Carbachol-stimulated calcium entry in SH-SY5Y human neuroblastoma cells: Which route?
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Cited by (15)
Involvement of store-operated Ca<sup>2+</sup> entry in activation of AMP-activated protein kinase and stimulation of glucose uptake by M<inf>3</inf> muscarinic acetylcholine receptors in human neuroblastoma cells
2014, Biochimica et Biophysica Acta - Molecular Cell ResearchCitation Excerpt :Collectively, these data indicate that the sustained AMPK phosphorylation induced by CCh required the influx of extracellular Ca2 +. Previous studies have shown that in SH-SY5Y cells the mAChR-induced [Ca2 +]i plateau requires the continued presence of the agonist [26,28]. Accordingly, addition of atropine (100 nM) to cells pre-treated with CCh (10 μM) induced a drop of [Ca2 +]i plateau to resting levels (Fig. 3D).
Transcriptional response to muscarinic acetylcholine receptor stimulation: Regulation of Egr-1 biosynthesis by ERK, Elk-1, MKP-1, and calcineurin in carbachol-stimulated human neuroblastoma cells
2008, Archives of Biochemistry and BiophysicsCitation Excerpt :An anti-phospho-Elk-1 antibody (Santa Cruz, Heidelberg, Germany, #sc-8406) was used for immunoprecipitation. SH-SY5Y neuroblastoma cells were used for this study because these cells express a relatively high density of pharmacologically homogenous M3 muscarinic acetylcholine receptors [1–7]. The expression of type M3 muscarinic acetylcholine receptor in SH-SY5Y cells was confirmed via RNase protection mapping.
Store-operated Ca<sup>2+</sup>-channels are sensitive to changes in extracellular pH
2005, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Agonist-induced entry of Ca2+ into cells often exhibits a biphasic pattern: binding of the agonist to its cell surface receptor initiates a sharp rise in intracellular Ca2+ concentration ([Ca2+]i) followed by a recovery to a level which is higher than that of the original level and is therefore referred to as a “plateau.” This pattern of Ca2+-signal has been observed in a variety of different cell types (both excitable and non-excitable cells) following stimulation with a variety of agents, e.g., endothelin-1 in aortic smooth muscle cells [18], thrombin in platelets [27], or activation of muscarinic acetylcholine receptors in neuroblastoma cells with carbachol [20,28]. It has been established that the sharp rise is attributed to the opening of inositol-1,4,5-trisphosphate (IP3)-sensitive Ca2+-channels on the endoplasmic reticulum [24] membrane, whereas the plateau is the result of the opening of SOCs present in the plasma membrane [29–31].