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https://www.readbyqxmd.com/read/29783744/interplay-between-er-ca-2-binding-proteins-stim1-and-stim2-is-required-for-store-operated-ca-2-entry
#1
Heather A Nelson, Colin A Leech, Richard F Kopp, Michael W Roe
Store-operated calcium entry (SOCE), a fundamentally important homeostatic and Ca2+ signaling pathway in many types of cells, is activated by the direct interaction of stromal interaction molecule 1 (STIM1), an endoplasmic reticulum (ER) Ca2+ -binding protein, with Ca2+ -selective Orai1 channels localized in the plasma membrane. While much is known about the regulation of SOCE by STIM1, the role of stromal interaction molecule 2 (STIM2) in SOCE remains incompletely understood. Here, using clustered regularly interspaced short palindromic repeats -CRISPR associated protein 9 (CRISPR-Cas9) genomic editing and molecular imaging, we investigated the function of STIM2 in NIH 3T3 fibroblast and αT3 cell SOCE...
May 19, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29623030/on-the-role-of-store-operated-calcium-entry-in-acute-and-chronic-neurodegenerative-diseases
#2
REVIEW
Agnese Secondo, Giacinto Bagetta, Diana Amantea
In both excitable and non-excitable cells, calcium (Ca2+ ) signals are maintained by a highly integrated process involving store-operated Ca2+ entry (SOCE), namely the opening of plasma membrane (PM) Ca2+ channels following the release of Ca2+ from intracellular stores. Upon depletion of Ca2+ store, the stromal interaction molecule (STIM) senses Ca2+ level reduction and migrates from endoplasmic reticulum (ER)-like sites to the PM where it activates the channel proteins Orai and/or the transient receptor potential channels (TRPC) prompting Ca2+ refilling...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29581306/cross-linking-of-orai1-channels-by-stim-proteins
#3
Yandong Zhou, Robert M Nwokonko, Xiangyu Cai, Natalia A Loktionova, Raz Abdulqadir, Ping Xin, Barbara A Niemeyer, Youjun Wang, Mohamed Trebak, Donald L Gill
The transmembrane docking of endoplasmic reticulum (ER) Ca2+ -sensing STIM proteins with plasma membrane (PM) Orai Ca2+ channels is a critical but poorly understood step in Ca2+ signal generation. STIM1 protein dimers unfold to expose a discrete STIM-Orai activating region (SOAR1) that tethers and activates Orai1 channels within discrete ER-PM junctions. We reveal that each monomer within the SOAR dimer interacts independently with single Orai1 subunits to mediate cross-linking between Orai1 channels. Superresolution imaging and mobility measured by fluorescence recovery after photobleaching reveal that SOAR dimer cross-linking leads to substantial Orai1 channel clustering, resulting in increased efficacy and cooperativity of Orai1 channel function...
March 26, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29480205/inhibition-of-trpc1-dependent-store-operated-calcium-entry-improves-synaptic-stability-and-motor-performance-in-a-mouse-model-of-huntington-s-disease
#4
Jun Wu, Daniel Ryskamp, Lutz Birnbaumer, Ilya Bezprozvanny
BACKGROUND: Huntington disease (HD) is a dominantly inherited neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. We previously discovered that mutant Huntingtin sensitizes type 1 inositol 1,4,5-trisphosphate receptor (InsP3R1) to InsP3. This causes calcium leakage from the endoplasmic reticulum (ER) and a compensatory increase in neuronal store-operated calcium (nSOC) entry. We previously demonstrated that supranormal nSOC leads to synaptic loss in striatal medium spiny neurons (MSNs) in YAC128 HD mice...
2018: Journal of Huntington's Disease
https://www.readbyqxmd.com/read/29363328/molecular-physiology-and-pathophysiology-of-stromal-interaction-molecules
#5
Heather A Nelson, Michael W Roe
Ca2+ release from the endoplasmic reticulum is an important component of Ca2+ signal transduction that controls numerous physiological processes in eukaryotic cells. Release of Ca2+ from the endoplasmic reticulum is coupled to the activation of store-operated Ca2+ entry into cells. Store-operated Ca2+ entry provides Ca2+ for replenishing depleted endoplasmic reticulum Ca2+ stores and a Ca2+ signal that regulates Ca2+ -dependent intracellular biochemical events. Central to connecting discharge of endoplasmic reticulum Ca2+ stores following G protein-coupled receptor activation with the induction of store-operated Ca2+ entry are stromal interaction molecules (STIM1 and STIM2)...
