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https://www.readbyqxmd.com/read/29243589/defective-stim-mediated-store-operated-ca2-entry-in-hepatocytes-leads-to-metabolic-dysfunction-in-obesity
#1
Ana Paula Arruda, Benedicte Mengel Pers, Günes Parlakgul, Ekin Güney, Ted Goh, Erika Cagampan, Grace Yankun Lee, Renata L Goncalves, Gökhan S Hotamisligil
Defective Ca2+ handling is a key mechanism underlying hepatic endoplasmic reticulum (ER) dysfunction in obesity. ER Ca2+ level is in part monitored by the store-operated Ca2+ entry (SOCE) system, an adaptive mechanism that senses ER luminal Ca2+ concentrations through the STIM proteins and facilitates import of the ion from the extracellular space. Here, we show that hepatocytes from obese mice displayed significantly diminished SOCE as a result of impaired STIM1 translocation, which was associated with aberrant STIM1 O-GlycNAcylation...
December 15, 2017: ELife
https://www.readbyqxmd.com/read/29242293/variable-impairment-of-platelet-functions-in-patients-with-severe-genetically-linked-immune-deficiencies
#2
Magdolna Nagy, Tom G Mastenbroek, Nadine J A Mattheij, Susanne de Witt, Kenneth J Clemetson, Janbernd Kirschner, Ansgar S Schulz, Thomas Vraetz, Carsten Speckmann, Attila Braun, Judith M E M Cosemans, Barbara Zieger, Johan W M Heemskerk
In patients with dysfunctions of the Ca2+ channel ORAI1, stromal interaction molecule 1 (STIM1) or integrin-regulating kindlin-3 (FERMT3), severe immunodeficiency is frequently linked to abnormal platelet activity. In this paper, we studied in nine rare patients, including relatives, with confirmed genetic mutations of ORAI1, STIM1 or FERMT3, platelet responsiveness by multi-parameter assessment of whole blood thrombus formation under high-shear flow conditions. In platelets isolated from 5 out of 6 patients with ORAI1 or STIM1 mutations, store-operated Ca2+ entry (SOCE) was (in)completely defective compared to control platelets...
December 14, 2017: Haematologica
https://www.readbyqxmd.com/read/29241198/fam3a-protects-against-glutamate-induced-toxicity-by-preserving-calcium-homeostasis-in-differentiated-pc12-cells
#3
Qing Song, Wen-Li Gou, Yu-Liang Zou
BACKGROUND/AIMS: Stroke is the leading cause of adult disability, and glutamate-induced dysregulation of intracellular Ca2+ homeostasis is a key mechanism. FAM3A is the first member of the family with sequence similarity 3 (FAM3) gene family, and its biological function remains largely unknown. We have recently reported that FAM3A exerts protective effects against oxidative stress and mitochondrial dysfunction in HT22 cells. METHODS: Here, we investigated the protective effects of FAM3A using a glutamate-induced neuronal injury model in nerve growth factor (NGF)-differentiated PC12 cells...
December 12, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29237734/authentic-crac-channel-activity-requires-stim1-and-the-conserved-portion-of-the-orai-n-terminus
#4
Isabella Derler, Carmen Butorac, Adela Krizova, Michael Stadlbauer, Martin Muik, Marc Fahrner, Irene Frischauf, Christoph Romanin
Calcium (Ca2+) is an essential second messenger required for diverse signaling processes in immune cells. Ca2+ release-activated Ca2+ (CRAC) channels represent one main Ca2+ entry pathway into the cell. They are fully reconstituted via two proteins, the stromal interaction molecule 1 (STIM1), a Ca2+ sensor in the endoplasmic reticulum and the Ca2+ ion channel Orai in the plasma membrane. After Ca2+ store depletion, STIM1 and Orai couple to each other allowing Ca2+ influx. CRAC-/STIM1-mediated Orai channel currents display characteristic hallmarks such as high Ca2+ selectivity, an increase in current density when switching from a Ca2+-containing solution to a divalent-free Na+ one and fast Ca2+ dependent inactivation...
