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https://www.readbyqxmd.com/read/28707074/presenilin-1-delta-e9-mutant-induces-stim1-driven-store-operated-calcium-channel-hyperactivation-in-hippocampal-neurons
#1
Maria Ryazantseva, Anna Goncharova, Kseniia Skobeleva, Maksim Erokhin, Axel Methner, Pavel Georgiev, Elena Kaznacheyeva
Presenilins regulate calcium homeostasis in the endoplasmic reticulum, and dysregulation of intracellular calcium has been implicated in the pathogenesis of Alzheimer disease. Elevated presenilin-1 (PS1) holoprotein levels have been detected in postmortem brains of patients carrying familial Alzheimer disease (FAD) PS1 mutations. This study examines the effect of the FAD presenilin mutant that lacks the ninth exon (PS1 ∆E9) and does not undergo endoproteolysis on store-operated calcium (SOC) entry. Significant enhancement of SOC channel activation was detected by electrophysiological measurements in hippocampal neurons with PS1 ∆E9 mutant expression...
July 13, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28629579/role-of-soce-architects-stim-and-orai-proteins-in-cell-death
#2
REVIEW
Jyoti Tanwar, Rajender K Motiani
Calcium (Ca(2+)) signaling plays a critical role in regulating plethora of cellular functions including cell survival, proliferation and migration. The perturbations in cellular Ca(2+) homeostasis can lead to cell death either by activating autophagic pathways or through induction of apoptosis. Endoplasmic reticulum (ER) is the major storehouse of Ca(2+) within cells and a number of physiological agonists mediate ER Ca(2+) release by activating IP3 receptors (IP3R). This decrease in ER Ca(2+) levels is sensed by STIM, which physically interacts and activates plasma membrane Ca(2+) selective Orai channels...
June 9, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28615316/orai-calcium-channels
#3
REVIEW
Mohamed Trebak, James W Putney
In this review article, we discuss the different gene products and translational variants of ORAI proteins and their contribution to the makeup of different native calcium-conducting channels with distinct compositions and modes of activation. We also review the different modes of regulation of these distinct calcium channels and their impact on downstream cellular signaling controlling important physiological functions.
July 2017: Physiology
https://www.readbyqxmd.com/read/28592415/role-of-stim1-stromal-interaction-molecule-1-in-hypertrophy-related-contractile-dysfunction
#4
Constantine D Troupes, Markus Wallner, Giulia Borghetti, Chen Zhang, Sadia Mohsin, Dirk von Lewinski, Remus M Berretta, Hajime Kubo, Xiongwen Chen, Jonathan Soboloff, Steven Houser
RATIONALE: Pathological increases in cardiac afterload result in myocyte hypertrophy with changes in myocyte electrical and mechanical phenotype. Remodeling of contractile and signaling Ca(2+) occurs in pathological hypertrophy and is central to myocyte remodeling. STIM1 (stromal interaction molecule 1) regulates Ca(2+) signaling in many cell types by sensing low endoplasmic reticular Ca(2+) levels and then coupling to plasma membrane Orai channels to induce a Ca(2+) influx pathway. Previous reports suggest that STIM1 may play a role in cardiac hypertrophy, but its role in electrical and mechanical phenotypic alterations is not well understood...
July 7, 2017: Circulation Research
https://www.readbyqxmd.com/read/28591300/risk-factors-for-unstable-blood-glucose-level-integrative-review-of-the-risk-factors-related-to-the-nursing-diagnosis
#5
Andressa Magalhães Teixeira, Rosangela Tsukamoto, Camila Takáo Lopes, Rita de Cassia Gengo E Silva
Objective: to identify evidence in the literature on the possible risk factors for the risk of unstable blood glucose diagnosis in individuals with type 2 diabetes mellitus, and to compare them with the risk factors described by NANDA International. Method: an integrative literature review guided by the question: what are the risk factors for unstable blood glucose level in people with type 2 diabetes mellitus? Primary studies were included whose outcomes were variations in glycemic levels, published in English, Portuguese or Spanish, in PubMed or CINAHL between 2010 and 2015...
June 5, 2017: Revista Latino-americana de Enfermagem
https://www.readbyqxmd.com/read/28546857/chloroquine-inhibits-ca-2-permeable-ion-channels-mediated-ca-2-signaling-in-primary-b-lymphocytes
#6
Yi-Fan Wu, Ping Zhao, Xi Luo, Jin-Chao Xu, Lu Xue, Qi Zhou, Mingrui Xiong, Jinhua Shen, Yong-Bo Peng, Meng-Fei Yu, Weiwei Chen, Liqun Ma, Qing-Hua Liu
BACKGROUND: Chloroquine, a bitter tastant, inhibits Ca(2+) signaling, resulting in suppression of B cell activation; however, the inhibitory mechanism remains unclear. RESULTS: In this study, thapsigargin (TG), but not caffeine, induced sustained intracellular Ca(2+) increases in mouse splenic primary B lymphocytes, which were markedly inhibited by chloroquine. Under Ca(2+)-free conditions, TG elicited transient Ca(2+) increases, which additionally elevated upon the restoration of 2 mM Ca(2+)...
