Peer-Reviewed Journal Details
Mandatory Fields
Smith, LM;Walsh, PT;Rudiger, T;Cotter, TG;Mc Carthy, TV;Marx, A;O'Connor, R
2004
January
Experimental Cell Research
EphA3 is induced by CD28 and 1GF-1 and regulates cell adhesion
Validated
WOS: 34 ()
Optional Fields
RECEPTOR TYROSINE KINASE FACTOR-I RECEPTOR GROWTH-FACTOR RECEPTOR N-TERMINAL KINASES T-CELLS EXPRESSION LIGAND ACTIVATION APOPTOSIS GENE
292
295
303
Stimulation of CD28 alone has been shown to regulate cytokine gene transcription and expression of the type I insulin-like growth factor receptor (IGF-lR) in lymphocytes. In this study, the ephrin receptor tyrosine kinase ephA3, was identified as a new CD28-responsive gene in Jurkat cells by using a human cytokine/receptor array. EphA3 was not detected in normal peripheral T cells, in any subset of thymus-derived developing T cells, or in Hodgkin's lymphoma. However, contrary to previous findings, EphA3 was detected in a panel of T-cell lymphomas. Stimulation of Jurkat cells with ephrin-A5 resulted in loss of cell adhesion to fibronectin and recruitment of the adapter protein CrkII to EphA3. Interestingly, EphA3 expression in CD28-stimulated Jurkat cells was enhanced by IGF-1 or by overexpression of the IGF-IR, and was suppressed by anti-IGF-IR blocking antibodies. The data suggest that CD28- and IGF-1-regulated expression of EphA3 is associated with adherence and that it may be involved in the motility of malignant T cells. (C) 2003 Elsevier Inc. All rights reserved.
SAN DIEGO
0014-4827
10.1016/j.yexcr.2003.08.021
Grant Details