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Negative feedback regulation of antigen receptors through calmodulin inhibition of E2A
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Grundström)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Grundström)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Grundström)
2012 (English)In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 188, no 12, 6175-6183 p.Article in journal (Refereed) Published
Abstract [en]

Signaling from the BCR is used to judge Ag-binding strengths of the Abs of B cells. BCR signaling enables the selection for successive improvements in the Ag affinity over an extremely broad range of affinities during somatic hypermutation. We show that the mouse BCR is subject to general negative feedback regulation of the receptor proteins, as well as many coreceptors and proteins in signal pathways from the receptor. Thus, the BCR can downregulate itself, which can enable sensitive detection of successive improvements in the Ag affinity over a very large span of affinities. Furthermore, the feedback inhibition of the BCR signalosome and most of its proteins, as well as most other regulations of genes by BCR stimulation, is to a large extent through inhibition of the transcription factor E2A by Ca(2+)/calmodulin.

Place, publisher, year, edition, pages
2012. Vol. 188, no 12, 6175-6183 p.
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:umu:diva-55739DOI: 10.4049/jimmunol.1103105ISI: 000305077900043PubMedID: 22581853OAI: oai:DiVA.org:umu-55739DiVA: diva2:529338
Available from: 2012-05-30 Created: 2012-05-29 Last updated: 2017-12-07Bibliographically approved

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Verma-Gaur, JiyotiHauser, JannekGrundström, Thomas
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