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Kidins220/ARMS binds to the B cell antigen receptor and regulates B cell development and activation.
J Exp Med
September 2015
Department of Molecular Immunology, BioIII, Faculty of Biology, University of Freiburg and Max Planck Institute of Immunobiology and Epigenetics, 79104 Freiburg, Germany Centre for Biological Signaling Studies (BIOSS), Spemann Graduate School of Biology and Medicine (SGBM), Centre of Chronic Immunodeficiency (CCI), Department of Dermatology, Center for Biological Systems Analysis (ZBSA), Institute of Molecular Medicine and Cell Research, Comprehensive Cancer Centre Freiburg, and Institute of Pathology, University Medical Center Freiburg, University of Freiburg, 79104 Freiburg, Germany Centre for Biological Signaling Studies (BIOSS), Spemann Graduate School of Biology and Medicine (SGBM), Centre of Chronic Immunodeficiency (CCI), Department of Dermatology, Center for Biological Systems Analysis (ZBSA), Institute of Molecular Medicine and Cell Research, Comprehensive Cancer Centre Freiburg, and Institute of Pathology, University Medical Center Freiburg, University of Freiburg, 79104 Freiburg, Germany
B cell antigen receptor (BCR) signaling is critical for B cell development and activation. Using mass spectrometry, we identified a protein kinase D-interacting substrate of 220 kD (Kidins220)/ankyrin repeat-rich membrane-spanning protein (ARMS) as a novel interaction partner of resting and stimulated BCR. Upon BCR stimulation, the interaction increases in a Src kinase-independent manner.
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