December 13, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29237733/communication-between-n-terminus-and-loop2-tunes-orai-activation
#5
Marc Fahrner, Saurabh K Pandey, Martin Muik, Lukas Traxler, Carmen Butorac, Michael Stadlbauer, Vasilina Zayats, Adéla Krizova, Peter Plenk, Irene Frischauf, Rainer Schindl, Hermann J Gruber, Peter Hinterdorfer, Rüdiger Ettrich, Christoph Romanin, Isabella Derler
Ca2+ release-activated Ca2+ (CRAC) channels constitute the major Ca2+ entry pathway into the cell. They are fully reconstituted via intermembrane coupling of the Ca2+ selective Orai channel and the Ca2+ sensing protein STIM1. In addition to the Orai C-terminus, the main coupling site for STIM1, the Orai N-terminus is indispensable for Orai channel gating. Although the extended transmembrane Orai N-terminal (ETON) region (Orai1: aa73-91; Orai3: aa48-65) is fully conserved in the Orai1 and Orai3 isoforms, Orai3 tolerates larger N-terminal truncations than Orai1 in retaining store-operated activation...
December 13, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29227474/a-proteolytic-fragment-of-histone-deacetylase-4-protects-the-heart-from-failure-by-regulating-the-hexosamine-biosynthetic-pathway
#6
Lorenz H Lehmann, Zegeye H Jebessa, Michael M Kreusser, Axel Horsch, Tao He, Mariya Kronlage, Matthias Dewenter, Viviana Sramek, Ulrike Oehl, Jutta Krebs-Haupenthal, Albert H von der Lieth, Andrea Schmidt, Qiang Sun, Julia Ritterhoff, Daniel Finke, Mirko Völkers, Andreas Jungmann, Sven W Sauer, Christian Thiel, Alexander Nickel, Michael Kohlhaas, Michaela Schäfer, Carsten Sticht, Christoph Maack, Norbert Gretz, Michael Wagner, Ali El-Armouche, Lars S Maier, Juan E Camacho Londoño, Benjamin Meder, Marc Freichel, Hermann-Josef Gröne, Patrick Most, Oliver J Müller, Stephan Herzig, Eileen E M Furlong, Hugo A Katus, Johannes Backs
The stress-responsive epigenetic repressor histone deacetylase 4 (HDAC4) regulates cardiac gene expression. Here we show that the levels of an N-terminal proteolytically derived fragment of HDAC4, termed HDAC4-NT, are lower in failing mouse hearts than in healthy control hearts. Virus-mediated transfer of the portion of the Hdac4 gene encoding HDAC4-NT into the mouse myocardium protected the heart from remodeling and failure; this was associated with decreased expression of Nr4a1, which encodes a nuclear orphan receptor, and decreased NR4A1-dependent activation of the hexosamine biosynthetic pathway (HBP)...
December 11, 2017: Nature Medicine
https://www.readbyqxmd.com/read/29223474/fine-tuning-of-store-operated-calcium-entry-by-fast-and-slow-ca2-dependent-inactivation-involvement-of-saraf
#7
REVIEW
Isaac Jardín, Letizia Albarran, Ginés M Salido, Jose J López, Stewart O Sage, Juan A Rosado
Store-operated Ca2+ entry (SOCE) is a functionally relevant mechanism for Ca2+ influx present in electrically excitable and non-excitable cells. Regulation of Ca2+ entry through store-operated channels is essential to maintain an appropriate intracellular Ca2+ homeostasis and prevent cell damage. Calcium-release activated channels exhibit Ca2+-dependent inactivation mediated by two temporally separated mechanisms: fast Ca2+-dependent inactivation takes effect in the order of milliseconds and involves the interaction of Ca2+ with residues in the channel pore while slow Ca2+-dependent inactivation (SCDI) develops over tens of seconds, requires a global rise in [Ca2+]cyt and is a mechanism regulated by mitochondria...
December 6, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29212003/soce-is-important-for-maintaining-sarcoplasmic-calcium-content-and-release-in-skeletal-muscle-fibers
#8
Mónika Sztretye, Nikolett Geyer, János Vincze, Dána Al-Gaadi, Tamás Oláh, Péter Szentesi, Gréta Kis, Miklós Antal, Ildikó Balatoni, László Csernoch, Beatrix Dienes
Store-operated Ca2+ entry (SOCE) is a Ca2+-entry process activated by the depletion of intracellular stores and has an important role in many cell types. In skeletal muscle, however, its role during physiological muscle activation has been controversial. To address this question, sarcoplasmic reticulum (SR) calcium release in a mouse strain with a naturally occurring mutation in the myostatin gene (Compact (Cmpt)) leading to a hypermuscular yet reduced muscle-force phenotype was compared to that in wild-type mice...
