Bam32: A novel mediator of Erk activation in T cells

Connie L. Sommers; Jordan M. Gurson; Rishi Surana; Mira Barda-Saad; Jan Lee; Aparna Kishor; Wenmei Li; Adam J. Gasser; Valarie A. Barr; Michihiko Miyaji; Paul E. Love; Lawrence E. Samelson

doi:10.1093/intimm/dxn039

Bam32: A novel mediator of Erk activation in T cells

Connie L. Sommers, Jordan M. Gurson, Rishi Surana, Mira Barda-Saad, Jan Lee, Aparna Kishor, Wenmei Li, Adam J. Gasser, Valarie A. Barr, Michihiko Miyaji, Paul E. Love, Lawrence E. Samelson

Research output: Contribution to journal › Article › peer-review

18 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	811-818
Number of pages	8
Journal	International Immunology
Volume	20
Issue number	7
DOIs	https://doi.org/10.1093/intimm/dxn039
State	Published - Jul 2008
Externally published	Yes

Bibliographical note

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

Funding Information:
Intramural Research Program of the National Institutes of Health; National Cancer Institute; Center for Cancer Research.

Funding

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

Funders	Funder number
National Cancer Institute	ZIABC010304

Keywords

Erk
IL-4
Proliferation
T lymphocyte
TCR

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title = "Bam32: A novel mediator of Erk activation in T cells",

abstract = "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, T lymphocyte, TCR",

author = "Sommers, {Connie L.} and Gurson, {Jordan M.} and Rishi Surana and Mira Barda-Saad and Jan Lee and Aparna Kishor and Wenmei Li and Gasser, {Adam J.} and Barr, {Valarie A.} and Michihiko Miyaji and Love, {Paul E.} and Samelson, {Lawrence E.}",

year = "2008",

month = jul,

doi = "10.1093/intimm/dxn039",

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AU - Gurson, Jordan M.

AU - Surana, Rishi

AU - Barda-Saad, Mira

AU - Lee, Jan

AU - Kishor, Aparna

AU - Li, Wenmei

AU - Gasser, Adam J.

AU - Barr, Valarie A.

AU - Miyaji, Michihiko

AU - Love, Paul E.

AU - Samelson, Lawrence E.

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AB - 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.

KW - Erk

KW - IL-4

KW - Proliferation

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Bam32: A novel mediator of Erk activation in T cells

Abstract

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