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https://www.readbyqxmd.com/read/28393091/data-on-cytotoxicity-in-hela-and-su-dhl-4-cells-exposed-to-dpb162-ae-compound
#1
Mart Bittremieux, Katsuhiko Mikoshiba, Geert Bultynck
DPB162-AE is a valuable tool to study store-operated Ca(2+) entry (SOCE), as this compound was developed as a 2-APB analog that inhibits SOCE more potently and more selectively than 2-APB itself. In addition to this, we showed that, in some conditions, DPB162-AE can deplete the endoplasmic reticulum Ca(2+) stores in intact cells, including the cervical carcinoma HeLa cell line and the diffuse large B-cell lymphoma SU-DHL-4 cell line. Here, we present data regarding the toxicity of DPB162-AE in HeLa and SU-DHL-4 cells...
June 2017: Data in Brief
https://www.readbyqxmd.com/read/28385807/pyk2-phosphorylation-of-ve-ptp-downstream-of-stim1-induced-ca2-entry-regulates-disassembly-of-adherens-junctions
#2
Dheeraj Soni, Sushil C Regmi, Dong-Mei Wang, Auditi DebRoy, You-Yang Zhao, Stephen M Vogel, Asrar B Malik, Chinnaswamy Tiruppathi
VE-PTP stabilizes endothelial adherens junctions (AJs) through constitutive dephosphorylation of VE-cadherin. Here we investigated the role of STIM1 activation of store-operated Ca2+ entry (SOCE) in regulating adherens junction assembly. We observed that SOCE induced by STIM1 activated Pyk2 in human lung microvascular endothelial cells (ECs) and induced tyrosine phosphorylation of VE-PTP at Y1981. Pyk2-induced tyrosine phosphorylation of VE-PTP promoted Src binding to VE-PTP, Src activation, and subsequent VE-cadherin phosphorylation, and thereby increased the endothelial permeability response...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28372809/the-role-of-stim1-and-soce-in-smooth-muscle-contractility
#3
REVIEW
C H Feldman, C A Grotegut, P B Rosenberg
Contraction is a central feature for skeletal, cardiac and smooth muscle; this unique feature is largely dependent on calcium (Ca(2+)) signaling and therefore maintenance of internal Ca(2+) stores. Stromal interaction molecule 1 (STIM1) is a single-pass transmembrane protein that functions as a Ca(2+) sensor for the activation store-operated calcium channels (SOCCs) on the plasma membrane in response to depleted internal sarco(endo)plasmic (S/ER) reticulum Ca(2+) stores. STIM1 was initially characterized in non-excitable cells; however, evidence from both animal models and human mutations suggests a role for STIM1 in modulating Ca(2+) homeostasis in excitable tissues as well...
March 10, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28364693/the-%C3%AF-1-receptor-agonist-pentazocine-increases-store-operated-ca-2-entry-in-mcf7%C3%AF-1-and-sk-n-sh-cell-lines
#4
Giuseppe Gasparre, Carmen Abate, Roberto Carlucci, Francesco Berardi, Giuseppe Cassano
BACKGROUND: The intracellular [Ca(2+)] is modulated by σ receptors. An important component of the cellular machinery governing the intracellular [Ca(2+)] is Store-Operated Calcium Entry (SOCE). Here we want to investigate whether ligands of σ receptors affect SOCE. METHODS: The intracellular [Ca(2+)] was monitored, with the fluorescent Ca(2+)-sensitive probe Fura-2, in four cell lines with a different expression of σ receptors, namely MCF7 (expressing σ1 receptors with a low density and overexpressing σ2 receptors), MCF7σ1 (overexpressing σ1 receptors), SK-N-SH, and HT-29...
January 28, 2017: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/28364016/reduced-membrane-cholesterol-limits-pulmonary-endothelial-ca-2-entry-following-chronic-hypoxia
#5
Bojun Zhang, Jay S Naik, Nikki L Jernigan, Benjimen R Walker, Thomas C Resta
Chronic hypoxia (CH)-induced pulmonary hypertension is associated with diminished production of endothelium-derived Ca(2+)-dependent vasodilators such as nitric oxide. Interestingly, ATP-induced endothelial Ca(2+) entry as well as membrane cholesterol (Chol) are decreased in pulmonary arteries from CH rats (4 wk, PB = 380 Torr) compared to normoxic controls. Store-operated Ca(2+) entry (SOCE) and depolarization-induced Ca(2+) entry are major components of the response to ATP and are similarly decreased after CH...