March 2018: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/29358461/stim2-stromal-interaction-molecule-2-mediated-increase-in-resting-cytosolic-free-ca-2-concentration-stimulates-pasmc-proliferation-in-pulmonary-arterial-hypertension
#6
Shanshan Song, Shane G Carr, Kimberly M McDermott, Marisela Rodriguez, Aleksandra Babicheva, Angela Balistrieri, Ramon J Ayon, Jian Wang, Ayako Makino, Jason X-J Yuan
An increase in cytosolic free Ca2+ concentration ([Ca2+ ]cyt ) in pulmonary artery smooth muscle cells (PASMCs) triggers pulmonary vasoconstriction and stimulates PASMC proliferation leading to vascular wall thickening. Here, we report that STIM2 (stromal interaction molecule 2), a Ca2+ sensor in the sarcoplasmic reticulum membrane, is required for raising the resting [Ca2+ ]cyt in PASMCs from patients with pulmonary arterial hypertension (PAH) and activating signaling cascades that stimulate PASMC proliferation and inhibit PASMC apoptosis...
March 2018: Hypertension
https://www.readbyqxmd.com/read/29351410/hypoxia-selectively-upregulates-cation-channels-and-increases-cytosolic-ca-2-in-pulmonary-but-not-coronary-arterial-smooth-muscle-cells
#7
Xi He, Shanshan Song, Ramon J Ayon, Angela Balisterieri, Stephen M Black, Ayako Makino, W Gil Wier, Wei-Jin Zang, Jason X-J Yuan
Ca2+ signaling, particularly the mechanism via store-operated Ca2+ entry (SOCE) and receptor-operated Ca2+ entry (ROCE), plays a critical role in the development of acute hypoxia-induced pulmonary vasoconstriction and chronic hypoxia-induced pulmonary hypertension. This study aimed to test the hypothesis that chronic hypoxia differentially regulates the expression of proteins that mediate SOCE and ROCE [stromal interacting molecule (STIM), Orai, and canonical transient receptor potential channel TRPC6] in pulmonary (PASMC) and coronary (CASMC) artery smooth muscle cells...
April 1, 2018: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29298434/coiled-coil-formation-conveys-a-stim1-signal-from-er-lumen-to-cytoplasm
#8
Nupura Hirve, Vangipurapu Rajanikanth, Patrick G Hogan, Aparna Gudlur
STIM1 and STIM2 are endoplasmic reticulum (ER) membrane proteins that sense decreases in ER-luminal free Ca2+ and, through a conformational change in the STIM cytoplasmic domain, control gating of the plasma membrane Ca2+ channel ORAI1. To determine how STIM1 conveys a signal from the ER lumen to the cytoplasm, we studied the Ca2+ -dependent conformational change of engineered STIM1 proteins in isolated ER membranes and, in parallel, physiological activation of these proteins in cells. We find that conserved "sentinel" features of the CC1 region help to prevent activation while Ca2+ is bound to STIM ER-luminal domains...
January 2, 2018: Cell Reports
https://www.readbyqxmd.com/read/29247211/stim2-eb3-association-and-morphology-of-dendritic-spines-in-hippocampal-neurons
#9
Ekaterina Pchitskaya, Nina Kraskovskaya, Daria Chernyuk, Elena Popugaeva, Hua Zhang, Olga Vlasova, Ilya Bezprozvanny
Mushroom spines form strong synaptic contacts and are essential for memory storage. We have previously demonstrated that neuronal store-operated calcium entry (nSOC) in hippocampal neurons is regulated by STIM2 protein. This pathway plays a key role in stability of mushroom spines and is compromised in different mice models of Alzheimer's disease (AD). Actin was thought to be the sole cytoskeleton compartment presented in dendritic spines, however, recent studies demonstrated that dynamic microtubules with EB3 capped plus-ends transiently enter spines...
