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https://www.readbyqxmd.com/read/28108672/stromal-interaction-molecule-1-stim1-regulates-growth-cell-cycle-and-apoptosis-of-human-tongue-squamous-carcinoma-cells
#1
Xiaobo Cui, Laixiao Song, Yunfei Bai, Yaping Wang, Boqian Wang, Wei Wang
Oral tongue squamous carcinoma (OTSCC) is the most common type of cancer of oral carcinomas. However, the molecular mechanism by which OTSCC development is not fully identified. Stromal interaction molecule 1 (STIM1) is a transmembrane protein, mainly located in the endoplasmic reticulum (ER). STIM1 is involved in several types of cancers. Here we report that STIM1 contributes to the development of human OTSCC. We knocked down STIM1 in OTSCC cell line Tca-8113 with lentivirus-mediated shRNA and found that SITM1 knockdown repressed the proliferation of Tca-8113 cells...
January 20, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28108030/pore-opening-mechanism-of-crac-channels
#2
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/28095277/long-term-follow-up-of-the-french-stop-imatinib-stim1-study-in-patients-with-chronic-myeloid-leukemia
#3
Gabriel Etienne, Joëlle Guilhot, Delphine Rea, Françoise Rigal-Huguet, Franck Nicolini, Aude Charbonnier, Agnès Guerci-Bresler, Laurence Legros, Bruno Varet, Martine Gardembas, Viviane Dubruille, Michel Tulliez, Marie-Pierre Noel, Jean-Christophe Ianotto, Bruno Villemagne, Martin Carré, François Guilhot, Philippe Rousselot, François-Xavier Mahon
Purpose Imatinib (IM) can safely be discontinued in patients with chronic myeloid leukemia (CML) who have had undetectable minimal residual disease (UMRD) for at least 2 years. We report the final results of the Stop Imatinib (STIM1) study with a long follow-up. Patients and Methods IM was prospectively discontinued in 100 patients with CML with UMRD sustained for at least 2 years. Molecular recurrence (MR) was defined as positivity of BCR-ABL transcript in a quantitative reverse transcriptase polymerase chain reaction assay confirmed by a second analysis point that indicated an increase of one log in relation to the first analysis point at two successive assessments or loss of major molecular response at one point...
January 20, 2017: Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology
https://www.readbyqxmd.com/read/28089266/trpc1-orai1-and-stim1-in-soce-friends-in-tight-spaces
#4
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/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 undercovered by the prominent function of STIM1, STIM2 became to be 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/28087079/the-stim-orai-coupling-interface-and-gating-of-the-orai1-channel
#7
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
#8
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/28043696/regulation-of-crac-channels-by-ca-2-dependent-inactivation
#9
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
#10
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
https://www.readbyqxmd.com/read/28018901/regulation-of-store-operated-ca-2-entry-by-septins
#11
Bipan K Deb, Gaiti Hasan
The mechanism of store-operated Ca(2+) entry (SOCE) brings extracellular Ca(2+) into cells after depletion of intracellular Ca(2+) stores. Regulation of Ca(2+) homeostasis by SOCE helps control various intracellular signaling functions in both non-excitable and excitable cells. Whereas essential components of the SOCE pathway are well characterized, molecular mechanisms underlying regulation of this pathway need investigation. A class of proteins recently demonstrated as regulating SOCE is septins. These are filament-forming GTPases that assemble into higher order structures...
2016: Frontiers in Cell and Developmental Biology
https://www.readbyqxmd.com/read/28018223/pharmacological-characterization-of-the-native-store-operated-calcium-channels-of-cortical-neurons-from-embryonic-mouse-brain
#12
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/28003364/stromal-interaction-molecule-1-stim1-regulates-atp-sensitive-potassium-katp-and-store-operated-ca2-channels-in-min6-%C3%AE-cells
#13
Colin A Leech, Richard F Kopp, Heather A Nelson, Jyotirmoy Nandi, Michael W Roe
Stromal interaction molecule 1 (STIM1) regulates store-operated Ca(2+) entry (SOCE) and other ion channels, either as an endoplasmic reticulum (ER) Ca(2+) sensing protein or when present in the plasma membrane. However, the role of STIM1 in insulin-secreting β-cells is unresolved. We report that lowering expression of STIM1, the gene that encodes STIM1, in insulin-secreting MIN6 β-cells with RNA interference inhibits SOCE and ATP-sensitive K(+) (KATP) channel activation. The effects of STIM1 knockdown were reversed by transduction of MIN6 cells with an adenovirus gene shuttle vector that expressed human STIM1 Immunoprecipitation studies revealed that STIM1 binds to nucleotide binding fold-1 (NBF1) of the sulfonylurea receptor 1 (SUR1) subunit of the KATP channel...
December 21, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27929067/the-stim1-binding-site-nexus-remotely-controls-orai1-channel-gating
#14
Yandong Zhou, Xiangyu Cai, Natalia A Loktionova, Xianming Wang, Robert M Nwokonko, Xizhuo Wang, Youjun Wang, Brad S Rothberg, Mohamed Trebak, Donald L Gill
The ubiquitously expressed Orai Ca(2+) channels are gated through a unique process of intermembrane coupling with the Ca(2+)-sensing STIM proteins. Despite the significance of Orai1-mediated Ca(2+) signals, how gating of Orai1 is triggered by STIM1 remains unknown. A widely held gating model invokes STIM1 binding directly to Orai1 pore-forming helix. Here we report that an Orai1 C-terminal STIM1-binding site, situated far from the N-terminal pore helix, alone provides the trigger that is necessary and sufficient for channel gating...