March 31, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28356979/inhibition-of-store-operated-ca-2-entry-counteracts-the-apoptosis-of-nasopharyngeal-carcinoma-cells-induced-by-sodium-butyrate
#6
Wei Huang, Caiping Ren, Guoling Huang, Jie Liu, Weidong Liu, Lei Wang, Bin Zhu, Xiangling Feng, Jia Shi, Jinlong Li, Xiaomeng Xia, Wei Jia, Jiawen Chen, Yuxiang Chen, Xingjun Jiang
Sodium butyrate (NaBu), a histone deacetylase inhibitor, has demonstrated anti-tumor effects in several cancers, and is a promising candidate chemotherapeutic agent. However, its roles in nasopharyngeal carcinoma (NPC), an endemic malignant disease in Southern China and Southeast Asia, has rarely been studied. In the present study, MTT assay, colony formation assay, flow cytometry analysis and western blotting were performed to explore the influence of NaBu on NPC cells and its underlying mechanism. NaBu induced morphological changes and inhibited proliferation in 5-8F and 6-10B cells...
February 2017: Oncology Letters
https://www.readbyqxmd.com/read/28352661/store-operated-ca-2-entry-controls-ameloblast-cell-function-and-enamel-development
#7
Miriam Eckstein, Martin Vaeth, Cinzia Fornai, Manikandan Vinu, Timothy G Bromage, Meerim K Nurbaeva, Jessica L Sorge, Paulo G Coelho, Youssef Idaghdour, Stefan Feske, Rodrigo S Lacruz
Loss-of-function mutations in stromal interaction molecule 1 (STIM1) impair the activation of Ca(2+) release-activated Ca(2+) (CRAC) channels and store-operated Ca(2+) entry (SOCE), resulting in a disease syndrome called CRAC channelopathy that is characterized by severe dental enamel defects. The cause of these enamel defects has remained unclear given a lack of animal models. We generated Stim1/2(K14cre) mice to delete STIM1 and its homolog STIM2 in enamel cells. These mice showed impaired SOCE in enamel cells...
March 23, 2017: JCI Insight
https://www.readbyqxmd.com/read/28341841/regulation-of-membrane-ruffling-by-polarized-stim1-and-orai1-in-cortactin-rich-domains
#8
Aida M Lopez-Guerrero, Patricia Tomas-Martin, Carlos Pascual-Caro, Thomas Macartney, Alejandro Rojas-Fernandez, Graeme Ball, Dario R Alessi, Eulalia Pozo-Guisado, Francisco Javier Martin-Romero
Cell motility and migration requires the reorganization of the cortical cytoskeleton at the leading edge of cells and extracellular Ca(2+) entry is essential for this reorganization. However the molecular nature of the regulators of this pathway is unknown. This work contributes to understanding the role of STIM1 and ORAI1 in the promotion of membrane ruffling by showing that phospho-STIM1 localizes at the leading edge of cells, and that both phospho-STIM1 and ORAI1 co-localize with cortactin (CTTN), a regulator of the cytoskeleton at membrane ruffling areas...
March 24, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28326487/enhanced-stim1-expression-is-associated-with-acquired-chemo-resistance-of-cisplatin-in-osteosarcoma-cells
#9
Xilong Sun, Qiang Wei, Jie Cheng, Yanzhu Bian, Congna Tian, Yujing Hu, Huijie Li
Osteosarcoma is the most common primary malignant bone tumor. Although cisplatin is the primary chemotherapy used in osteosarcoma treatment, the cisplatin resistance remains a big challenge for improving overall survival. The store-operated calcium (Ca(2+)) entry (SOCE) and its major mediator Stim1 have been shown to be implicated in a number of pathological processes typical for cancer. In this study, we showed that Stim1 expression was significantly increased in chemo-resistant osteosarcoma tissues compared with chemo-sensitivity tissues...
March 22, 2017: Human Cell
https://www.readbyqxmd.com/read/28303257/neurod2-regulates-stim1-expression-and-store-operated-calcium-entry-in-cortical-neurons
#10
Gokhan Guner, Gizem Guzelsoy, Fatma Sadife Isleyen, Gulcan Semra Sahin, Cansu Akkaya, Efil Bayam, Eser Ilgin Kotan, Alkan Kabakcioglu, Gulayse Ince-Dunn
Calcium signaling controls many key processes in neurons, including gene expression, axon guidance, and synaptic plasticity. In contrast to calcium influx through voltage- or neurotransmitter-gated channels, regulatory pathways that control store-operated calcium entry (SOCE) in neurons are poorly understood. Here, we report a transcriptional control of Stim1 (stromal interaction molecule 1) gene, which is a major sensor of endoplasmic reticulum (ER) calcium levels and a regulator of SOCE. By using a genome-wide chromatin immunoprecipitation and sequencing approach in mice, we find that NEUROD2, a neurogenic transcription factor, binds to an intronic element within the Stim1 gene...
