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store operated channels

Yuzuki Kanda, Miho Okada, Rina Ikarashi, Eri Morioka, Takashi Kondo, Masayuki Ikeda
Clozapine (Clz) and olanzapine (Olz) are second generation (atypical) antipsychotics, used widely for treating schizophrenia and bipolar disorder. These drugs share multiple sites of actions, however their mechanisms remain incompletely understood. Here, we analyzed the effects of these drugs on primary cultures of rat cortical astrocytes and C6 glioma cells using fura-2-based Ca(2+) imaging. C6 cells, but not cortical astrocytes, express the serotonin 2A receptor subtype, which couples to phospholipase C. Clz (1μM) significantly blocked serotonin-induced Ca(2+) transients in C6 cells, consistent with known antagonistic actions of Clz...
October 18, 2016: Neuroscience Letters
Jian Shi, Francesc Miralles, Lutz Birnbaumer, William A Large, Anthony P Albert
In vascular smooth muscle cells (VSMCs), stimulation of TRPC1-based SOCs mediate Ca(2+) entry pathways which regulate contractility, proliferation and migration. It is therefore important to understand how these channels are activated. Studies have shown that stimulation of TRPC1-based SOCs requires Gαq/PLCβ1 activities and PKC phosphorylation, but it is unclear how store depletion stimulates this gating pathway. The present work examines this issue by focusing on the role of STIM1, an endo/sarcoplasmic reticulum Ca(2+) sensor...
October 18, 2016: Journal of Physiology
Ming Wei, Yandong Zhou, Aomin Sun, Guolin Ma, Lian He, Lijuan Zhou, Shuce Zhang, Jin Liu, Shenyuan L Zhang, Donald L Gill, Youjun Wang
Store-operated Ca(2+) entry (SOCE) mediated by STIM1 and Orai1 is crucial for Ca(2+) signaling and homeostasis in most cell types. 2-Aminoethoxydiphenyl borate (2-APB) is a well-described SOCE inhibitor, but its mechanisms of action remain largely elusive. Here, we show that 2-APB does not affect the dimeric state of STIM1, but enhances the intramolecular coupling between the coiled-coil 1 (CC1) and STIM-Orai-activating region (SOAR) of STIM1, with subsequent reduction in the formation of STIM1 puncta in the absence of Orai1 overexpression...
October 10, 2016: Pflügers Archiv: European Journal of Physiology
Axel R Concepcion, Martin Vaeth, Larry E Wagner, Miriam Eckstein, Lee Hecht, Jun Yang, David Crottes, Maximilian Seidl, Hyosup P Shin, Carl Weidinger, Scott Cameron, Stuart E Turvey, Thomas Issekutz, Isabelle Meyts, Rodrigo S Lacruz, Mario Cuk, David I Yule, Stefan Feske
Eccrine sweat glands are essential for sweating and thermoregulation in humans. Loss-of-function mutations in the Ca2+ release-activated Ca2+ (CRAC) channel genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and patients with these CRAC channel mutations suffer from anhidrosis and hyperthermia at high ambient temperatures. Here we have shown that CRAC channel-deficient patients and mice with ectodermal tissue-specific deletion of Orai1 (Orai1K14Cre) or Stim1 and Stim2 (Stim1/2K14Cre) failed to sweat despite normal sweat gland development...
October 10, 2016: Journal of Clinical Investigation
A Young Han, Hui Su Lee, Geun Hee Seol
This study assessed the effects of essential oil of Foeniculum vulgare Mill. (fennel oil) and of trans-anethole, the main component of fennel oil, on extracellular Ca(2+)-induced store-operated Ca(2+) entry (SOCE) into vascular endothelial (EA) cells and their mechanisms of action. Components of fennel oil were analyzed by gas chromatography-mass spectrometry. Cytosolic Ca(2+) concentration ([Ca(2+)]c) in EA cells was determined using Fura-2 fluorescence. In the presence of extracellular Ca(2+), fennel oil significantly increased [Ca(2+)]c in EA cells; this increase was significantly inhibited by the Ca(2+) channel blockers La(3+) and nifedipine...
