ArticleCell calcium2007
Ca2+ refilling of the endoplasmic reticulum is largely preserved albeit reduced Ca2+ entry in endothelial cells.
Article in Cell calcium, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- The Molecular Heterogeneity of Store-Operated CaInternational journal of molecular sciences · 2023Review
- Enforced tethering elongates the cortical endoplasmic reticulum and limits store-operated Ca2+ entry.Journal of cell science · 2022Article
- PCV2 Triggers PK-15 Cell Apoptosis Through the PLC-IP3R-CaFrontiers in microbiology · 2021Article
- The Endoplasmic Reticulum and Calcium Homeostasis in Pancreatic Beta Cells.Endocrinology · 2020Review
- Stim and Orai mediate constitutive CaOncotarget · 2018Article
- The Role of Endothelial CaInternational journal of molecular sciences · 2018Review
- NaPflugers Archiv : European journal of physiology · 2017Article
- Development of novel FP-based probes for live-cell imaging of nitric oxide dynamics.Nature communications · 2016Article
- The STIM1-ORAI1 microdomain.Cell calcium · 2015Review
- Double-stranded RNA attenuates the barrier function of human pulmonary artery endothelial cells.PloS one · 2014Article
- The endocannabinoid N-arachidonoyl glycine (NAGly) inhibits store-operated Ca2+ entry by preventing STIM1-Orai1 interaction.Journal of cell science · 2013Article
- Mitochondrial Ca2+ uptake 1 (MICU1) and mitochondrial ca2+ uniporter (MCU) contribute to metabolism-secretion coupling in clonal pancreatic β-cells.The Journal of biological chemistry · 2012Article
- Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters.World journal of biological chemistry · 2012Article
- ESCRT machinery potentiates HIV-1 utilization of the PI(4,5)P(2)-PLC-IP3R-Ca(2+) signaling cascade.Journal of molecular biology · 2011Article
- GPR55-dependent and -independent ion signalling in response to lysophosphatidylinositol in endothelial cells.British journal of pharmacology · 2010Article
- Osteoblasts modulate Ca2+ signaling in bone-metastatic prostate and breast cancer cells.Clinical & experimental metastasis · 2009Article
- Cytosolic Ca2+ prevents the subplasmalemmal clustering of STIM1: an intrinsic mechanism to avoid Ca2+ overload.Journal of cell science · 2008Article
- Enhanced spontaneous Ca2+ events in endothelial cells reflect signalling through myoendothelial gap junctions in pressurized mesenteric arteries.Cell calcium · 2008Article
- Mitochondria and Ca(2+) signaling: old guests, new functions.Pflugers Archiv : European journal of physiology · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In this study the relationship between the efficiency of endoplasmic reticulum (ER) Ca2+ refilling and the extent of Ca2+ entry was investigated in endothelial cells. ER and mitochondrial Ca2+ concentration were measured using genetically encoded Ca2+ sensors, while the amount of entering Ca2+ was controlled by varying either the extracellular Ca2+ or the electrical driving force for Ca2+ by changing the plasma membrane potential. In the absence of an agonist, ER Ca2+ replenishment was fully accomplished even if the Ca2+ concentration applied was reduced from 2 to 0.5mM. A similar strong efficiency of ER Ca2+ refilling was obtained under condition of plasma membrane depolarization. However, in the presence of histamine, ER Ca2+ refilling depended on mitochondrial Ca2+ transport and was more susceptible to membrane depolarization. Store-operated Ca2+ entry (SOCE), was strongly reduced under low Ca2+ and depolarizing conditions but increased if ER Ca2+ uptake was blocked or if ER Ca2+ was released continuously by IP(3). A correlation of the kinetics of ER Ca2+refilling with cytosolic Ca2+ signals revealed that termination of SOCE is a rapid event that is not delayed compared to ER refilling. Our data indicate that ER refilling occurs in priority to, and independently from the cytosolic Ca2+ elevation upon Ca2+ entry and that this important process is widely achieved even under conditions of diminished Ca2+entry.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.