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https://www.readbyqxmd.com/read/28203685/sgk1-up-regulates-orai1-expression-and-vsmc-migration-during-neointima-formation-after-arterial-injury
#1
Britta Walker-Allgaier, Malte Schaub, Ioana Alesutan, Jakob Voelkl, Sascha Geue, Patrick Münzer, José M Rodríguez, Dietmar Kuhl, Florian Lang, Meinrad Gawaz, Oliver Borst
No abstract text is available yet for this article.
February 16, 2017: Thrombosis and Haemostasis
https://www.readbyqxmd.com/read/28196740/dpb162-ae-an-inhibitor-of-store-operated-ca-2-entry-can-deplete-the-endoplasmic-reticulum-ca-2-store
#2
Mart Bittremieux, Julia V Gerasimenko, Marleen Schuermans, Tomas Luyten, Eloise Stapleton, Kamil J Alzayady, Humbert De Smedt, David I Yule, Katsuhiko Mikoshiba, Peter Vangheluwe, Oleg V Gerasimenko, Jan B Parys, Geert Bultynck
Store-operated Ca(2+) entry (SOCE), an important Ca(2+) signaling pathway in non-excitable cells, regulates a variety of cellular functions. To study its physiological role, pharmacological tools, like 2-aminoethyl diphenylborinate (2-APB), are used to impact SOCE. 2-APB is one of the best characterized SOCE inhibitors. However, 2-APB also activates SOCE at lower concentrations, while it inhibits inositol 1,4,5-trisphosphate receptors (IP3Rs), sarco/endoplasmic reticulum Ca(2+)-ATPases (SERCAs) and other ion channels, like TRP channels...
February 1, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28185894/trpc1-and-trpc4-channels-functionally-interact-with-stim1l-to-promote-myogenesis-and-maintain-fast-repetitive-ca-2-release-in-human-myotubes
#3
Fabrice Antigny, Jessica Sabourin, Sophie Saüc, Laurent Bernheim, Stéphane Koenig, Maud Frieden
STIM1 and Orai1 are essential players of store-operated Ca(2+) entry (SOCE) in human skeletal muscle cells and are required for adult muscle differentiation. Besides these two proteins, TRPC (transient receptor potential canonical) channels and STIM1L (a longer STIM1 isoform) are also present on muscle cells. In the present study, we assessed the role of TRPC1, TRPC4 and STIM1L in SOCE, in the maintenance of repetitive Ca(2+) transients and in muscle differentiation. Knockdown of TRPC1 and TRPC4 reduced SOCE by about 50% and significantly delayed the onset of Ca(2+) entry, both effects similar to STIM1L invalidation...
February 6, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28179072/orai3-channel-is-the-2-apb-induced-endoplasmic-reticulum-calcium-leak
#4
Daniel Leon-Aparicio, Jonathan Pacheco, Jesus Chavez-Reyes, Jose M Galindo, Jesus Valdes, Luis Vaca, Agustin Guerrero-Hernandez
We have studied in HeLa cells the molecular nature of the 2-APB induced ER Ca(2+) leak using synthetic Ca(2+) indicators that report changes in both the cytoplasmic ([Ca(2+)]i) and the luminal ER ([Ca(2+)]ER) Ca(2+) concentrations. We have tested the hypothesis that Orai channels participate in the 2-APB-induced ER Ca(2+) leak that was characterized in the companion paper. The expression of the dominant negative Orai1 E106A mutant, which has been reported to block the activity of all three types of Orai channels, inhibited the effect of 2-APB on the [Ca(2+)]ER but did not decrease the ER Ca(2+) leak after thapsigargin (TG)...
January 23, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28167653/orai1-activates-proliferation-of-lymphatic-endothelial-cells-in-response-to-laminar-flow-through-kr%C3%A3-ppel-like-factors-2-and-4
#5
Dongwon Choi, Eunkyung Park, Eunson Jung, Young Jin Seong, Mingu Hong, Sunju Lee, James Burford, Georgina Gyarmati, Janos Peti-Peterdi, Sonal Srikanth, Yousang Gwack, Chester J Koh, Evgenii Boriushkin, Anne Hamik, Alex K Wong, Young-Kwon Hong
RATIONALE: Lymphatic vessels function to drain interstitial fluid from a variety of tissues. Although shear stress generated by fluid flow is known to trigger lymphatic expansion and remodeling, the molecular basis underlying flow-induced lymphatic growth is unknown. OBJECTIVE: We aimed to gain a better understanding of the mechanism by which laminar shear stress activates lymphatic proliferation. METHODS AND RESULTS: Primary endothelial cells from dermal blood and lymphatic vessels (BECs and LECs) were exposed to low-rate steady laminar flow...
