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https://www.readbyqxmd.com/read/28247021/store-operated-calcium-entry-is-essential-for-glial-calcium-signalling-in-cns-white-matter
#1
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/28222911/store-operated-ca-2-entry-is-not-required-for-fertilization-induced-ca-2-signaling-in-mouse-eggs
#2
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/28202489/nicotinamide-phosphoribosyltransferase-promotes-pulmonary-vascular-remodeling-and-is-a-therapeutic-target-in-pulmonary-arterial-hypertension
#3
Jiwang Chen, Justin R Sysol, Sunit Singla, Shuangping Zhao, Aya Yamamura, Daniela Valdez-Jasso, Taimur Abbasi, Krystyna M Shioura, Sakshi Sahni, Vamsi Reddy, Arvind Sridhar, Hui Gao, Jaime Torres, Sara M Camp, Haiyang Tang, Shui Quing Ye, Suzy Comhair, Raed Dweik, Paul Hassoun, Jason X-J Yuan, Joe G N Garcia, Roberto F Machado
Background -Pulmonary arterial hypertension (PAH) is a severe and progressive disease, a hallmark of which is pulmonary vascular remodeling. Nicotinamide phosphoribosyltransferase (NAMPT), is a cytozyme which regulates intracellular NAD levels and cellular redox state, regulates histone deacetylases, promotes cell proliferation and inhibits apoptosis. We hypothesized that NAMPT promotes pulmonary vascular remodeling, and that inhibition of NAMPT could attenuate pulmonary hypertension. Methods -Plasma and mRNA and protein levels of NAMPT were measured in the lungs and isolated pulmonary artery endothelial cells (PAECs) from PAH patients, as well as in lungs of rodent models of pulmonary hypertension (PH)...
February 15, 2017: Circulation
https://www.readbyqxmd.com/read/28132808/store-operated-ca-2-entry-controls-induction-of-lipolysis-and-the-transcriptional-reprogramming-to-lipid-metabolism
#4
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...
March 7, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28087881/role-of-stim2-in-cell-function-and-physiopathology
#5
Alejandro Berna-Erro, Isaac Jardin, Gines M Salido, Juan A Rosado
An endoplasmic reticulum (ER)-resident protein that regulates cytosolic and ER free-Ca(2+) concentration by induction of store-operated calcium entry: that is the original definition of STIM2 and its function. While its activity strongly depends on the amount of calcium stored in the ER, its function goes further, to intracellular signalling and gene expression. Initially under-studied owing to the prominent function of STIM1, STIM2 came to be regarded as vital in mice, gradually emerging as an important player in the nervous system, and cooperating with STIM1 in the immune system...
January 14, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28087343/calcium-remodeling-in-colorectal-cancer
#6
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/28030855/a-rare-de-novo-interstitial-duplication-at-4p15-2-in-a-boy-with-severe-congenital-heart-defects-limb-anomalies-hypogonadism-and-global-developmental-delay
#7
Liyang Liang, Yingjun Xie, Yiping Shen, Qibin Yin, Haiming Yuan
Proximal 4p deletion syndrome is a relatively rare genetic condition characterized by dysmorphic facial features, limb anomalies, minor congenital heart defects, hypogonadism, cafe-au-lait spots, developmental delay, tall and thin habitus, and intellectual disability. At present, over 20 cases of this syndrome have been published. However, duplication of the same region in proximal 4p has never been reported. Here, we describe a 2-year-5-month-old boy with severe congenital heart defects, limb anomalies, hypogonadism, distinctive facial features, pre- and postnatal developmental delay, and mild cognitive impairments...
2016: Cytogenetic and Genome Research
https://www.readbyqxmd.com/read/28018223/pharmacological-characterization-of-the-native-store-operated-calcium-channels-of-cortical-neurons-from-embryonic-mouse-brain
#8
Sylvain Chauvet, Louis Jarvis, Mireille Chevallet, Niroj Shrestha, Klaus Groschner, Alexandre Bouron
In the murine brain, the first post-mitotic cortical neurons formed during embryogenesis express store-operated channels (SOCs) sensitive to Pyr3, initially proposed as a blocker of the transient receptor potential channel of C type 3 (TRPC3 channel). However, Pyr3 does not discriminate between Orai and TRPC3 channels, questioning the contribution of TRPC3 in SOCs. This study was undertaken to clarify the molecular identity and the pharmacological profile of native SOCs from E13 cortical neurons. The mRNA expression of STIM1-2 and Orai1-3 was assessed by quantitative reverse transcription polymerase chain reaction...