December 5, 2017: Biophysical Journal
https://www.readbyqxmd.com/read/29210464/ca2-and-lipid-signals-hold-hands-at-er-plasma-membrane-contact-sites
#9
Tamas Balla
Discovery of the STIM1 and Orai proteins as the principal components of store-operated Ca2+ entry (SOCE) has drawn attention to contact sites between the ER and the plasma membrane (PM). Such contacts between adjacent membranes of different cellular organelles, primarily between the mitochondria and the ER, had already been known as the sites where Ca2+ released from the ER can be efficiently channeled to the mitochondria and also where phosphatidylserine synthesis and transfer takes place. Recent studies have identified contact sites between virtually every organelle and the ER and the functional importance of these small specialized membrane domains is increasingly recognized...
December 6, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/29203863/orai-channels-are-critical-for-receptor-mediated-endocytosis-of-albumin
#10
Bo Zeng, Gui-Lan Chen, Eliana Garcia-Vaz, Sunil Bhandari, Nikoleta Daskoulidou, Lisa M Berglund, Hongni Jiang, Thomas Hallett, Lu-Ping Zhou, Li Huang, Zi-Hao Xu, Viji Nair, Robert G Nelson, Wenjun Ju, Matthias Kretzler, Stephen L Atkin, Maria F Gomez, Shang-Zhong Xu
Impaired albumin reabsorption by proximal tubular epithelial cells (PTECs) has been highlighted in diabetic nephropathy (DN), but little is known about the underlying molecular mechanisms. Here we find that ORAI1-3, are preferentially expressed in PTECs and downregulated in patients with DN. Hyperglycemia or blockade of insulin signaling reduces the expression of ORAI1-3. Inhibition of ORAI channels by BTP2 and diethylstilbestrol or silencing of ORAI expression impairs albumin uptake. Transgenic mice expressing a dominant-negative Orai1 mutant (E108Q) increases albuminuria, and in vivo injection of BTP2 exacerbates albuminuria in streptozotocin-induced and Akita diabetic mice...
December 4, 2017: Nature Communications
https://www.readbyqxmd.com/read/29188077/orai1-2-3-and-stim1-promote-store-operated-calcium-entry-in-pulmonary-arterial-smooth-muscle-cells
#11
Jian Wang, Chuyi Xu, Qiuyu Zheng, Kai Yang, Ning Lai, Tao Wang, Haiyang Tang, Wenju Lu
Previous studies have demonstrated that besides the classic canonical transient receptor potential channel family, Orai family and stromal interaction molecule 1 (STIM1) might also be involved in the regulation of store-operated calcium channels (SOCCs). An increase in cytosolic free Ca2+ concentration promoted by store-operated Ca2+ entry (SOCE) in pulmonary arterial smooth muscle cells (PASMCs) is a major trigger for pulmonary vasoconstriction and proliferation and migration of PASMCs. In this study, our data revealed the following: (1) in both rat distal pulmonary arteries and PASMCs, chronic hypoxia exposure upregulated the expression of Orai1 and Orai2, without affecting Orai3 and STIM1; (2) either heterozygous knockout of HIF-1α in mice or knockdown of HIF-1α in PASMCs abolished the hypoxic upregulation of Orai2, but not Orai1, suggesting the hypoxic upregulation of Orai2 depends on HIF-1α; and (3) using small interference RNA knockdown strategies, Orai1, 2, 3 and STIM1 were all shown to mediate SOCE in hypoxic PASMCs...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/29184418/fgf2-promotes-metastasis-of-uveal-melanoma-cells-via-store-operated-calcium-entry
#12
Yanyan Wang, Xiuli Bao, Zhiyong Zhang, Yi Sun, Xiyuan Zhou
Uveal melanoma (UM), the most common primary intraocular malignancy in adults, is highly metastatic and associated with dismal prognosis. Fibroblast growth factor 2 (FGF2) has been shown to induce cell proliferation and angiogenesis of melanoma and other malignancies. However, the expression of FGF2 in UM and its effects on melanoma cell migration are not well known. In this study, we found FGF2 expression was related to UM histological subtype and presence of metastasis. In vitro experiments showed that FGF2 treatment caused increased horizontal and vertical migration and F-actin cytoskeleton assembly as well as decreased adhesive activity of MUM2B cells, together with increased intracellular calcium concentration and expression of ORAI1 and STIM1 - two key regulatory proteins of store-operated calcium entry (SOCE)...