February 6, 2017: Circulation Research
https://www.readbyqxmd.com/read/28165446/identification-of-bpifa1-splunc1-as-an-epithelium-derived-smooth-muscle-relaxing-factor
#6
Tongde Wu, Julianne Huang, Patrick J Moore, Michael S Little, William G Walton, Robert C Fellner, Neil E Alexis, Y Peter Di, Matthew R Redinbo, Stephen L Tilley, Robert Tarran
Asthma is a chronic airway disease characterized by inflammation, mucus hypersecretion and abnormal airway smooth muscle (ASM) contraction. Bacterial permeability family member A1, BPIFA1, is a secreted innate defence protein. Here we show that BPIFA1 levels are reduced in sputum samples from asthmatic patients and that BPIFA1 is secreted basolaterally from healthy, but not asthmatic human bronchial epithelial cultures (HBECs), where it suppresses ASM contractility by binding to and inhibiting the Ca(2+) influx channel Orai1...
February 6, 2017: Nature Communications
https://www.readbyqxmd.com/read/28164587/high-expression-of-orai1-enhances-cell-proliferation-and-is-associated-with-poor-prognosis-in-human-colorectal-cancer
#7
Lin Gui, Zhenjun Wang, Jiagang Han, Huachong Ma, Zhulin Li
BACKGROUND: Store-operated Ca2+ entry (SOCE) is the predominant Ca2+ influx mechanism in non-excitable cells and regulates a variety of cellular functions. As the essential channel pore-forming protein of SOCE, Orai1 has recently been implicated in carcinogenesis and tumor progression in multiple malignancies. However, the role of Orai1 in colorectal cancer (CRC) has not been investigated. METHODS: The expression of Orai1 in 21 CRC specimens was examined by immunohistochemistry (IHC) staining, Western blot, and qRT-PCR...
September 1, 2016: Clinical Laboratory
https://www.readbyqxmd.com/read/28145580/sp-2-iminosugar-%C3%AE-glucosidase-inhibitor-1-c-octyl-2-oxa-3-oxocastanospermine-specifically-affected-breast-cancer-cell-migration-through-stim1-%C3%AE-1-integrin-and-fak-signaling-pathways
#8
Nahla Gueder, Ghada Allan, Marie-Sophie Telliez, Frédéric Hague, José M Garcia Fernandez, Elena M Sanchez-Fernandez, Carmen Ortiz-Mellet, Ahmed Ahidouch, Halima Ouadid-Ahidouch
Aberrant glycosylation changes on many glycoproteins are often related to cancer progression and metastasis. sp(2) -Iminosugar-type castanospermine analogues, inhibitors of α-glucosidases, have been reported to exhibit antitumor activity. However, their effects on cell migration and the underlying molecular mechanism are not fully understood. Here, we investigated the effect of the pseudo- C-octyl glycoside 2-oxa-3-oxocastanospermine derivatives (CO-OCS) on breast cancer cells (MCF-7 and MDA-MB-231 cells), and MCF-10A mammary normal cell lines...
February 1, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28132808/store-operated-ca-2-entry-controls-induction-of-lipolysis-and-the-transcriptional-reprogramming-to-lipid-metabolism
#9
Mate Maus, Mario Cuk, Bindi Patel, Jayson Lian, Mireille Ouimet, Ulrike Kaufmann, Jun Yang, Rita Horvath, Hue-Tran Hornig-Do, Zofia M Chrzanowska-Lightowlers, Kathryn J Moore, Ana Maria Cuervo, Stefan Feske
Ca(2+) signals were reported to control lipid homeostasis, but the Ca(2+) channels and pathways involved are largely unknown. Store-operated Ca(2+) entry (SOCE) is a ubiquitous Ca(2+) influx pathway regulated by stromal interaction molecule 1 (STIM1), STIM2, and the Ca(2+) channel ORAI1. We show that SOCE-deficient mice accumulate pathological amounts of lipid droplets in the liver, heart, and skeletal muscle. Cells from patients with loss-of-function mutations in STIM1 or ORAI1 show a similar phenotype, suggesting a cell-intrinsic role for SOCE in the regulation of lipid metabolism...
January 21, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28130257/hydrogen-peroxide-is-a-critical-regulator-of-the-hypoxia-induced-alterations-of-store-operated-ca2-entry-into-rat-pulmonary-arterial-smooth-muscle-cells
#10
Taoxiang Chen, Xiaoya Xu, Zhao Zhao, Fangyu Zhao, Yimei Gao, Xiaohong Yan, Yu Wan
To investigate the association between store-operated Ca2+ entry (SOCE) and reactive oxygen species (ROS) during hypoxia, this study determined the changes of transient receptor potential canonical 1 (TRPC1) and Orai1, two candidate proteins for store-operated Ca2+ (SOC) channels and their gate regulator, stromal interaction molecule 1 (STIM1) in a hypoxic environment and their relationship with ROS in pulmonary arterial smooth muscle cells (PASMCs). Exposing to hypoxia, a transient Ca2+ spike and subsequent Ca2+ plateau of SOCE in PASMCs were intensified when TRPC1, STIM1 and Orai1 were upregulated...