December 8, 2016: Nature Communications
https://www.readbyqxmd.com/read/27913208/the-functions-of-store-operated-calcium-channels
#15
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/27913207/overexpression-of-stim1-in-neurons-in-mouse-brain-improves-contextual-learning-and-impairs-long-term-depression
#16
Łukasz Majewski, Filip Maciąg, Paweł M Boguszewski, Iga Wasilewska, Grzegorz Wiera, Tomasz Wójtowicz, Jerzy Mozrzymas, Jacek Kuznicki
STIM1 is an endoplasmic reticulum calcium sensor that is involved in several processes in neurons, including store-operated calcium entry. STIM1 also inhibits voltage-gated calcium channels, such as Cav1.2 and Cav3.1, and is thus considered a multifunctional protein. The aim of this work was to investigate the ways in which transgenic neuronal overexpression of STIM1 in FVB/NJ mice affects animal behavior and the electrophysiological properties of neurons in acute hippocampal slices. We overexpressed STIM1 from the Thy1...
November 29, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27879676/calcium-dyshomeostasis-in-tubular-aggregate-myopathy
#17
REVIEW
Jong-Mok Lee, Satoru Noguchi
Calcium is a crucial mediator of cell signaling in skeletal muscles for basic cellular functions and specific functions, including contraction, fiber-type differentiation and energy production. The sarcoplasmic reticulum (SR) is an organelle that provides a large supply of intracellular Ca(2+) in myofibers. Upon excitation, it releases Ca(2+) into the cytosol, inducing contraction of myofibrils. During relaxation, it takes up cytosolic Ca(2+) to terminate the contraction. During exercise, Ca(2+) is cycled between the cytosol and the SR through a system by which the Ca(2+) pool in the SR is restored by uptake of extracellular Ca(2+) via a specific channel on the plasma membrane...
November 22, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27878958/inhibition-of-orai1-mediated-ca-2-entry-enhances-chemosensitivity-of-hepg2-hepatocarcinoma-cells-to-5-fluorouracil
#18
Bao-Dong Tang, Xin Xia, Xiao-Fei Lv, Bei-Xin Yu, Jia-Ni Yuan, Xiao-Yi Mai, Jin-Yan Shang, Jia-Guo Zhou, Si-Jia Liang, Rui-Ping Pang
Increasing evidence supports that activation of store-operated Ca(2+) entry (SOCE) is implicated in the chemoresistance of cancer cells subjected to chemotherapy. However, the molecular mechanisms underlying chemoresistance are not well understood. In this study, we aim to investigate whether 5-FU induces hepatocarcinoma cell death through regulating Ca(2+) -dependent autophagy. [Ca(2+) ]i was measured using fura2/AM dye. Protein expression was determined by Western blotting and immunohistochemistry. We found that 5-fluorouracil (5-FU) induced autophagic cell death in HepG2 hepatocarcinoma cells by inhibiting PI3K/AKT/mTOR pathway...
November 23, 2016: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/27876257/tubular-aggregate-myopathy-with-features-of-stormorken-disease-due-to-a-new-stim1-mutation
#19
Jean-Baptiste Noury, Johann Böhm, Georges Arielle Peche, Lucie Guyant-Marechal, Anne-Laure Bedat-Millet, Léa Chiche, Robert-Yves Carlier, Edoardo Malfatti, Norma B Romero, Tanya Stojkovic
STIM1 is a reticular Ca(2+) sensor composed of a luminal and a cytosolic domain. Missense mutations in the luminal domain have been associated with tubular aggregate myopathy (TAM), while cytosolic mutations can cause Stormorken syndrome, a multisystemic disease associating TAM with asplenia, thrombocytopenia, miosis, ichthyosis, short stature and dyslexia. Here we present the case of a 41-year-old female complaining of exercise intolerance. Clinical examination showed short stature, scoliosis, proximal muscle weakness with lower limb predominance, and ophthalmoplegia...
October 14, 2016: Neuromuscular Disorders: NMD
https://www.readbyqxmd.com/read/27868128/the-role-of-stim1-in-the-cr-vi-induced-ca-2-i-increase-and-cell-injury-in-l-02-hepatocytes
#20
Xing Yi, Yujing Zhang, Caigao Zhong, Xiali Zhong, Fang Xiao
Hexavalent chromium [Cr(vi)] is a potent cytotoxin and carcinogen. In recent years, drinking water contamination with Cr(vi) has become a worldwide problem of significant public health importance, thus much attention has been paid to the investigation of Cr(vi)-induced hepatotoxicity. The concentration of intracellular calcium ions ([Ca(2+)]i) was found to be increased after Cr(vi) exposure, but the exact underlying mechanisms involved in the Ca(2+) homeostasis imbalance remain poorly characterized. In the present study, by utilizing the antagonist of store-operated calcium channels (SOCCs) 2-aminoethoxydiphenyl borate (2-APB), small interfering RNA against stromal interaction molecule 1 (si-STIM1) and antioxidant N-acetylcysteine (NAC), we found that Cr(vi) induces [Ca(2+)]i increase, cell viability loss and transaminase (AST/ALT) leakage, and that these could be suppressed by both 2-APB and si-STIM1...
December 7, 2016: Metallomics: Integrated Biometal Science
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