Hao, Shengli and August, Avery (2005) Actin Depolymerization Transduces the Strength of B-Cell Receptor Stimulation. Molecular Biology of the Cell, 16 (5). pp. 2275-2284. ISSN 1059-1524 http://resolver.caltech.edu/CaltechAUTHORS:HAOmbc05
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Polymerization of the actin cytoskeleton has been found to be essential for B-cell activation. We show here, however, that stimulation of BCR induces a rapid global actin depolymerization in a BCR signal strength-dependent manner, followed by polarized actin repolymerization. Depolymerization of actin enhances and blocking actin depolymerization inhibits BCR signaling, leading to altered BCR and lipid raft clustering, ERK activation, and transcription factor activation. Furthermore actin depolymerization by itself induces altered lipid raft clustering and ERK activation, suggesting that F-actin may play a role in separating lipid rafts and in setting the threshold for cellular activation.
|Additional Information:||Copyright © 2005 by The American Society for Cell Biology. Submitted October 8, 2004; Revised January 3, 2005; Accepted February 13, 2005. Monitoring Editor: Anne Ridley. This article was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E04–10–0881) on February 23, 2005. We thank members of the Immunology Research Labs at Penn State for their critical feedback. We also thank the investigators mentioned in the materials section for the kind gifts of crucial reagents. This work was supported by a Johnson & Johnson Focused Giving Program Award and in part by grants from the American Heart Association (award 0330036N) and the National Institutes of Health (AI51626), all to A.A. S.H. was a graduate fellow of the Huck Institutes for Life Sciences at Penn State University. The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).|
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|Deposited On:||23 Jun 2008|
|Last Modified:||26 Dec 2012 10:07|
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