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Disruption of the cortical actin cytoskeleton does not affect store operated Ca2+ channels in human T-cells

Mueller, P. and Quintana, A. and Griesemer, D. and Hoth, M. and Pieters, J.. (2007) Disruption of the cortical actin cytoskeleton does not affect store operated Ca2+ channels in human T-cells. FEBS Letters, 581 (18). pp. 3557-3562.

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Abstract

Lymphocyte signaling and activation leads to the influx of extracellular Ca(2+) via the activation of Ca(2+) release activated Ca(2+) (CRAC) channels in the plasma membrane. Activation of CRAC channels occurs following emptying of the endoplasmic reticulum intracellular Ca(2+) stores. One model to explain the coupling of store-emptying to CRAC activation is the secretion-like conformational coupling model. This model proposes that store depletion increases junctions between the endoplasmic reticulum and the plasma membrane in a manner that could be regulated by the cortical actin cytoskeleton. Here, we show that stabilization or depolymerization of the actin cytoskeleton failed to affect CRAC activation. We therefore conclude that rearrangement of the actin cytoskeleton is dispensable for store-operated Ca(2+) entry in T-cells.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Infection Biology > Biochemistry (Pieters)
UniBasel Contributors:Pieters, Jean
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Elsevier Science
ISSN:0014-5793
Note:Publication type according to Uni Basel Research Database: Journal article
Language:English
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edoc DOI:
Last Modified:26 Sep 2017 10:32
Deposited On:22 Mar 2012 13:22

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