December 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29163766/epigallocatechin-3-gallate-egcg-up-regulates-mir-15b-expression-thus-attenuating-store-operated-calcium-entry-soce-into-murine-cd4-t-cells-and-human-leukaemic-t-cell-lymphoblasts
#10
Shaqiu Zhang, Tamer Al-Maghout, Rosi Bissinger, Ni Zeng, Lisann Pelzl, Madhuri S Salker, Anchun Cheng, Yogesh Singh, Florian Lang
CD4+ T cells are key elements in immune responses and inflammation. Activation of T cell receptors in CD4+ T cells triggers cytosolic Ca2+ release with subsequent store operated Ca2+ entry (SOCE), which is accomplished by the pore forming Ca2+ release activated Ca2+ (CRAC) channel Orai1 and its regulator stromal cell-interaction molecule 2 (STIM2). Green tea polyphenol epigallocatechin-3-gallate (EGCG) acts as a potent anti-inflammatory and anti-oxidant agent for various types of cells including immune cells...
October 27, 2017: Oncotarget
https://www.readbyqxmd.com/read/29155098/orai1-mutations-abolishing-store-operated-ca-2-entry-cause-anhidrotic-ectodermal-dysplasia-with-immunodeficiency
#11
Jayson Lian, Mario Cuk, Sascha Kahlfuss, Lina Kozhaya, Martin Vaeth, Frédéric Rieux-Laucat, Capucine Picard, Melina J Benson, Antonia Jakovcevic, Karmen Bilic, Iva Martinac, Peter Stathopulos, Imre Kacskovics, Thomas Vraetz, Carsten Speckmann, Stephan Ehl, Thomas Issekutz, Derya Unutmaz, Stefan Feske
BACKGROUND: Store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ channels is an essential signaling pathway in many cell types. Ca2+ release-activated Ca2+ channels are formed by ORAI1, ORAI2, and ORAI3 proteins and activated by stromal interaction molecule (STIM) 1 and STIM2. Mutations in the ORAI1 and STIM1 genes that abolish SOCE cause a combined immunodeficiency (CID) syndrome that is accompanied by autoimmunity and nonimmunologic symptoms. OBJECTIVE: We performed molecular and immunologic analysis of patients with CID, anhidrosis, and ectodermal dysplasia of unknown etiology...
November 16, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/29145451/stromal-interaction-molecule-1-haploinsufficiency-causes-maladaptive-response-to-pressure-overload
#12
Takayoshi Ohba, Hiroyuki Watanabe, Manabu Murakami, Kenji Iino, Takeshi Adachi, Yoshihiro Baba, Tomohiro Kurosaki, Kyoichi Ono, Hiroshi Ito
Stromal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum Ca2+ sensor, has been shown to control a Ca2+-dependent signal that promotes cardiac hypertrophy. However, whether STIM1 has adaptive role that helps to protect against cardiac overload stress remains unknown. We hypothesized that STIM1 deficiency causes a maladaptive response to pressure overload stress. We investigated STIM1 heterozygous KO (STIM1+/-) mice hearts, in which STIM1 protein levels decreased to 27% of wild-type (WT) with no compensatory increase in STIM2...
2017: PloS One
https://www.readbyqxmd.com/read/29054597/stim1-but-not-stim2-is-the-calcium-sensor-critical-for-sweat-secretion
#13
Chang-Yi Cui, Ji Heon Noh, Marc Michel, Myriam Gorospe, David Schlessinger
No abstract text is available yet for this article.
March 2018: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/29030115/store-operated-ca-2-entry-controls-clonal-expansion-of-t-cells-through-metabolic-reprogramming
#14
Martin Vaeth, Mate Maus, Stefan Klein-Hessling, Elizaveta Freinkman, Jun Yang, Miriam Eckstein, Scott Cameron, Stuart E Turvey, Edgar Serfling, Friederike Berberich-Siebelt, Richard Possemato, Stefan Feske
Store-operated Ca2+ entry (SOCE) is the main Ca2+ influx pathway in lymphocytes and is essential for T cell function and adaptive immunity. SOCE is mediated by Ca2+ release-activated Ca2+ (CRAC) channels that are activated by stromal interaction molecule (STIM) 1 and STIM2. SOCE regulates many Ca2+ -dependent signaling molecules, including calcineurin, and inhibition of SOCE or calcineurin impairs antigen-dependent T cell proliferation. We here report that SOCE and calcineurin regulate cell cycle entry of quiescent T cells by controlling glycolysis and oxidative phosphorylation...