2017: OncoTargets and Therapy
https://www.readbyqxmd.com/read/29184031/transmembrane-helix-connectivity-in-orai1-controls-two-gates-for-calcium-dependent-transcription
#13
Irene Frischauf, Monika Litviňuková, Romana Schober, Vasilina Zayats, Barbora Svobodová, Daniel Bonhenry, Victoria Lunz, Sabrina Cappello, Laura Tociu, David Reha, Amrutha Stallinger, Anna Hochreiter, Teresa Pammer, Carmen Butorac, Martin Muik, Klaus Groschner, Ivan Bogeski, Rüdiger H Ettrich, Christoph Romanin, Rainer Schindl
The channel Orai1 requires Ca2+ store depletion in the endoplasmic reticulum and an interaction with the Ca2+ sensor STIM1 to mediate Ca2+ signaling. Alterations in Orai1-mediated Ca2+ influx have been linked to several pathological conditions including immunodeficiency, tubular myopathy, and cancer. We screened large-scale cancer genomics data sets for dysfunctional Orai1 mutants. Five of the identified Orai1 mutations resulted in constitutively active gating and transcriptional activation. Our analysis showed that certain Orai1 mutations were clustered in the transmembrane 2 helix surrounding the pore, which is a trigger site for Orai1 channel gating...
November 28, 2017: Science Signaling
https://www.readbyqxmd.com/read/29179526/calcium-influx-and-sperm-evoked-calcium-responses-during-oocyte-maturation-and-egg-activation
#14
REVIEW
Ya-Ru Xu, Wan-Xi Yang
Under the guidance and regulation of hormone signaling, large majority of mammalian oocytes go through twice cell cycle arrest-resumption prior to the fertilized egg splits: oocyte maturation and egg activation. Cytosolic free calcium elevations and endoplasmic reticulum calcium store alternations are actively involved in triggering the complex machineries and events during oogenesis. Among these, calcium influx had been implicated in the replenishment of endoplasmic reticulum store during oocyte maturation and calcium oscillation during egg activation...
October 24, 2017: Oncotarget
https://www.readbyqxmd.com/read/29176619/stim1-promotes-migration-phagosomal-maturation-and-antigen-cross-presentation-in-dendritic-cells
#15
Paula Nunes-Hasler, Sophia Maschalidi, Carla Lippens, Cyril Castelbou, Samuel Bouvet, Daniele Guido, Flavien Bermont, Esen Y Bassoy, Nicolas Page, Doron Merkler, Stéphanie Hugues, Denis Martinvalet, Bénédicte Manoury, Nicolas Demaurex
Antigen cross-presentation by dendritic cells (DC) stimulates cytotoxic T cell activation to promote immunity to intracellular pathogens, viruses and cancer. Phagocytosed antigens generate potent T cell responses, but the signalling and trafficking pathways regulating their cross-presentation are unclear. Here, we show that ablation of the store-operated-Ca2+-entry regulator STIM1 in mouse myeloid cells impairs cross-presentation and DC migration in vivo and in vitro. Stim1 ablation reduces Ca2+ signals, cross-presentation, and chemotaxis in mouse bone-marrow-derived DCs without altering cell differentiation, maturation or phagocytic capacity...
November 24, 2017: Nature Communications
https://www.readbyqxmd.com/read/29174092/rare-copy-number-variants-identified-in-prune-belly-syndrome
#16
Nansi S Boghossian, Robert J Sicko, Andreas Giannakou, Aggeliki Dimopoulos, Michele Caggana, Michael Y Tsai, Edwina H Yeung, Nathan Pankratz, Benjamin R Cole, Paul A Romitti, Marilyn L Browne, Ruzong Fan, Aiyi Liu, Denise M Kay, James L Mills
Prune belly syndrome (PBS), also known as Eagle-Barrett syndrome, is a rare congenital disorder characterized by absence or hypoplasia of the abdominal wall musculature, urinary tract anomalies, and cryptorchidism in males. The etiology of PBS is largely unresolved, but genetic factors are implicated given its recurrence in families. We examined cases of PBS to identify novel pathogenic copy number variants (CNVs). A total of 34 cases (30 males and 4 females) with PBS identified from all live births in New York State (1998-2005) were genotyped using Illumina HumanOmni2...
