scholarly journals Endoplasmic Reticulum Stress and Store-Operated Calcium Entry Contribute to Usnic Acid-Induced Toxicity in Hepatic Cells

2015 ◽  
Vol 146 (1) ◽  
pp. 116-126 ◽  
Author(s):  
Si Chen ◽  
Zhuhong Zhang ◽  
Yuanfeng Wu ◽  
Qiang Shi ◽  
Hua Yan ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Usnic Acid ◽  
Calcium Entry ◽  
Hepatic Cells ◽  
Store Operated Calcium Entry

scholarly journals Impaired Store-Operated Calcium Entry and STIM1 Loss Lead to Reduced Insulin Secretion and Increased Endoplasmic Reticulum Stress in the Diabetic β-Cell

Diabetes ◽  
2018 ◽  
Vol 67 (11) ◽  
pp. 2293-2304 ◽  
Author(s):  
Tatsuyoshi Kono ◽  
Xin Tong ◽  
Solaema Taleb ◽  
Robert N. Bone ◽  
Hitoshi Iida ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Insulin Secretion ◽  
Endoplasmic Reticulum Stress ◽  
Calcium Entry ◽  
Β Cell ◽  
Store Operated Calcium Entry

scholarly journals Synthesis and Pharmacological Characterization of 2-Aminoethyl Diphenylborinate (2-APB) Derivatives for Inhibition of Store-Operated Calcium Entry (SOCE) in MDA-MB-231 Breast Cancer Cells

2020 ◽  
Vol 21 (16) ◽  
pp. 5604 ◽  
Author(s):  
Achille Schild ◽  
Rajesh Bhardwaj ◽  
Nicolas Wenger ◽  
Dominic Tscherrig ◽  
Palanivel Kandasamy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Structural Changes ◽  
Calcium Entry ◽  
Imaging Plate ◽  
Ip3 Receptors ◽  
Pharmacological Characterization ◽  
Store Operated Calcium Entry

Calcium ions regulate a wide array of physiological functions including cell differentiation, proliferation, muscle contraction, neurotransmission, and fertilization. The endoplasmic reticulum (ER) is the major intracellular Ca2+ store and cellular events that induce ER store depletion (e.g., activation of inositol 1,4,5-triphosphate (IP3) receptors) trigger a refilling process known as store-operated calcium entry (SOCE). It requires the intricate interaction between the Ca2+ sensing stromal interaction molecules (STIM) located in the ER membrane and the channel forming Orai proteins in the plasma membrane (PM). The resulting active STIM/Orai complexes form highly selective Ca2+ channels that facilitate a measurable Ca2+ influx into the cytosol followed by successive refilling of the ER by the sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA). STIM and Orai have attracted significant therapeutic interest, as enhanced SOCE has been associated with several cancers, and mutations in STIM and Orai have been linked to immunodeficiency, autoimmune, and muscular diseases. 2-Aminoethyl diphenylborinate (2-APB) is a known modulator and depending on its concentration can inhibit or enhance SOCE. We have synthesized several novel derivatives of 2-APB, introducing halogen and other small substituents systematically on each position of one of the phenyl rings. Using a fluorometric imaging plate reader (FLIPR) Tetra-based calcium imaging assay we have studied how these structural changes of 2-APB affect the SOCE modulation activity at different compound concentrations in MDA-MB-231 breast cancer cells. We have discovered 2-APB derivatives that block SOCE at low concentrations, at which 2-APB usually enhances SOCE.

scholarly journals The tethering function of mitofusin2 controls osteoclast differentiation by modulating the Ca2+–NFATc1 axis

2020 ◽  
Vol 295 (19) ◽  
pp. 6629-6640 ◽  
Author(s):  
Anna Ballard ◽  
Rong Zeng ◽  
Allahdad Zarei ◽  
Christine Shao ◽  
Linda Cox ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Bone Mass ◽  
Intracellular Signaling ◽  
Osteoclast Differentiation ◽  
Calcium Entry ◽  
Calcium Handling ◽  
Mitochondrial Network ◽  
Female Mice ◽  
Mitochondrial Functions ◽  
Store Operated Calcium Entry