2016: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/27913208/the-functions-of-store-operated-calcium-channels
#9
REVIEW
James W Putney, Natacha Steinckwich-Besançon, Takuro Numaga-Tomita, Felicity M Davis, Pooja N Desai, Diane M D'Agostin, Shilan Wu, Gary S Bird
Store-operated calcium channels provide calcium signals to the cytoplasm of a wide variety of cell types. The basic components of this signaling mechanism include a mechanism for discharging Ca(2+) stores (commonly but not exclusively phospholipase C and inositol 1,4,5-trisphosphate), a sensor in the endoplasmic reticulum that also serves as an activator of the plasma membrane channel (STIM1 and STIM2), and the store-operated channel (Orai1, 2 or 3). The advent of mice genetically altered to reduce store-operated calcium entry globally or in specific cell types has provided important tools to understand the functions of these widely encountered channels in specific and clinically important physiological systems...
November 30, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27881772/store-operated-calcium-channel-complex-in-postsynaptic-spines-a-new-therapeutic-target-for-alzheimer-s-disease-treatment
#10
Hua Zhang, Suya Sun, Lili Wu, Ekaterina Pchitskaya, Olga Zakharova, Klementina Fon Tacer, Ilya Bezprozvanny
Mushroom dendritic spine structures are essential for memory storage and the loss of mushroom spines may explain memory defects in aging and Alzheimer's disease (AD). The stability of mushroom spines depends on stromal interaction molecule 2 (STIM2)-mediated neuronal-store-operated Ca(2+) influx (nSOC) pathway, which is compromised in AD mouse models, in aging neurons, and in sporadic AD patients. Here, we demonstrate that the Transient Receptor Potential Canonical 6 (TRPC6) and Orai2 channels form a STIM2-regulated nSOC Ca(2+) channel complex in hippocampal mushroom spines...
November 23, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27826230/ampa-receptors-are-involved-in-store-operated-calcium-entry-and-interact-with-stim-proteins-in-rat-primary-cortical-neurons
#11
Joanna Gruszczynska-Biegala, Maria Sladowska, Jacek Kuznicki
The process of store-operated calcium entry (SOCE) leads to refilling the endoplasmic reticulum (ER) with calcium ions (Ca(2+)) after their release into the cytoplasm. Interactions between (ER)-located Ca(2+) sensors (stromal interaction molecule 1 [STIM1] and STIM2) and plasma membrane-located Ca(2+) channel-forming protein (Orai1) underlie SOCE and are well described in non-excitable cells. In neurons, however, SOCE appears to be more complex because of the importance of Ca(2+) influx via voltage-gated or ionotropic receptor-operated Ca(2+) channels...
2016: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/27721237/store-operated-ca2-entry-regulates-ca2-activated-chloride-channels-and-eccrine-sweat-gland-function
#12
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...
November 1, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27659710/emerging-pathways-driving-early-synaptic-pathology-in-alzheimer-s-disease
#13
REVIEW
Clark A Briggs, Shreaya Chakroborty, Grace E Stutzmann
The current state of the AD research field is highly dynamic is some respects, while seemingly stagnant in others. Regarding the former, our current lack of understanding of initiating disease mechanisms, the absence of effective treatment options, and the looming escalation of AD patients is energizing new research directions including a much-needed re-focusing on early pathogenic mechanisms, validating novel targets, and investigating relevant biomarkers, among other exciting new efforts to curb disease progression and foremost, preserve memory function...
February 19, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27641664/dysregulation-of-neuronal-calcium-homeostasis-in-alzheimer-s-disease-a-therapeutic-opportunity
#14
REVIEW
Elena Popugaeva, Ekaterina Pchitskaya, Ilya Bezprozvanny
Alzheimer's disease (AD) is the disease of lost memories. Synaptic loss is a major reason for memory defects in AD. Signaling pathways involved in memory loss in AD are under intense investigation. The role of deranged neuronal calcium (Ca(2+)) signaling in synaptic loss in AD is described in this review. Familial AD (FAD) mutations in presenilins are linked directly with synaptic Ca(2+) signaling abnormalities, most likely by affecting endoplasmic reticulum (ER) Ca(2+) leak function of presenilins. Excessive ER Ca(2+) release via type 2 ryanodine receptors (RyanR2) is observed in AD spines due to increase in expression and function of RyanR2...
