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International Immunology Advance Access originally published online on April 29, 2008
International Immunology 2008 20(7):811-818; doi:10.1093/intimm/dxn039
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Published by Oxford University Press 2008.

Bam32: a novel mediator of Erk activation in T cells

Connie L. Sommers1, Jordan M. Gurson1, Rishi Surana1, Mira Barda-Saad1, Jan Lee2, Aparna Kishor1, WenMei Li1, Adam J. Gasser1, Valarie A. Barr1, Michihiko Miyaji1, Paul E. Love3 and Lawrence E. Samelson1

1 Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
2 Division of Therapeutic Proteins, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892, USA
3 Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA

Correspondence to: L. E. Samelson; E-mail: samelson{at}helix.nih.gov

Bam32 (B lymphocyte adapter molecule of 32 kDa) is an adapter protein expressed in some hematopoietic cells including B and T lymphocytes. It was previously shown that Bam32-deficient mice have defects in various aspects of B cell activation including B cell receptor (BCR)-induced Erk activation, BCR-induced proliferation and T-independent antibody responses. In this study, we have examined the role of Bam32 in T cell activation using Bam32-deficient mice. By comparing CD4+ T cells from lymph nodes of wild-type and Bam32-deficient mice, we found that Bam32 was required for optimal TCR-induced Erk activation, cytokine production, proliferation and actin-mediated spreading of CD4+ T cells. These results indicate a novel pathway to Erk activation in T cells involving the adapter protein Bam32.

Keywords: Erk, IL-4, proliferation, TCR, T lymphocyte

Transmitting editor: M. Nussenzweig

Received 9 October 2007, accepted 1 April 2008.


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