January 27, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28126709/enhanced-store-operated-ca2-influx-and-orai1-expression-in-ventricular-fibroblasts-from-human-failing-heart
#11
Gracious R Ross, Tanvir Bajwa, Stacie Edwards, Larisa Emelyanova, Farhan Rizvi, Ekhson L Holmuhamedov, Paul Werner, Francis X Downey, A Jamil Tajik, Arshad Jahangir
Excessive cardiac fibrosis, characterized by increased collagen-rich extracellular matrix (ECM) deposition, is a major predisposing factor for mechanical and electrical dysfunction in heart failure (HF). The human ventricular fibroblast (hVF) remodeling mechanisms that cause excessive collagen deposition in HF are unclear, although reports suggest a role for [Ca(2+)]i in fibrosis. Therefore, we determined the association of differences in cellular Ca(2+) dynamics and collagen secretion/deposition between hVFs from failing and normal (control) hearts...
January 26, 2017: Biology Open
https://www.readbyqxmd.com/read/28114279/the-sigmar1-chaperone-drives-breast-and-colorectal-cancer-cell-migration-by-tuning-sk3-dependent-ca-2-homeostasis
#12
M Gueguinou, D Crottès, A Chantôme, R Rapetti-Mauss, M Potier-Cartereau, L Clarysse, A Girault, Y Fourbon, P Jézéquel, C Guérin-Charbonnel, G Fromont, P Martin, B Pellissier, R Schiappa, E Chamorey, O Mignen, A Uguen, F Borgese, C Vandier, O Soriani
The remodeling of calcium homeostasis contributes to the cancer hallmarks and the molecular mechanisms involved in calcium channel regulation in tumors remain to be characterized. Here, we report that SigmaR1, a stress-activated chaperone, is required to increase calcium influx by triggering the coupling between SK3, a Ca(2+)-activated K(+) channel (KCNN3) and the voltage-independent calcium channel Orai1. We show that SigmaR1 physically binds SK3 in BC cells. Inhibition of SigmaR1 activity, either by molecular silencing or by the use of sigma ligand (igmesine), decreased SK3 current and Ca(2+) entry in breast cancer (BC) and colorectal cancer (CRC) cells...
January 23, 2017: Oncogene
https://www.readbyqxmd.com/read/28108030/pore-opening-mechanism-of-crac-channels
#13
REVIEW
Priscilla S-W Yeung, Megumi Yamashita, Murali Prakriya
Three decades ago, James W. Putney Jr. conceptualized the idea of store-operated calcium entry (SOCE) to explain how depletion of endoplasmic reticulum (ER) Ca(2+) stores evokes Ca(2+) influx across the plasma membrane. Since the publication of this highly influential idea, it is now established that SOCE is universal among non-excitable and probably even many types of excitable cells, and contributes to numerous effector functions impacting immunity, muscle contraction, and brain function. The molecules encoding SOCE, the STIM and Orai proteins, are now known and our understanding of how this pathway is activated in response to ER Ca(2+) store depletion has advanced significantly...
December 23, 2016: Cell Calcium
https://www.readbyqxmd.com/read/28089266/trpc1-orai1-and-stim1-in-soce-friends-in-tight-spaces
#14
REVIEW
Indu S Ambudkar, Lorena Brito de Souza, Hwei Ling Ong
Store-operated calcium entry (SOCE) is a ubiquitous Ca(2+) entry pathway that is activated in response to depletion of ER-Ca(2+) stores and critically controls the regulation of physiological functions in miscellaneous cell types. The transient receptor potential canonical 1 (TRPC1) is the first member of the TRPC channel subfamily to be identified as a molecular component of SOCE. While TRPC1 has been shown to contribute to SOCE and regulate various functions in many cells, none of the reported TRPC1-mediated currents resembled ICRAC, the highly Ca(2+)-selective store-dependent current first identified in lymphocytes and mast cells...
December 30, 2016: Cell Calcium
https://www.readbyqxmd.com/read/28087343/calcium-remodeling-in-colorectal-cancer
#15
REVIEW
Carlos Villalobos, Diego Sobradillo, Miriam Hernández-Morales, Lucía Núñez
: Colorectal cancer (CRC) is the third most frequent form of cancer and the fourth leading cause of cancer-related death in the world. Basic and clinical data indicate that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) may prevent colon cancer but mechanisms remain unknown. Aspirin metabolite salicylate and other NSAIDs may inhibit tumor cell growth acting on store-operated Ca(2+) entry (SOCE), suggesting an important role for this pathway in CRC. Consistently, SOCE is emerging as a novel player in different forms of cancer, including CRC...
