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https://www.readbyqxmd.com/read/28331181/multi-walled-carbon-nanotubes-act-as-a-chemokine-and-recruit-macrophages-by-activating-the-plc-ip3-crac-channel-signaling-pathway
#1
Hui Li, Xiao-Qiu Tan, Li Yan, Bo Zeng, Jie Meng, Hai-Yan Xu, Ji-Min Cao
The impact of nanomaterials on immune cells is gaining attention but is not well documented. Here, we report a novel stimulating effect of carboxylated multi-walled carbon nanotubes (c-MWCNTs) on the migration of macrophages and uncover the underlying mechanisms, especially the upstream signaling, using a series of techniques including transwell migration assay, patch clamp, ELISA and confocal microscopy. c-MWCNTs dramatically stimulated the migration of RAW264.7 macrophages when endocytosed, and this effect was abolished by inhibiting phospholipase C (PLC) with U-73122, antagonizing the IP3 receptor with 2-APB, and blocking calcium release-activated calcium (CRAC) channels with SK&F96365...
March 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28326487/enhanced-stim1-expression-is-associated-with-acquired-chemo-resistance-of-cisplatin-in-osteosarcoma-cells
#2
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
#3
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/28301277/evidence-that-orai1-does-not-contribute-to-store-operated-trpc1-channels-in-vascular-smooth-muscle-cells
#4
Jian Shi, Francesc Miralles, Jean-Pierre Kinet, Lutz Birnbaumer, William A Large, Anthony P Albert
Ca(2+)-permeable store-operated channels (SOCs) mediate Ca(2+) entry pathways which are involved in many cellular functions such as contraction, growth, and proliferation. Prototypical SOCs are formed of Orai1 proteins and are activated by the endo/sarcoplasmic reticulum Ca(2+) sensor stromal interaction molecule 1 (STIM1). There is considerable debate about whether canonical transient receptor potential 1 (TRPC1) proteins also form store-operated channels (SOCs), and if they do, is Orai1 involved. We recently showed that stimulation of TRPC1-based SOCs involves store depletion inducing STIM1-evoked Gαq/PLCβ1 activity in contractile vascular smooth muscle cells (VSMCs)...
March 16, 2017: Channels
https://www.readbyqxmd.com/read/28296184/long-term-administration-of-pyridostigmine-attenuates-pressure-overload-induced-cardiac-hypertrophy-by-inhibiting-calcineurin-signalling
#5
Yi Lu, Ming Zhao, Jin-Jun Liu, Xi He, Xiao-Jiang Yu, Long-Zhu Liu, Lei Sun, Li-Na Chen, Wei-Jin Zang
Cardiac hypertrophy is associated with autonomic imbalance, characterized by enhanced sympathetic activity and withdrawal of parasympathetic control. Increased parasympathetic function improves ventricular performance. However, whether pyridostigmine, a reversible acetylcholinesterase inhibitor, can offset cardiac hypertrophy induced by pressure overload remains unclear. Hence, this study aimed to determine whether pyridostigmine can ameliorate pressure overload-induced cardiac hypertrophy and identify the underlying mechanisms...
March 10, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28293066/udp-induced-phagocytosis-and-atp-stimulated-chemotactic-migration-are-impaired-in-stim1-microglia-in-vitro-and-in-vivo
#6
Hye Min Lim, Heo Woon, Jung Woo Han, Yoshihiro Baba, Tomohiro Kurosaki, Min Goo Lee, Joo Young Kim
STIM1 is the only currently known intracellular calcium sensor that functions as the calcium influx regulator controlling immune cell activation. STIM1 function in immune cell calcium signalling has been studied extensively; however, its role in microglia, innate immune cells in brain, has not been fully understood. Here, we report that STIM1(-/-) murine microglia lost store-operated calcium influx and displayed aberrant immunological functions. Microglial functions regulated by chronic and global [Ca(2+)]i changes were reduced significantly, including cytokine releases and opsonin-dependent phagocytosis...
2017: Mediators of Inflammation
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
#7
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/28290212/spirodela-polyrhiza-extract-modulates-the-activation-of-atopic-dermatitis-related-ion-channels-orai1-and-trpv3-and-inhibits-mast-cell-degranulation
#8
Joo Hyun Nam, Hyo Won Jung, Young-Won Chin, Won-Mo Yang, Hyo Sang Bae, Woo Kyung Kim
CONTEXT: Spirodela polyrhiza (L.) Schleid. (Lemnaceae), Spirodelae Herba (SH), has been known to relieve inflammation, urticaria and skin symptoms including pruritus, eczema and rash. OBJECTIVE: The effects of SH extract on two calcium ion channels, Orai1 and TRPV3, and their potential as novel therapeutics for atopic dermatitis (AD) were investigated. The regulatory role of Orai1 on mast cell degranulation was evaluated. MATERIALS AND METHODS: The dried leaves of SH were extracted by 70% methanol...
