Capacitative Calcium Entry

Holda, Jaclyn R.; Klishin, Andrey; Sedova, Marina; Hüser, Jörg; Blatter, Lothar A.

doi:10.1152/physiologyonline.1998.13.4.157

Cited by 33 publications

(40 citation statements)

References 15 publications

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“…Notice that the capacitative Ca 2ϩ entry (CCE) becomes significantly larger in cells pretreated with ryanodine. The result is consistent with the suggestion that sustained depletion of ER Ca 2ϩ is required for full activation of the CCE pathway (28,29).…”

Section: Stable Expression Of Ryr and Bcl-xl In Cho Cells-supporting

confidence: 92%

Depletion of Intracellular Ca2+ by Caffeine and Ryanodine Induces Apoptosis of Chinese Hamster Ovary Cells Transfected with Ryanodine Receptor

Pan

Damron

Nieminen

et al. 2000

Journal of Biological Chemistry

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Section: Stable Expression Of Ryr and Bcl-xl In Cho Cells-supporting

confidence: 92%

Depletion of Intracellular Ca2+ by Caffeine and Ryanodine Induces Apoptosis of Chinese Hamster Ovary Cells Transfected with Ryanodine Receptor

Pan

Damron

Nieminen

et al. 2000

Journal of Biological Chemistry

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“…These latter data are inconsistent with the involvement of a physical interaction between the ER and the plasma membrane in the activation of SOC. Another model which has received some consideration involves vesicle fusion as a mechanism whereby Ca2+ influx channels are inserted into the plasma membrane upon internal Ca2+ store depletion (Holda et al, 1998). However, Hoth and Penner (1992) had previously reported that there was no change in the capacitance during activation of Ca2+ influx, a finding inconsistent with vesicle fusion.…”

mentioning

confidence: 99%

Regulation of Calcium in Salivary Gland Secretion

Ambudkar

2000

Critical Reviews in Oral Biology & Medicine

102

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Neurotransmitter-regulation of fluid secretion in the salivary glands is achieved by a coordinated sequence of intracellular signaling events, including the activation of membrane receptors, generation of the intracellular second messenger, inositol 1,4,5, trisphosphate, internal Ca2l release, and Ca2+ influx. The resulting increase in cytosolic lCa2+l (lCa2+l1) regulates a number of ion transporters, e.g., Ca2+-activated K+ channel, Na+/K+/2ClI co-transporter in the basolateral membrane, and the Ca2l-activated Cl-channel in the luminal membrane, which are intricately involved in fluid secretion. Thus, regulation of lCa2+l1 is central to the regulation of salivary acinar cell function and is achieved by the concerted activities of several ion channels and Ca2+-pumps localized in various cellular membranes. Ca2+ pumps, present in the endoplasmic reticulum and the plasma membrane, serve to remove Ca2+ from the cytosol. Ca2+ channels present in the endoplasmic reticulum and the plasma membrane facilitate rapid influx of Ca2+ into the cytosol from the internal Ca2+ stores and from the external medium, respectively. It is well-established that prolonged fluid secretion is regulated via a sustained elevation in lCa2+l, that is primarily achieved by the influx of Ca2+ into the cell from the external medium. This Ca2`influx occurs via a putative plasma-membranestore-operated Ca2+ channel which has not yet been identified in any non-excitable cell type. Understanding the molecular nature of this Ca2+ influx mechanism is critical to our understanding of Ca2+ signaling in salivary gland cells. This review focuses on the various active and passive Ca2+ transport mechanisms in salivary gland cells-their localization, regulation, and role in neurotransmitter-regulation of fluid secretion. In addition to a historical perspective of Ca2+ signaling, recent findings and challenging problems facing this field are highlighted.

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“…1; for review see Refs. [2][3][4][5][6]. Elevations of [Ca 2ϩ ] i mediate the signal transduction from the plasma membrane agonist receptors to the Ca 2ϩ -sensitive intracellular targets, modulating a variety of cellular functions, including secretion, enzyme activation, gene expression, and proliferation.…”

mentioning

confidence: 99%