October 17, 2017: Immunity
https://www.readbyqxmd.com/read/28900907/the-stim-orai-pathway-stim-orai-structures-isolated-and-in-complex
#15
REVIEW
Jinhui Zhu, Qingping Feng, Peter B Stathopulos
Considerable progress has been made elucidating the molecular mechanisms of calcium (Ca2+ ) sensing by stromal interaction molecules (STIMs) and the basis for Orai channel activity. This chapter focuses on the available high-resolution structural details of STIM and Orai proteins with respect to the regulation of store-operated Ca2+ entry (SOCE). Solution structures of the Ca2+ -sensing domains of STIM1 and STIM2 are reviewed in detail, crystal structures of cytosolic coiled-coil STIM fragments are discussed, and an overview of the closed Drosophila melanogaster Orai hexameric structure is provided...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28732182/stim1-regulates-enamel-mineralization-and-ameloblast-modulation
#16
Y Furukawa, N Haruyama, M Nikaido, M Nakanishi, N Ryu, M Oh-Hora, K Kuremoto, K Yoshizaki, Y Takano, I Takahashi
Loss-of-function mutations in the Ca(2+) release-activated Ca(2+) channel genes ORAI1 and STIM1 abolish store-operated Ca(2+) entry (SOCE) and result in ectodermal dysplasia with amelogenesis imperfecta. However, because of the limited availability of patient tissue, analyses of enamel mineralization or possible changes in ameloblast function or morphology have not been possible. Here, we generated mice with ectodermal tissue-specific deletion of Stim1 ( Stim1 cKO [conditional knockout]), Stim2 ( Stim2 cKO), and Stim1 and Stim2 ( Stim1/2 cKO) and analyzed their enamel phenotypes as compared with those of control ( Stim1/2(fl/fl)) animals...
November 2017: Journal of Dental Research
https://www.readbyqxmd.com/read/28724541/stim1-and-stim2-cooperatively-regulate-mouse-neutrophil-store-operated-calcium-entry-and-cytokine-production
#17
Regina A Clemens, Joshua Chong, Derayvia Grimes, Yongmei Hu, Clifford A Lowell
Neutrophils are key effector cells of the innate immune system. Calcium-dependent signaling pathways initiated by store-operated calcium entry (SOCE) are known to regulate neutrophil activation; however, the precise mechanism of this process remains unclear. STIM1 and STIM2 are calcium-sensing molecules that link calcium depletion of the endoplasmic reticulum with opening of plasma membrane calcium channels. Although a role for STIM1 in neutrophil SOCE and activation has been established, the function of STIM2 is unknown...
September 28, 2017: Blood
https://www.readbyqxmd.com/read/28707074/presenilin-1-delta-e9-mutant-induces-stim1-driven-store-operated-calcium-channel-hyperactivation-in-hippocampal-neurons
#18
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
#19
REVIEW
Jyoti Tanwar, Rajender K Motiani
Calcium (Ca2+ ) signaling plays a critical role in regulating plethora of cellular functions including cell survival, proliferation and migration. The perturbations in cellular Ca2+ homeostasis can lead to cell death either by activating autophagic pathways or through induction of apoptosis. Endoplasmic reticulum (ER) is the major storehouse of Ca2+ within cells and a number of physiological agonists mediate ER Ca2+ release by activating IP3 receptors (IP3 R). This decrease in ER Ca2+ levels is sensed by STIM, which physically interacts and activates plasma membrane Ca2+ selective Orai channels...
January 2018: Cell Calcium
https://www.readbyqxmd.com/read/28479254/stim1-and-stim2-differently-regulate-endogenous-ca-2-entry-and-promote-tgf-%C3%AE-induced-emt-in-breast-cancer-cells
#20
Siheng Zhang, Yutian Miao, Xianchong Zheng, Yong Gong, Jinxin Zhang, Fei Zou, Chunqing Cai
The Ca2+ sensor proteins STIM1 and STIM2 are crucial elements of store-operated calcium entry (SOCE) in breast cancer cells. Increased SOCE activity may contribute to epithelial-mesenchymal transitions (EMT) and increase cell migration and invasion. However, the roles of STIM1 and STIM2 in TGF-β-induced EMT are still unclear. In this study, we demonstrate roles of STIMs in TGF-β-induced EMT in breast cancer cells. In particular, STIM1 and STIM2 expression affected TGF-β-induced EMT by mediating SOCE in MDA-MB-231 and MCF-7 breast cancer cells...
June 17, 2017: Biochemical and Biophysical Research Communications
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