Dynamic regulation of the mitochondrial network by mitofusins (MFNs) modulates energy production, cell survival, and many intracellular signaling events, including calcium handling. However, the relative importance of specific mitochondrial functions and their dependence on MFNs vary greatly among cell types. Osteoclasts have many mitochondria, and increased mitochondrial biogenesis and oxidative phosphorylation enhance bone resorption, but little is known about the mitochondrial network or MFNs in osteoclasts. Because expression of each MFN isoform increases with osteoclastogenesis, we conditionally deleted MFN1 and MFN2 (double conditional KO (dcKO)) in murine osteoclast precursors, finding that this increased bone mass in young female mice and abolished osteoclast precursor differentiation into mature osteoclasts in vitro. Defective osteoclastogenesis was reversed by overexpression of MFN2 but not MFN1; therefore, we generated mice lacking only MFN2 in osteoclasts. MFN2-deficient female mice had increased bone mass at 1 year and resistance to Receptor Activator of NF-κB Ligand (RANKL)-induced osteolysis at 8 weeks. To explore whether MFN-mediated tethering or mitophagy is important for osteoclastogenesis, we overexpressed MFN2 variants defective in either function in dcKO precursors and found that, although mitophagy was dispensable for differentiation, tethering was required. Because the master osteoclastogenic transcriptional regulator nuclear factor of activated T cells 1 (NFATc1) is calcium-regulated, we assessed calcium release from the endoplasmic reticulum and store-operated calcium entry and found that the latter was blunted in dcKO cells. Restored osteoclast differentiation by expression of intact MFN2 or the mitophagy-defective variant was associated with normalization of store-operated calcium entry and NFATc1 levels, indicating that MFN2 controls mitochondrion–endoplasmic reticulum tethering in osteoclasts.

scholarly journals Regulation of store-operated calcium entry during cell division

2012 ◽  
Vol 40 (1) ◽  
pp. 119-123 ◽  
Author(s):  
Jeremy T. Smyth ◽  
James W. Putney
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Division ◽  
Recent Work ◽  
Calcium Entry ◽  
Store Operated Calcium Entry ◽  
Dividing Cells ◽  
Complex Mechanisms ◽  
Molecular Components ◽  
Ca2 Channels

Store-operate Ca2+ channels gate Ca2+ entry into the cytoplasm in response to the depletion of Ca2+ from endoplasmic reticulum Ca2+ stores. The major molecular components of store-operated Ca2+ entry are STIM (stromal-interacting molecule) 1 (and in some instances STIM2) that serves as the endoplasmic reticulum Ca2+ sensor, and Orai (Orai1, Orai2 and Orai3) which function as pore-forming subunits of the store-operated channel. It has been known for some time that store-operated Ca2+ entry is shut down during cell division. Recent work has revealed complex mechanisms regulating the functions and locations of both STIM1 and Orai1 in dividing cells.

Calcium entry via TRPC6 mediates albumin overload-induced endoplasmic reticulum stress and apoptosis in podocytes

Cell Calcium ◽  
2011 ◽  
Vol 50 (6) ◽  
pp. 523-529 ◽  
Author(s):  
Shan Chen ◽  
Fang-Fang He ◽  
Hui Wang ◽  
Zhan Fang ◽  
Ning Shao ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Calcium Entry

scholarly journals Remodelling of the endoplasmic reticulum during store-operated calcium entry

2011 ◽  
Vol 103 (8) ◽  
pp. 365-380 ◽  
Author(s):  
Wei-Wei Shen ◽  
Maud Frieden ◽  
Nicolas Demaurex
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Entry ◽  
Store Operated Calcium Entry

scholarly journals Sertraline induces endoplasmic reticulum stress in hepatic cells

Toxicology ◽  
2014 ◽  
Vol 322 ◽  
pp. 78-88 ◽  
Author(s):  
Si Chen ◽  
Jiekun Xuan ◽  
Letha Couch ◽  
Advait Iyer ◽  
Yuanfeng Wu ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Hepatic Cells

scholarly journals Reticulon 4 Is Necessary for Endoplasmic Reticulum Tubulation, STIM1-Orai1 Coupling, and Store-operated Calcium Entry

2014 ◽  
Vol 289 (13) ◽  
pp. 9380-9395 ◽  
Author(s):  
Levente Jozsef ◽  
Keitaro Tashiro ◽  
Andrew Kuo ◽  
Eon Joo Park ◽  
Athanasia Skoura ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Entry ◽  
Store Operated Calcium Entry
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