal Transduction
T-Lymphocytes
rap1 GTP-Binding Proteins