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Blood, 15 March 2004, Vol. 103, No. 6, pp. 2248-2256.
Prepublished online as a Blood First Edition Paper on November 26, 2003; DOI 10.1182/blood-2003-08-2671.
Submitted August 5, 2003
Accepted November 17, 2003
Homer-3 regulates activation of serum response element in T cells via its EVH1 domain
Kazuhiro Ishiguro and Ramnik Xavier*
Department of Medicine, Massachusetts General Hospital, Boston, MA, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA
* Corresponding author; email: xavier{at}molbio.mgh.harvard.edu.
EVH1 domain proteins regulate signal transduction at the neuronal and immunological synapse. Despite shared cell biological machinery at these synapses, the regulation of client proteins that transmit synaptic activity to the nucleus is likely to be different. Homer-3, a member of the Ena/VASP homology 1 (EVH1) family, is expressed in the thymus, suggesting a role for this protein in T cell signal transduction. Upon TCR engagement, Homer-3 was recruited to the contact area of Jurkat cells to anti-CD3 and CD28 antibody-coated beads prior to actin accumulation, and subsequently translocated into the nucleus. Overexpression of Homer-3 reduced transcriptional activation via the serum response element (SRE) in response to anti-CD3 antibody, phorbol ester or dominant active Ha-Ras. Consistent with these results, knockdown of Homer-3 increased SRE activation. Homer-3 coprecipitated with CCAAT/enhancer binding protein (C/EBP)  , one of the transcription factors that binds to the SRE and has a consensus motif binding to EVH1 domain. Moreover, Homer-3 and its EVH1 domain fragment reduced transcriptional activation of C/EBP. These findings suggest that Homer-3 may be involved in the regulation of SRE activation in T cells via interaction between its EVH1 domain and C/EBP.
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