October 6, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Jon Andoni Sánchez, Amparo Alfonso, Olivier P Thomas, Luís M Botana
Previous works with autumnalamide reported that Store Operated Calcium (SOC) channels were blocked through mitochondrial modulation. In the present paper we studied the effect of autumnalamide on ionomycin Ca(2+) fluxes. Thus, autumnalamide did not modify ionomycin-sensitive intracellular pools while the ionomycin-induced Ca(2+) influx was blocked with similar potency whether the incubation was done before or after ionomycin-sensitive pools depletion. Nevertheless, autumnalamide was not able to inhibit ionomycin-induced Ca(2+) influx once the membrane channels were activated...
September 28, 2016: Immunobiology
Edgar Flores-Soto, Jorge Reyes-García, Abril Carbajal-García, Elías Campuzano-González, Mercedes Perusquía, Bettina Sommer, Luis M Montaño
: Testosterone (TES), other androgens and female sex steroids induce non-genomic rapid relaxing effects in airway smooth muscle (ASM). In guinea pig ASM, basal tension was relaxed by dehydroepiandrosterone (DHEA) and TES; 17β-estradiol (E2) had a small effect. Blockers of L-type voltage dependent Ca(2+) channel (L-VDCC, D-600) and store operated Ca(2+) channel (SOC, 2-APB) also relaxed the basal tone. In tracheal myocytes, DHEA and TES diminished intracellular basal Ca(2+) concentrations (b[Ca(2+)]i) as D-600+2-APB but to a higher extend...
October 4, 2016: Molecular and Cellular Endocrinology
Hong-Tai Chang, Chiang-Ting Chou, I-Shu Chen, Chia-Cheng Yu, Ti Lu, Shu-Shong Hsu, Pochuen Shieh, Chung-Ren Jan, Wei-Zhe Liang
Cytochalasin B, a cell-permeable mycotoxin isolated from the fungus Phoma spp., shows a wide range of biological effects, among which its potent antitumor activity has raised great interests in different models. However, the cytotoxic activity of cytochalasin B and its underlying mechanisms have not been elucidated in breast cells. This study examined the effect of cytochalasin B on MCF 10A human breast epithelial cells and ZR-75-1 human breast cancer cells. Cytochalasin B (10-20μM) concentration-dependently induced cytotoxicity, cell cycle arrest, and [Ca(2+)]i rises in ZR-75-1 cells but not in MCF 10A cells...
October 1, 2016: Toxicology
Estella Zuccolo, Silvia Dragoni, Valentina Poletto, Paolo Catarsi, Daniele Guido, Alessandra Rappa, Marta Reforgiato, Francesco Lodola, Dmitry Lim, Vittorio Rosti, Germano Guerra, Francesco Moccia
Arachidonic acid (AA) stimulates endothelial cell (EC) proliferation through an increase in intracellular Ca(2+) concentration ([Ca(2+)]i), that, in turn, promotes nitric oxide (NO) release. AA-evoked Ca(2+) signals are mainly mediated by Transient Receptor Potential Vanilloid 4 (TRPV4) channels. Circulating endothelial colony forming cells (ECFCs) represent the only established precursors of ECs. In the present study, we therefore, sought to elucidate whether AA promotes human ECFC (hECFC) proliferation through an increase in [Ca(2+)]i and the following activation of the endothelial NO synthase (eNOS)...
September 12, 2016: Vascular Pharmacology
Judith A Stolwijk, Xuexin Zhang, Maxime Gueguinou, Wei Zhang, Khalid Matrougui, Christian Renken, Mohamed Trebak
Endothelial barrier function is tightly regulated by plasma membrane receptors and is crucial for tissue fluid homeostasis; its dysfunction causes disease, including sepsis and inflammation. The ubiquitous activation of Ca2+ signaling upon phospholipase C (PLC)-coupled receptor ligation leads quite naturally to the assumption that Ca2+ signaling is required for receptor-regulated endothelial barrier function. This widespread hypothesis draws analogy from smooth muscle and proposes the requirement of G protein coupled receptor (GPCR)-generated Ca2+ signaling in activating the endothelial contractile apparatus and generating inter-endothelial gaps...