2017: Cell & Bioscience
https://www.readbyqxmd.com/read/28516266/constitutive-calcium-entry-and-cancer-updated-views-and-insights
#7
REVIEW
Olivier Mignen, Bruno Constantin, Marie Potier-Cartereau, Aubin Penna, Mathieu Gautier, Maxime Guéguinou, Yves Renaudineau, Kenji F Shoji, Romain Félix, Elsa Bayet, Paul Buscaglia, Marjolaine Debant, Aurélie Chantôme, Christophe Vandier
Tight control of basal cytosolic Ca(2+) concentration is essential for cell survival and to fine-tune Ca(2+)-dependent cell functions. A way to control this basal cytosolic Ca(2+) concentration is to regulate membrane Ca(2+) channels including store-operated Ca(2+) channels and secondary messenger-operated channels linked to G-protein-coupled or tyrosine kinase receptor activation. Orai, with or without its reticular STIM partner and Transient Receptor Potential (TRP) proteins, were considered to be the main Ca(2+) channels involved...
May 17, 2017: European Biophysics Journal: EBJ
https://www.readbyqxmd.com/read/28500564/calcium-signaling-from-normal-b-cell-development-to-tolerance-breakdown-and-autoimmunity
#8
REVIEW
Patrice Hemon, Yves Renaudineau, Marjolaine Debant, Nelig Le Goux, Sreya Mukherjee, Wesley Brooks, Olivier Mignen
Maintenance of self-tolerance of auto-reactive lymphocytes is a fundamental mechanism to prevent the onset of autoimmune diseases. Deciphering the mechanisms involved in the deregulations leading to tolerance disruption and autoimmunity is still a major area of interest to identify new therapeutic targets and options. Ca(2+) signaling plays a major role in B cell normal development and is therefore finely tuned by B cell receptor (BCR)-dependent and independent pathways. Developmental changes in the characteristics of BCR-dependent Ca(2+) signals as well as the modulation of basal intracellular concentration ([Ca(2+)]i) contribute strongly to self-tolerance maintaining mechanisms responsible for the physical or functional elimination of autoreactive B cells such as clonal deletion, receptor editing, and anergy...
May 13, 2017: Clinical Reviews in Allergy & Immunology
https://www.readbyqxmd.com/read/28497275/na-ca-2-exchangers-and-orai-channels-jointly-refill-endoplasmic-reticulum-er-ca-2-via-er-nanojunctions-in-vascular-endothelial-cells
#9
Cristiana M L Di Giuro, Niroj Shrestha, Roland Malli, Klaus Groschner, Cornelis van Breemen, Nicola Fameli
We investigated the role of Na(+)/ Ca(2+) exchange (NCX) in the refilling of endoplasmic reticulum (ER) Ca(2+) in vascular endothelial cells under various conditions of cell stimulation and plasma membrane (PM) polarization. Better understanding of the mechanisms behind basic ER Ca(2+) content regulation is important, since current hypotheses on the possible ultimate causes of ER stress point to deterioration of the Ca(2+) transport mechanism to/from ER itself. We measured [Ca(2+)]i temporal changes by Fura-2 fluorescence under experimental protocols that inhibit a host of transporters (NCX, Orai, non-selective transient receptor potential canonical (TRPC) channels, sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA), Na(+)/ K(+) ATPase (NKA)) involved in the Ca(2+) communication between the extracellular space and the ER...
May 11, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28489162/endoscopic-sleeve-gastroplasty-for-obesity-treatment-two-years-of-experience
#10
Gontrand Lopez-Nava, M P Galvão, I Bautista-Castaño, J P Fernandez-Corbelle, M Trell, N Lopez
Background: Bariatric endoscopic techniques are minimally invasive and induce gastric volume reduction to treat obesity. Aim : To evaluate endoscopic sleeve gastroplasty (Apollo method) using a suturing method directed at the greater curvature, as well as the perioperative care, two year safety and weight loss. Method: Prospective single-center study over 154 patients (108 females) using the endoscopic sleeve gastroplasty procedure under general anesthesia with overnight inpatient observation...
