scholarly journals Pathophysiological Significance of Store-Operated Calcium Entry in Megakaryocyte Function: Opening New Paths for Understanding the Role of Calcium in Thrombopoiesis

2016 ◽  
Vol 17 (12) ◽  
pp. 2055 ◽  
Author(s):  
Christian Di Buduo ◽  
Alessandra Balduini ◽  
Francesco Moccia
Keyword(s):  
Calcium Entry ◽  
Store Operated Calcium Entry

scholarly journals A CRITICAL ROLE OF TRPC1-ORAI1-STIM1 MEDIATED STORE OPERATED CALCIUM ENTRY IN CARDIAC HYPERTROPHY

2015 ◽  
Vol 65 (10) ◽  
pp. A902
Author(s):  
Senthil Selvaraj ◽  
Brij Singh ◽  
Christian Bollensdorff ◽  
Jassim Al Suwaidi ◽  
Magdi Yacoub
Keyword(s):  
Cardiac Hypertrophy ◽  
Critical Role ◽  
Calcium Entry ◽  
Store Operated Calcium Entry

scholarly journals The Role of S-Acylation in Store Operated Calcium Entry

2019 ◽  
Vol 116 (3) ◽  
pp. 237a-238a
Author(s):  
Savannah J. West ◽  
Qiaochu Wang ◽  
Michael X. Zhu ◽  
Askar M. Akimzhanov ◽  
Darren Boehning
Keyword(s):  
Calcium Entry ◽  
Store Operated Calcium Entry

Role of Store-Operated Calcium Entry During Meiotic Progression and Fertilization of Mammalian Oocytes

2012 ◽  
pp. 291-328 ◽  
Author(s):  
Francisco Javier Martín-Romero ◽  
Aida M. López-Guerrero ◽  
Ignacio S. Álvarez ◽  
Eulalia Pozo-Guisado
Keyword(s):  
Calcium Entry ◽  
Meiotic Progression ◽  
Store Operated Calcium Entry

scholarly journals Dominant regulation of interendothelial cell gap formation by calcium-inhibited type 6 adenylyl cyclase

2002 ◽  
Vol 157 (7) ◽  
pp. 1267-1278 ◽  
Author(s):  
Donna L. Cioffi ◽  
Timothy M. Moore ◽  
Jerry Schaack ◽  
Judy R. Creighton ◽  
Dermot M.F. Cooper ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Physiological Role ◽  
Cell Types ◽  
Cytosolic Calcium ◽  
Calcium Entry ◽  
Gap Formation ◽  
Calcium Stimulation ◽  
Store Operated Calcium Entry ◽  
Stimulation Of

Acute transitions in cytosolic calcium ([Ca2+]i) through store-operated calcium entry channels catalyze interendothelial cell gap formation that increases permeability. However, the rise in [Ca2+]i only disrupts barrier function in the absence of a rise in cAMP. Discovery that type 6 adenylyl cyclase (AC6; EC 4.6.6.1) is inhibited by calcium entry through store-operated calcium entry pathways provided a plausible explanation for how inflammatory [Ca2+]i mediators may decrease cAMP necessary for endothelial cell gap formation. [Ca2+]i mediators only modestly decrease global cAMP concentrations and thus, to date, the physiological role of AC6 is unresolved. Present studies used an adenoviral construct that expresses the calcium-stimulated AC8 to convert normal calcium inhibition into stimulation of cAMP, within physiologically relevant concentration ranges. Thrombin stimulated a dose-dependent [Ca2+]i rise in both pulmonary artery (PAECs) and microvascular (PMVEC) endothelial cells, and promoted intercellular gap formation in both cell types. In PAECs, gap formation was progressive over 2 h, whereas in PMVECs, gap formation was rapid (within 10 min) and gaps resealed within 2 h. Expression of AC8 resulted in a modest calcium stimulation of cAMP, which virtually abolished thrombin-induced gap formation in PMVECs. Findings provide the first direct evidence that calcium inhibition of AC6 is essential for endothelial gap formation.

scholarly journals The Knockout for G Protein-Coupled Receptor-Like PfSR25 Increases the Susceptibility of Malaria Parasites to the Antimalarials Lumefantrine and Piperaquine but Not to Medicine for Malaria Venture Compounds

2021 ◽  
Vol 12 ◽  
Author(s):  
Benedito M. Santos ◽  
Bárbara K. M. Dias ◽  
Myna Nakabashi ◽  
Celia R. S. Garcia
Keyword(s):  
G Protein ◽  
Calcium Entry ◽  
G Protein Coupled Receptor ◽  
Intracellular Calcium Signaling ◽  
Store Operated Calcium Entry ◽  
G Protein Coupled ◽  
Internal Calcium ◽  
Shed Light ◽  
Antimalarial Compounds

Previously we have reported that the G protein-coupled receptor (GPCR)-like PfSR25 in Plasmodium falciparum is a potassium (K+) sensor linked to intracellular calcium signaling and that knockout parasites (PfSR25-) are more susceptible to oxidative stress and antimalarial compounds. Here, we explore the potential role of PfSR25 in susceptibility to the antimalarial compounds atovaquone, chloroquine, dihydroartemisinin, lumefantrine, mefloquine, piperaquine, primaquine, and pyrimethamine and the Medicine for Malaria Venture (MMV) compounds previously described to act on egress/invasion (MMV006429, MMV396715, MMV019127, MMV665874, MMV665878, MMV665785, and MMV66583) through comparative assays with PfSR25- and 3D7 parasite strains, using flow cytometry assays. The IC50 and IC90 results show that lumefantrine and piperaquine have greater activity on the PfSR25- parasite strain when compared to 3D7. For MMV compounds, we found no differences between the strains except for the compound MMV665831, which we used to investigate the store-operated calcium entry (SOCE) mechanism. The results suggest that PfSR25 may be involved in the mechanism of action of the antimalarials lumefantrine and piperaquine. Our data clearly show that MMV665831 does not affect calcium entry in parasites after we depleted their internal calcium pools with thapsigargin. The results demonstrated here shed light on new possibilities on the antimalarial mechanism, bringing evidence of the involvement of the GPCR-like PfSR25.

scholarly journals Role of the store-operated calcium entry on differentiation of dental epithelial cells

2018 ◽  
Vol WCP2018 (0) ◽  
pp. PO4-7-19
Author(s):  
Kaori Murata ◽  
Takao Morita ◽  
Akihiro Nezu ◽  
Masato Saitoh ◽  
Akihiko Tanimura
Keyword(s):  
Epithelial Cells ◽  
Calcium Entry ◽  
Store Operated Calcium Entry

The Role of Orai1 in Store-Operated Calcium Entry in Porcine Oocytes.

2010 ◽  
Vol 83 (Suppl_1) ◽  
pp. 560-560 ◽  
Author(s):  
Chunmin Wang ◽  
Kiho Lee ◽  
Zoltan Machaty
Keyword(s):  
Calcium Entry ◽  
Store Operated Calcium Entry
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