September 13, 2016: Journal of Biological Chemistry
Dalia Alansary, Barbara Schmidt, Kathrin Dörr, Ivan Bogeski, Heiko Rieger, Achim Kless, Barbara A Niemeyer
Store-operated Ca(2+) entry mediated by STIM1-gated Orai1 channels is essential to activate immune cells and its inhibition or gain-of-function can lead to immune dysfunction and other pathologies. Reactive oxygen species interacting with cysteine residues can alter protein function. Pretreatment of the Ca(2+) selective Orai1 with the oxidant H2O2 reduces ICRAC with C195, distant to the pore, being its major redox sensor. However, the mechanism of inhibition remained elusive. Here we combine experimental and theoretical approaches and show that oxidation of Orai1 leads to reduced subunit interaction, slows diffusion and that either oxidized C195 or its oxidomimetic mutation C195D located at the exit of transmembrane helix 3 virtually eliminates channel activation by intramolecular interaction with S239 of transmembrane helix 4, thereby locking the channel in a closed conformation...
2016: Scientific Reports
Zili Zhang, Jian Wang, Jianxing He, Xiansheng Zeng, Xindong Chen, Mingmei Xiong, Qipeng Zhou, Meihua Guo, Defu Li, Wenju Lu
OBJECTIVE: Store operated calcium channels (SOCCs) and Receptor-operated calcium channels (ROCCs) are important pathways participating in regulation of intracellular Ca(2 +) concentration in various cell types. The purpose of our study is to determine whether genetic variations in key components of SOCCs and ROCCs are associated with lung cancer risk. METHODS: We identified 236 tagSNPs in 9 key genes related to SOCCs and ROCCs (TRPC1, TRPC3, TRPC4, TRPC6, TRPC7, ORAI1, ORAI2, STIM1, and STIM2) and evaluated their association with lung cancer risk in a two-stage case-control study with a total of 2433 lung cancer cases and 2433 cancer-free controls using Illumina high throughput genotyping platform...
September 2016: Meta Gene
Vijaya Lakshmi Bodiga, Santhi Priya Inapurapu, Praveen Kumar Vemuri, Madhukar Rao Kudle, Sreedhar Bodiga
Platinum-based chemotherapeutic regimen induces vascular dysfunction. Action of cisplatin on endothelial cells is mediated by protein kinase C (PKC-α), which further activates nuclear factor-κB (NF-κB) and induces canonical transient receptor potential channel (TRPC1) and intercellular adhesion molecule (ICAM-1) expression. Increased ICAM-1 contributes to hyperadhesion of monocytes and endothelial dysfunction. PKC-α is also involved in phosphorylation of TRPC1, resulting in store-operated calcium entry (SOCE) and further activation of NF-κB...
September 8, 2016: European Journal of Pharmacology
Amit Jairaman, Chelsea H Maguire, Robert P Schleimer, Murali Prakriya
Aberrant immune responses to environmental allergens including insect allergens from house dust mites and cockroaches contribute to allergic inflammatory diseases such as asthma in susceptible individuals. Airway epithelial cells (AECs) play a critical role in this process by sensing the proteolytic activity of allergens via protease-activated receptors (PAR2) to initiate inflammatory and immune responses in the airway. Elevation of cytosolic Ca(2+) is an important signaling event in this process, yet the fundamental mechanism by which allergens induce Ca(2+) elevations in AECs remains poorly understood...
2016: Scientific Reports
He-Hsiung Cheng, Chiang-Ting Chou, Wei-Zhe Liang, Jin-Shiung Cheng, Hong-Tai Chang, Chun-Chi Kuo, I-S Chen, Ti Lu, C-C Yu, Fu-An Chen, Daih-Huang Kuo, Pochuen Shieh, Chung-Ren Jan
NPC15199 is a synthesized compound that inhibits inflammation in some models. However, whether NPC15199 affects Ca²⁺ homeostasis in human gastric cancer is unclear. This study examined the effect of NPC15199 on cytosolic free Ca²⁺ concentrations ([Ca²⁺]i) and viability in SCM1 human gastric cancer cells. The Ca²⁺-sensitive fluorescent dye fura-2 was used to measure [Ca²⁺]i. NPC15199 evoked [Ca²⁺]i rises concentration-dependently. The response was reduced by removing extracellular Ca²⁺. NPC15199-evoked Ca²⁺ entry was not inhibited by store-operated channel inhibitors (nifedipine, econazole and SKF96365) and protein kinase C (PKC) activator (phorbol 12-myristate 13 acetate, PMA), or PKC inhibitor (GF109203X)...