January 2017: ENeuro
https://www.readbyqxmd.com/read/28298362/negative-regulation-of-smad1-pathway-and-collagen-iv-expression-by-store-operated-ca2-entry-in-glomerular-mesangial-cells
#11
Peiwen Wu, Yuezhong Ren, Yuhong Ma, Yanxia Wang, Hui Jiang, Sarika Chaudhari, Mark E Davis, Jonathan E Zuckerman, Rong Ma
Collagen IV (Col IV) is a major component of expanded glomerular extracellular matrix in diabetic nephropathy and Smad1 is a key molecule regulating Col IV expression in mesangial cells (MCs). The present study was conducted to determine if Smad1 pathway and Col IV protein abundance were regulated by store-operated Ca2+ entry (SOCE). In cultured human MCs, pharmacological inhibition of SOCE significantly increased the total amount of Smad1 protein. Activation of SOCE blunted high glucose-increased Smad1 protein content...
March 15, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28294127/orai2-modulates-store-operated-calcium-entry-and-t-cell-mediated-immunity
#12
Martin Vaeth, Jun Yang, Megumi Yamashita, Isabelle Zee, Miriam Eckstein, Camille Knosp, Ulrike Kaufmann, Peter Karoly Jani, Rodrigo S Lacruz, Veit Flockerzi, Imre Kacskovics, Murali Prakriya, Stefan Feske
Store-operated Ca(2+) entry (SOCE) through Ca(2+) release-activated Ca(2+) (CRAC) channels is critical for lymphocyte function and immune responses. CRAC channels are hexamers of ORAI proteins that form the channel pore, but the contributions of individual ORAI homologues to CRAC channel function are not well understood. Here we show that deletion of Orai1 reduces, whereas deletion of Orai2 increases, SOCE in mouse T cells. These distinct effects are due to the ability of ORAI2 to form heteromeric channels with ORAI1 and to attenuate CRAC channel function...
March 15, 2017: Nature Communications
https://www.readbyqxmd.com/read/28254622/molecular-analyses-on-neospora-caninum-triggered-netosis-in-the-caprine-system
#13
R Villagra-Blanco, L M R Silva, U Gärtner, H Wagner, K Failing, A Wehrend, A Taubert, C Hermosilla
Neospora caninum is an obligate intracellular protozoan parasite causing serious reproductive disorders in large and small ruminants worldwide. Polymorphonuclear neutrophils (PMN) react against multiple invading pathogens through different mechanisms including the release of neutrophil extracellular traps (NETs). Here, in vitro interactions of caprine PMN and N. caninum tachyzoites were studied. Scanning electron microscopic- and immunofluorescence-analyses demonstrated that caprine PMN undergo NETosis upon contact with tachyzoites of N...
July 2017: Developmental and Comparative Immunology
https://www.readbyqxmd.com/read/28247051/oocyte-activation-and-fertilisation-crucial-contributors-from-the-sperm-and-oocyte
#14
Marc Yeste, Celine Jones, Siti Nornadhirah Amdani, Kevin Coward
This chapter intends to summarise the importance of sperm- and oocyte-derived factors in the processes of sperm-oocyte binding and oocyte activation. First, we describe the initial interaction between sperm and the zona pellucida, with particular regard to acrosome exocytosis. We then describe how sperm and oocyte membranes fuse, with special reference to the discovery of the sperm protein IZUMO1 and its interaction with the oocyte membrane receptor JUNO. We then focus specifically upon oocyte activation, the fundamental process by which the oocyte is alleviated from metaphase II arrest by a sperm-soluble factor...
2017: Results and Problems in Cell Differentiation
https://www.readbyqxmd.com/read/28247021/store-operated-calcium-entry-is-essential-for-glial-calcium-signalling-in-cns-white-matter
#15
M Papanikolaou, A Lewis, A M Butt
'Calcium signalling' is the ubiquitous response of glial cells to multiple extracellular stimuli. The primary mechanism of glial calcium signalling is by release of calcium from intracellular stores of the endoplasmic reticulum (ER). Replenishment of ER Ca(2+) stores relies on store-operated calcium entry (SOCE). However, despite the importance of calcium signalling in glial cells, little is known about their mechanisms of SOCE. Here, we investigated SOCE in glia of the mouse optic nerve, a typical CNS white matter tract that comprises bundles of myelinated axons and the oligodendrocytes and astrocytes that support them...