February 19, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27617218/identification-of-trpcs-genetic-variants-that-modify-risk-for-lung-cancer-based-on-the-pathway-and-two-stage-study
#15
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
https://www.readbyqxmd.com/read/27572320/deficient-for-endoplasmic-reticulum-calcium-sensors-stim1-and-stim2-affects-aberrant-antibody-affinity-maturation-in-b-cells
#16
Xuhua Mao, Jianfeng Zhang, Yue Han, Chao Luan, Yu Hu, Zhimin Hao, Min Chen
Antigen specific B cells undergo a process termed affinity maturation in the germinal centers of secondary lymphoid organs where B cells with high affinity receptors are selected to mature into antibody-producing cells or to the memory B cell pool. It is known that B cell antigen receptor (BCR) signaling plays pivotal role in this selection process. Calcium influx is an essential component of BCR signaling. The current report is to determine the effect of calcium influx on antibody affinity maturation. In our studies, mice deficient for both endoplasmic reticulum calciumsensor Stim1 and Stim2 was immunized with T-cell dependent and independent antigens...
September 20, 2016: Oncotarget
https://www.readbyqxmd.com/read/27544849/stim2-regulates-ampa-receptor-trafficking-and-plasticity-at-hippocampal-synapses
#17
Kenrick An Fu Yap, Mahesh Shivarama Shetty, Gisela Garcia-Alvarez, Bo Lu, Durgadevi Alagappan, Masatsugu Oh-Hora, Sreedharan Sajikumar, Marc Fivaz
STIM2 is an integral membrane protein of the endoplasmic reticulum (ER) that regulates the activity of plasma membrane (PM) channels at ER-PM contact sites. Recent studies show that STIM2 promotes spine maturation and surface expression of the AMPA receptor (AMPAR) subunit GluA1, hinting at a probable role in synaptic plasticity. Here, we used a Stim2 cKO mouse to explore the function of STIM2 in Long-Term Potentiation (LTP) and Depression (LTD), two widely-studied models of synaptic plasticity implicated in information storage...
August 18, 2016: Neurobiology of Learning and Memory
https://www.readbyqxmd.com/read/27393042/the-role-of-the-store-operated-calcium-entry-channel-orai1-in-cultured-rat-hippocampal-synapse-formation-and-plasticity
#18
Eduard Korkotian, Efrat Oni-Biton, Menahem Segal
KEY POINTS: The role of non-synaptic calcium entry in the formation and functions of dendritic spines was studied in dissociated cultured rat hippocampal neurons. Orai1, a store-operated calcium channel, is found in dendritic spines. Orai1 co-localizes in dendritic spines with STIM2 under conditions of lower [Ca(2+) ]o. Orai1 channels are associated with the formation of new dendritic spines in response to elevated [Ca(2+) ]o. Lack of Orai1, either by transfection with a dominant negative construct or with small interfering RNA to Orai1, results in retarded dendritic spines, an increase in density of filopodia, lower synaptic connectivity and the ability to undergo plastic changes...
January 1, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/27281129/targeting-stim-and-orai-proteins-as-an-alternative-approach-in-anticancer-therapy
#19
REVIEW
Francesco Moccia, Estella Zuccolo, Valentina Poletto, Ilaria Turin, Germano Guerra, Paolo Pedrazzoli, Vittorio Rosti, Camillo Porta, Daniela Montagna
An increase in intracellular Ca2+ concentration plays a key role in the establishment of many cancer hallmarks, including aberrant proliferation, migration, invasion, resistance to apoptosis and angiogenesis. The dysregulation of Ca2+ entry is one of the most subtle mechanisms by which cancer cells overwhelm their normal counterparts and gain the adaptive advantages that result in tumour growth, vascularisation and dissemination throughout the organism. Both constitutive and agonist-induced Ca2+ influx may be mediated by store-dependent as well as store-independent Ca2+ entry routes...
2016: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/27261277/store-operated-ca-2-entry-in-follicular-t-cells-controls-humoral-immune-responses-and-autoimmunity
#20
Martin Vaeth, Miriam Eckstein, Patrick J Shaw, Lina Kozhaya, Jun Yang, Friederike Berberich-Siebelt, Robert Clancy, Derya Unutmaz, Stefan Feske
T follicular helper (Tfh) cells promote affinity maturation of B cells in germinal centers (GCs), whereas T follicular regulatory (Tfr) cells limit the GC reaction. Store-operated Ca(2+) entry (SOCE) through Ca(2+) release-activated Ca(2+) (CRAC) channels mediated by STIM and ORAI proteins is a fundamental signaling pathway in T lymphocytes. Conditional deletion of Stim1 and Stim2 genes in T cells abolished SOCE and strongly reduced antibody-mediated immune responses following viral infection caused by impaired differentiation and function of Tfh cells...
June 21, 2016: Immunity
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