January 2017: Arquivos Brasileiros de Cirurgia Digestiva: ABCD, Brazilian Archives of Digestive Surgery
https://www.readbyqxmd.com/read/28294127/orai2-modulates-store-operated-calcium-entry-and-t-cell-mediated-immunity
#11
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/28292887/orai-and-trpc-channel-characterization-in-fc%C3%AE%C2%B5ri-mediated-calcium-signaling-and-mediator-secretion-in-human-mast-cells
#12
Hannah E Wajdner, Jasmine Farrington, Claire Barnard, Peter T Peachell, Christine G Schnackenberg, Joseph P Marino, Xiaoping Xu, Karen Affleck, Malcolm Begg, Elizabeth P Seward
Inappropriate activation of mast cells via the FcεRI receptor leads to the release of inflammatory mediators and symptoms of allergic disease. Calcium influx is a critical regulator of mast cell signaling and is required for exocytosis of preformed mediators and for synthesis of eicosanoids, cytokines and chemokines. Studies in rodent and human mast cells have identified Orai calcium channels as key contributors to FcεRI-initiated mediator release. However, until now the role of TRPC calcium channels in FcεRI-mediated human mast cell signaling has not been published...
March 2017: Physiological Reports
https://www.readbyqxmd.com/read/28262262/ca-2-influx-at-the-er-pm-junctions
#13
Woo Young Chung, Archana Jha, Malini Ahuja, Shmuel Muallem
Ca(2+) influx across the plasma membrane is a key component of the receptor-evoked Ca(2+) signaling that mediate numerous cell functions and reload the ER after partial or full ER Ca(2+) store depletion. Ca(2+) influx is activated in response to Ca(2+) release from the ER, a concept developed by Jim Putney, and the channels mediating the influx are thus called store-operated Ca(2+) influx channels, or SOCs. The molecular identity of the SOCs has been determined with the identification of the TRPC channels, STIM1 and the Orai channels...
May 2017: Cell Calcium
https://www.readbyqxmd.com/read/28247021/store-operated-calcium-entry-is-essential-for-glial-calcium-signalling-in-cns-white-matter
#14
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
#15
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
#16
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/28209043/-bortezomib-inhibits-hypoxia-induced-increase-of-orai-1-expression-in-pulmonary-arterial-smooth-muscle-cell
#17
L Xu, G Y Tian, L H Wang, Y B Liu, Z F Gao, G H Li, X H Fu
Objective: In this study, a primary culture system for the rat distal pulmonary arterial smooth muscle cell (PASMC) was established to observe the effect of Bortezomib a treatment on the basal intracellular calcium concentration ([Ca(2+) ](i)), store operated calcium entry (SOCE) and Orai-1 expression in rat PASMC. Methods: We employed the primary culture method for the rat distal PASMC including the enzymatically dissociation of PASMC from the freshly isolated distal pulmonary artery and the culture of PASMC...
February 12, 2017: Chinese Journal of Tuberculosis and Respiratory Diseases
https://www.readbyqxmd.com/read/28183802/differential-effects-of-anoctamins-on-intracellular-calcium-signals
#18
Inês Cabrita, Roberta Benedetto, Ana Fonseca, Podchanart Wanitchakool, Lalida Sirianant, Boris V Skryabin, Laura K Schenk, Hermann Pavenstädt, Rainer Schreiber, Karl Kunzelmann
The Ca(2+) activated Cl(-) channel TMEM16A [anoctamin (ANO)1] is homologous to yeast Ist2 and has been shown to tether the cortical endoplasmic reticulum (ER) to the plasma membrane. We therefore examined whether ANO1 and other members of the ANO family affect intracellular Ca(2+) ([Ca(2+)]i) signals. It is shown that expression of ANO1 augments Ca(2+) store release upon stimulation of GPCRs, whereas knockdown of ANO1, or lack of Ano1 expression in Ano1(-/-) animals as shown in an earlier report, inhibits Ca(2+) release...
February 9, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28179072/orai3-channel-is-the-2-apb-induced-endoplasmic-reticulum-calcium-leak
#19
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)...
July 2017: Cell Calcium
https://www.readbyqxmd.com/read/28155613/functional-upregulation-of-stim-1-orai-1-mediated-store-operated-ca2-contributing-to-the-hypertension-development-elicited-by-chronic-etoh-consumption
#20
Guilherme Henrique Souza Bomfim, Iago Mendez-Lopez, Juan Alberto Arranz-Tagarro, Adriana Aparecida Ferraz Carbonel, Danilo Roman-Campos, Juan Fernando Padín, Antonio Garcia Garcia, Aron Jurkiewicz, Neide Hyppolito Jurkiewicz
BACKGROUND: Chronic ethanol (EtOH) consumption has been associated with deleterious effects on the cardiovascular system by abnormal calcium (Ca2+) handling. Store-operated Ca2+ entry (SOCE) is related to cardiovascular remodeling which leads to the hypertension development, and the coupling between STIM-1 (ER Ca2+ sensor) and Orai-1 (channel pore) is a key mechanism to control SOCE through of store-operated Ca2+ channels (SOCCs). However, the role of STIM-1/Orai-1-mediated SOCE and its cross-talk with EtOH-triggered vascular remodeling and hypertension remain poorly understood...
2017: Current Vascular Pharmacology
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