December 2017: Pharmaceutical Biology
https://www.readbyqxmd.com/read/28286123/the-enhancement-of-txa2-receptors-mediated-contractile-response-in-intrarenal-artery-dysfunction-in-type-2-diabetic-mice
#9
Su-Juan Kuang, Jie-Sheng Qian, Hui Yang, Fang Rao, Xiao-Yan Chen, Meng-Zhen Zhang, Zhi-Xin Shan, Qiu-Xiong Lin, Yu-Mei Xue, Shu-Lin Wu, Li Jiang, Chun-Bo Chen, Chun-Yu Deng
Thromboxane A2 (TXA2) has been implicated in the pathogenesis of diabetic vascular complications, although the underlying mechanism remains unclear. The present study investigated the alterations in TXA2 receptor signal transduction in type 2 diabetic renal arteries. The contraction of renal arterial rings in control (db/m+) mice and type 2 diabetic (db/db) mice was measured by a Multi Myograph System. Intracellular calcium concentration ([Ca(2+)]i) in vascular smooth muscle cells was measured by Fluo-4/AM dye and confocal laser scanning microscopy...
March 9, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28262262/ca-2-influx-at-the-er-pm-junctions
#10
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...
February 20, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28258168/inhibition-of-l-type-ca-2-channels-by-trpc1-stim1-complex-is-essential-for-the-protection-of-dopaminergic-neurons
#11
Yuyang Sun, Haopeng Zhang, Senthil Selvaraj, Pramod Sukumaran, Saobo Lei, Lutz Birnbaumer, Brij B Singh
Loss of dopaminergic (DA) neurons leads to Parkinson's disease, however, the mechanism(s) for the vulnerability of DA neurons is not fully understood. We demonstrate that TRPC1 regulates the L-type Ca(2+) channel that contributes to the rhythmic activity of adult DA neurons in the substantia nigra (SN) region. Store-depletion that activates TRPC1, via STIM1, inhibits the frequency and amplitude of the rhythmic activity in DA neurons of wild-type, but not in TRPC1(-/-) mice. Similarly, TRPC1(-/-) SN neurons showed increased L-type Ca(2+) currents, decreased stimulation-dependent STIM1-Cav1...
March 3, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28247021/store-operated-calcium-entry-is-essential-for-glial-calcium-signalling-in-cns-white-matter
#12
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
#13
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
#14
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/28238652/the-er-stress-sensor-perk-coordinates-er-plasma-membrane-contact-site-formation-through-interaction-with-filamin-a-and-f-actin-remodeling
#15
Alexander R van Vliet, Francesca Giordano, Sarah Gerlo, Inmaculada Segura, Sofie Van Eygen, Geert Molenberghs, Susana Rocha, Audrey Houcine, Rita Derua, Tom Verfaillie, Jeroen Vangindertael, Herlinde De Keersmaecker, Etienne Waelkens, Jan Tavernier, Johan Hofkens, Wim Annaert, Peter Carmeliet, Afshin Samali, Hideaki Mizuno, Patrizia Agostinis
Loss of ER Ca(2+) homeostasis triggers endoplasmic reticulum (ER) stress and drives ER-PM contact sites formation in order to refill ER-luminal Ca(2+). Recent studies suggest that the ER stress sensor and mediator of the unfolded protein response (UPR) PERK regulates intracellular Ca(2+) fluxes, but the mechanisms remain elusive. Here, using proximity-dependent biotin identification (BioID), we identified the actin-binding protein Filamin A (FLNA) as a key PERK interactor. Cells lacking PERK accumulate F-actin at the cell edges and display reduced ER-PM contacts...
March 2, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28222911/store-operated-ca-2-entry-is-not-required-for-fertilization-induced-ca-2-signaling-in-mouse-eggs
#16
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/28220789/stim1-activates-crac-channels-through-rotation-of-the-pore-helix-to-open-a-hydrophobic-gate
#17
Megumi Yamashita, Priscilla S-W Yeung, Christopher E Ing, Beth A McNally, Régis Pomès, Murali Prakriya
Store-operated Ca(2+) release-activated Ca(2+) (CRAC) channels constitute a major pathway for Ca(2+) influx and mediate many essential signalling functions in animal cells, yet how they open remains elusive. Here, we investigate the gating mechanism of the human CRAC channel Orai1 by its activator, stromal interacting molecule 1 (STIM1). We find that two rings of pore-lining residues, V102 and F99, work together to form a hydrophobic gate. Mutations of these residues to polar amino acids produce channels with leaky gates that conduct ions in the resting state...
February 21, 2017: Nature Communications
https://www.readbyqxmd.com/read/28218251/stim1-phosphorylation-at-y361-recruits-orai1-to-stim1-puncta-and-induces-ca-2-entry
#18
Pascal Yazbeck, Mohammad Tauseef, Kevin Kruse, Md-Ruhul Amin, Rayees Sheikh, Stefan Feske, Yulia Komarova, Dolly Mehta
Store-operated Ca(2+) entry (SOCE) mediates the increase in intracellular calcium (Ca(2+)) in endothelial cells (ECs) that regulates several EC functions including tissue-fluid homeostasis. Stromal-interaction molecule 1 (STIM1), upon sensing the depletion of (Ca(2+)) from the endoplasmic reticulum (ER) store, organizes as puncta that trigger store-operated Ca(2+) entry (SOCE) via plasmalemmal Ca(2+)-selective Orai1 channels. While the STIM1 and Orai1 binding interfaces have been mapped, signaling mechanisms activating STIM1 recruitment of Orai1 and STIM1-Orai1 interaction remains enigmatic...
February 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28196740/dpb162-ae-an-inhibitor-of-store-operated-ca-2-entry-can-deplete-the-endoplasmic-reticulum-ca-2-store
#19
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
#20
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...
May 2017: Biochimica et Biophysica Acta
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