October 31, 2016: Chinese Journal of Physiology
Benjamin Chun-Kit Tong, Claire Shuk-Kwan Lee, Wing-Hei Cheng, Kwok-On Lai, J Kevin Foskett, King-Ho Cheung
Some forms of familial Alzheimer's disease (FAD) are caused by mutations in presenilins (PSs), catalytic components of a γ-secretase complex that cleaves target proteins, including amyloid precursor protein (APP). Calcium (Ca(2+)) dysregulation in cells with these FAD-causing PS mutants has been attributed to attenuated store-operated Ca(2+) entry [SOCE; also called capacitative Ca(2+) entry (CCE)]. CCE occurs when STIM1 detects decreases in Ca(2+) in the endoplasmic reticulum (ER) and activates ORAI channels to replenish Ca(2+) stores in the ER...
2016: Science Signaling
Sumita Chakraborty, Bipan K Deb, Tetyana Chorna, Vera Konieczny, Colin W Taylor, Gaiti Hasan
Store-operated Ca(2+) entry (SOCE) occurs when loss of Ca(2+) from the endoplasmic reticulum (ER) stimulates the Ca(2+) sensor, STIM, to cluster and activate the plasma membrane Ca(2+) channel Orai (encoded by Olf186-F in flies). Inositol 1,4,5-trisphosphate receptors (IP3Rs, which are encoded by a single gene in flies) are assumed to regulate SOCE solely by mediating ER Ca(2+) release. We show that in Drosophila neurons, mutant IP3R attenuates SOCE evoked by depleting Ca(2+) stores with thapsigargin. In normal neurons, store depletion caused STIM and the IP3R to accumulate near the plasma membrane, association of STIM with Orai, clustering of STIM and Orai at ER-plasma-membrane junctions and activation of SOCE...
October 15, 2016: Journal of Cell Science
Jessica Sabourin, Florent Allagnat
Normal plasma glucose level is ensured by the action of insulin, the major hypoglycemic hormone. Therefore, it is not surprising that insulin release from pancreatic β-cells of the Langerhans islets is controlled by an array of balanced mechanisms in which glucose plays the leading role. Glucose triggers insulin secretion through the well described pathway of ATP-driven closure of ATP-sensitive potassium channels (KATP), depolarization of the plasma membrane and opening of the voltage-dependent Ca2+ channels (VDCC)...
September 2, 2016: Journal of Molecular Endocrinology
Ellie M Carrell, Aundrea R Coppola, Helen J McBride, Robert T Dirksen
Orai1 is a transmembrane protein that forms homomeric, calcium-selective channels activated by stromal interaction molecule 1 (STIM1) after depletion of intracellular calcium stores. In adult skeletal muscle, depletion of sarcoplasmic reticulum calcium activates STIM1/Orai1-dependent store-operated calcium entry. Here, we used constitutive and inducible muscle-specific Orai1 knockout (KO) mice to determine the acute and long-term developmental effects of Orai1 ablation on muscle structure and function. Skeletal muscles from constitutive, muscle-specific Orai1 KO mice exhibited normal postnatal growth and fiber type differentiation...
September 1, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
G Y Peng, J Xu, R M Liu, W Hong, X M He, Y E Lin
OBJECTIVE: To determine whether store-operated Ca(2+) entry (SOCE) is involved in chronic hypoxia-induced alteration of intracellular Ca(2+) concentration ([Ca(2+) ]i) and proliferation in pulmonary arterial smooth muscle cells (PASMC). METHODS: Rat PASMCs were cultured and treated in normoxia (21%O2) or hypoxia (4%O2) condition. The proliferation of PASMC was detected by cell counting kit-8 (CCK-8) assay. [Ca(2+) ]i, SOCE and the effects of store-operated Ca(2+) channel (SOCC) inhibitors, SKF96365 and NiCl2, on SOCE in hypoxic PASMCs were tested by InCyte [Ca(2+) ]i measurement system...
September 1, 2016: Zhonghua Nei Ke za Zhi [Chinese Journal of Internal Medicine]
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