November 22, 2017: European Journal of Medical Genetics
https://www.readbyqxmd.com/read/29167149/three-dimensional-imaging-reveals-endo-sarco-plasmic-reticulum-containing-invaginations-within-the-muscle-nucleoplasm
#17
Shin-Haw Lee, Sina Hadipour-Lakmehsari, Tetsuaki Miyake, Anthony O Gramolini
The mammalian nucleus has invaginations from the cytoplasm, termed nucleoplasmic reticulum (NR). With increased resolution of cellular imaging, progress has been made in understanding the formation and function of NR. In fact, nucleoplasmic Ca2+ homeostasis has been implicated in the regulation of gene expression, DNA repair, and cell death. However, the majority of studies focus on cross-sectional or single plane analyses of NR invaginations, providing an incomplete assessment of its distribution and content...
November 22, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29166726/-interaction-between-trpc1-and-stim1-in-calcium-sensing-receptor-mediated-calcium-influx-and-nitric-oxide-production-in-human-umbilical-vein-endothelial-cells
#18
L M Wang, H Zhong, N Tang, L J Pang, C J Zhang, F He
Objective: To investigate the interaction of Ca(2+) protein TRPC1 and STIM1 in extracellular Ca(2+) -sensing receptor (CaR)-induced extracellular Ca(2+) influx and the production of nitric oxide (NO). Methods: Human umbilical vein endothelial cells (HUVECs) were cultured and incubated with CaR agonist spermine (activating store-operates cation channels (SOC) and receptor-operated channels (ROC)), CaR negative allosteric modulator Calhex231 (blocking SOC, activating ROC) and ROC analogue TPA (activating ROC, blocking SOC), protein kinase C (PKC) inhibitor Ro31-8220, PKCs and PKCμ inhibitor Go6967(activate SOC, blocking ROC), respectively...
November 24, 2017: Zhonghua Xin Xue Guan Bing za Zhi
https://www.readbyqxmd.com/read/29165691/estradiol-protects-proopiomelanocortin-neurons-against-insulin-resistance
#19
Jian Qiu, Martha A Bosch, Cecilia Meza, Uyen-Vy Navarro, Casey C Nestor, Edward J Wagner, Oline K Rønnekleiv, Martin J Kelly
Insulin resistance is at the core of the metabolic syndrome, and men exhibit a higher incidence of metabolic syndrome than women in early adult life, but this sex advantage diminishes sharply when women reach the postmenopausal state. Since 17β-estradiol (E2) augments the excitability of the anorexigenic POMC neurons, we investigated the neuroprotective effects of E2 against insulin resistance in POMC neurons from diet-induced obese (DIO) female and male mice. The efficacy of insulin to activate canonical transient receptor potential 5 (TRPC5) channels and depolarize POMC neurons was significantly reduced in DIO male but not in DIO female mice...
November 20, 2017: Endocrinology
https://www.readbyqxmd.com/read/29158474/unc93b1-interacts-with-the-calcium-sensor-stim1-for-efficient-antigen-cross-presentation-in-dendritic-cells
#20
Sophia Maschalidi, Paula Nunes-Hasler, Clarissa R Nascimento, Ignacio Sallent, Valérie Lannoy, Meriem Garfa-Traore, Nicolas Cagnard, Fernando E Sepulveda, Pablo Vargas, Ana-Maria Lennon-Duménil, Peter van Endert, Thierry Capiod, Nicolas Demaurex, Guillaume Darrasse-Jèze, Bénédicte Manoury
Dendritic cells (DC) have the unique ability to present exogenous antigens via the major histocompatibility complex class I pathway to stimulate naive CD8(+) T cells. In DCs with a non-functional mutation in Unc93b1 (3d mutation), endosomal acidification, phagosomal maturation, antigen degradation, antigen export to the cytosol and the function of the store-operated-Ca(2+)-entry regulator STIM1 are impaired. These defects result in compromised antigen cross-presentation and anti-tumor responses in 3d-mutated mice...
November 21, 2017: Nature Communications
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