January 10, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28087079/the-stim-orai-coupling-interface-and-gating-of-the-orai1-channel
#16
REVIEW
Yandong Zhou, Xiangyu Cai, Robert M Nwokonko, Natalia A Loktionova, Youjun Wang, Donald L Gill
In virtually all cells, store-operated Ca(2+) entry signals are vital in controlling a spectrum of functions. The signals are mediated by STIM proteins in the ER and Orai channels in the PM which undergo a dynamic coupling process within discrete ER-PM junctional regions. This coupling is initiated by depletion of ER stored Ca(2+) triggering STIM proteins to undergo an intricate activation process. Thereafter, STIM proteins become trapped in the ER-PM junctions where they tether and gate PM Orai Ca(2+) channels...
January 8, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28058752/orai1-mutations-with-distinct-channel-gating-defects-in-tubular-aggregate-myopathy
#17
Johann Böhm, Monica Bulla, Jill E Urquhart, Edoardo Malfatti, Simon G Williams, James O'Sullivan, Anastazja Szlauer, Catherine Koch, Giovanni Baranello, Marina Mora, Michela Ripolone, Raffaella Violano, Maurizio Moggio, Helen Kingston, Timothy Dawson, Christian G DeGoede, John Nixon, Anne Boland, Jean-François Deleuze, Norma Romero, William G Newman, Nicolas Demaurex, Jocelyn Laporte
Calcium (Ca(2+) ) is a physiological key factor, and the precise modulation of free cytosolic Ca(2+) levels regulates multiple cellular functions. Store-operated Ca(2+) entry (SOCE) is a major mechanism controlling Ca(2+) homeostasis, and is mediated by the concerted activity of the Ca(2+) sensor STIM1 and the Ca(2+) channel ORAI1. Dominant gain-of-function mutations in STIM1 or ORAI1 cause tubular aggregate myopathy (TAM) or Stormorken syndrome, while recessive loss-of-function mutations are associated with immunodeficiency...
January 6, 2017: Human Mutation
https://www.readbyqxmd.com/read/28057434/atopic-dermatitis-immune-deviation-barrier-dysfunction-ige-autoreactivity-and-new-therapies
#18
REVIEW
Masutaka Furue, Takahito Chiba, Gaku Tsuji, Dugarmaa Ulzii, Makiko Kido-Nakahara, Takeshi Nakahara, Takafumi Kadono
Atopic dermatitis (AD) is a chronic or chronically relapsing, eczematous, severely pruritic skin disorder mostly associated with IgE elevation and skin barrier dysfunction due to decreased filaggrin expression. The lesional skin of AD exhibits Th2- and Th22-deviated immune reactions that are progressive during disease chronicity. Th2 and Th22 cytokines further deteriorate the skin barrier by inhibiting filaggrin expression. Some IgEs are reactive to self-antigens. The IgE autoreactivity may precipitate the chronicity of AD...
January 2, 2017: Allergology International: Official Journal of the Japanese Society of Allergology
https://www.readbyqxmd.com/read/28043696/regulation-of-crac-channels-by-ca-2-dependent-inactivation
#19
REVIEW
Anant B Parekh
CRAC channels are a major route for Ca(2+) influx in eukaryotic cells. The channels show prominent Ca(2+)-dependent inactivation through two spatially and temporally distinct mechanisms: fast inactivation, which develops over milliseconds and is triggered by Ca(2+) near the mouth of the channel and slow inactivation, which arises over tens of seconds and requires a rise in global cytosolic Ca(2+). Slow inactivation is controlled physiologically by Ca(2+) uptake into mitochondria through the MCU. Site-directed mutagenesis studies on STIM1 and Orai1 have led to new molecular insight into how fast inactivation occurs...
December 16, 2016: Cell Calcium
https://www.readbyqxmd.com/read/28027799/regulation-of-epithelial-ion-transport-in-exocrine-glands-by-store-operated-ca-2-entry
#20
REVIEW
Axel R Concepcion, Stefan Feske
Store-operated Ca(2+) entry (SOCE) is a conserved mechanism of Ca(2+) influx that regulates Ca(2+) signaling in many cell types. SOCE is activated by depletion of endoplasmic reticulum (ER) Ca(2+) stores in response to physiological agonist stimulation. After it was first postulated by J.W. Putney Jr. in 1986, SOCE has been described in a large number of non-excitable cell types including secretory cells of different exocrine glands. Here we discuss the mechanisms by which SOCE controls salt and fluid secretion in exocrine glands, with a special focus on eccrine sweat glands...
December 21, 2016: Cell Calcium
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