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Agonist-induced calcium entry correlates with STIM1 translocation

Lookup NU author(s): Dr Kehinde Ross, Emeritus Professor Michael Whitaker, Professor Nick ReynoldsORCiD


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The mechanisms of agonist-induced calcium entry (ACE) following depletion of intracellular calcium stores have not been fully established. We report here that calcium-independent phospholipase A (iPLA2) is required for robust Ca2+ entry in HaCaT keratinocytes following ATP or UTP stimulation. Lysophosphatidic acid (LPA), an unrelated agonist, evoked Ca 2+ release without inducing robust Ca2- entry. Both LPA and UTP induced the redistribution of STIM1 into puncta which localized to regions near or at the plasma membrane, as well as within the cytoplasm. Plasma membrane-associated STIM1 remained high for up to 10 min after UTP stimulation, whereas it had returned almost to baseline by that time point in LPA-stimulated cells. This correlated with faster reloading of the endoplasmic reticulum Ca2+ stores in LPA treated cells. Thus by differentially regulating store-refilling after agonist-mediated depletion, LPA and UTP may exert distinct effects on the duration of STIM1 localization at the plasma membrane, and thus, on the magnitude and duration of ACE. © 2007 Wiley-Liss, Inc.

Publication metadata

Author(s): Ross K, Whitaker M, Reynolds NJ

Publication type: Article

Publication status: Published

Journal: Journal of Cellular Physiology

Year: 2007

Volume: 211

Issue: 3

Pages: 569-576

Print publication date: 01/06/2007

ISSN (print): 0021-9541

ISSN (electronic): 1097-4652

Publisher: John Wiley & Sons, Inc.


DOI: 10.1002/jcp.20993

PubMed id: 17299780


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Funder referenceFunder name
G0502242Medical Research Council