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Signal transduction

Gösta Winberg

The N-terminal cytoplasmic region of LMP2A has eight tyrosine residues,among them two with exact homology to the Immunoglobulin Transactivation Motifs (ITAMs), that upon phosphorylation bind the SH2 domains of the Syk tyrosine kinases and Y 112 motif that binds the Src family kinase Lyn.

The LMP2A N-terminal region also has two conserved PPPPY motifs. We have shown that the PPPPY motifs of LMP2A bind the WW domains of specific E3 protein-ubiquitin ligases, including AIP4/Itch and KIAA0439, both in vitro and in cultured B cells. In addition to a N-terminal C2 domain and four WW domains, these proteins have a C-terminal Hect catalytic domain implicated in the ubiquitination of target proteins. In cells expressing LMP2A, AIP4/Itch induces ubiquitination of Lyn and Syk. These results suggest that LMP2A serves as a molecular scaffold to recruit both B cell tyrosine kinases and C2/WW/Hect domain E3 protein-ubiquitin ligases, thereby promoting Lyn and Syk ubiquitination in a fashion that may contribute to a block in B cell signaling. LMP2A may therefore potentiate a normal mechanism in the regulation of B cell signaling (Winberg et al., submitted; Matskova et al., submitted).

This work is done by G�sta Winberg, docent; Ludmilla Matskova; graduate student; Ingemar Ernberg and FuChen, graduate student in close collaboration with Tony Pawsons group in Toronto.


Karolinska Institutet, MTC, Box 280, SE-171 77  Stockholm
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Phone: +46-8-728 62 62, Fax: +46-8-31 94 70

Last update: 2000-08-24 by Hong Zou

The latent membrane protein (LMP)2A of Epstein-Barr virus is implicated in the maintenance of viral latency, and appears to function in part by inhibiting B cell receptor (BCR) signaling. The latent membrane protein 2A (LMP2A) mRNA is consistently detected in NPC tumor biopsies and EBV malignancies and , along with EBNA1, is the only EBV-specific message detected in individuals harboring EBV latent infections, suggesting that LMP2 may plays an important role in vivo for control of latency and EBV-related diseases in humans.
Gösta Winberg