February 28, 2017: Brain Structure & Function
https://www.readbyqxmd.com/read/28243166/orai1-and-orai3-in-combination-with-stim1-mediate-the-majority-of-store-operated-calcium-entry-in-astrocytes
#16
Jea Kwon, Heeyoung An, Moonsun Sa, Joungha Won, Jeong Im Shin, C Justin Lee
Astrocytes are non-excitable cells in the brain and their activity largely depends on the intracellular calcium (Ca(2+)) level. Therefore, maintaining the intracellular Ca(2+) homeostasis is critical for proper functioning of astrocytes. One of the key regulatory mechanisms of Ca(2+) homeostasis in astrocytes is the store-operated Ca(2+) entry (SOCE). This process is mediated by a combination of the Ca(2+)-store-depletion-sensor, Stim, and the store-operated Ca(2+)-channels, Orai and TrpC families. Despite the existence of all those families in astrocytes, previous studies have provided conflicting results on the molecular identification of astrocytic SOCE...
February 2017: Experimental Neurobiology
https://www.readbyqxmd.com/read/28240257/atlastin-regulates-store-operated-calcium-entry-for-nerve-growth-factor-induced-neurite-outgrowth
#17
Jing Li, Bing Yan, Hongjiang Si, Xu Peng, Shenyuan L Zhang, Junjie Hu
Homotypic membrane fusion of the endoplasmic reticulum (ER) is mediated by a class of dynamin-like GTPases known as atlastin (ATL). Depletion of or mutations in ATL cause an unbranched ER morphology and hereditary spastic paraplegia (HSP), a neurodegenerative disease characterized by axon shortening in corticospinal motor neurons and progressive spasticity of the lower limbs. How ER shaping is linked to neuronal defects is poorly understood. Here, we show that dominant-negative mutants of ATL1 in PC-12 cells inhibit nerve growth factor (NGF)-induced neurite outgrowth...
February 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28222911/store-operated-ca-2-entry-is-not-required-for-fertilization-induced-ca-2-signaling-in-mouse-eggs
#18
Miranda L Bernhardt, Elizabeth Padilla-Banks, Paula Stein, Yingpei Zhang, Carmen J Williams
Repetitive oscillations in cytoplasmic Ca(2+) due to periodic Ca(2+) release from the endoplasmic reticulum (ER) drive mammalian embryo development following fertilization. Influx of extracellular Ca(2+) to support the refilling of ER stores is required for sustained Ca(2+) oscillations, but the mechanisms underlying this Ca(2+) influx are controversial. Although store-operated Ca(2+) entry (SOCE) is an appealing candidate mechanism, several groups have arrived at contradictory conclusions regarding the importance of SOCE in oocytes and eggs...
February 11, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28220846/cmt-linked-loss-of-function-mutations-in-gdap1-impair-store-operated-ca-2-entry-stimulated-respiration
#19
Paloma González-Sánchez, David Pla-Martín, Paula Martínez-Valero, Carlos B Rueda, Eduardo Calpena, Araceli Del Arco, Francesc Palau, Jorgina Satrústegui
GDAP1 is an outer mitochondrial membrane protein involved in Charcot-Marie-Tooth (CMT) disease. Lack of GDAP1 gives rise to altered mitochondrial networks and endoplasmic reticulum (ER)-mitochondrial interactions resulting in a decreased ER-Ca(2+) levels along with a defect on store-operated calcium entry (SOCE) related to a misallocation of mitochondria to subplasmalemmal sites. The defect on SOCE is mimicked by MCU silencing or mitochondrial depolarization, which prevent mitochondrial calcium uptake. Ca(2+) release from de ER and Ca(2+) inflow through SOCE in neuroblastoma cells result in a Ca(2+)-dependent upregulation of respiration which is blunted in GDAP1 silenced cells...
February 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28219928/mitochondria-control-store-operated-ca-2-entry-through-na-and-redox-signals
#20
Tsipi Ben-Kasus Nissim, Xuexin Zhang, Assaf Elazar, Soumitra Roy, Judith A Stolwijk, Yandong Zhou, Rajender K Motiani, Maxime Gueguinou, Nadine Hempel, Michal Hershfinkel, Donald L Gill, Mohamed Trebak, Israel Sekler
Mitochondria exert important control over plasma membrane (PM) Orai1 channels mediating store-operated Ca(2+) entry (SOCE). Although the sensing of endoplasmic reticulum (ER) Ca(2+) stores by STIM proteins and coupling to Orai1 channels is well understood, how mitochondria communicate with Orai1 channels to regulate SOCE activation remains elusive. Here, we reveal that SOCE is accompanied by a rise in cytosolic Na(+) that is critical in activating the mitochondrial Na(+)/Ca(2+) exchanger (NCLX) causing enhanced mitochondrial Na(+) uptake and Ca(2+) efflux...
March 15, 2017: EMBO Journal
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