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    2951 results match your criteria Cell Calcium[Journal]

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    The MCU complex in cell death.
    Cell Calcium 2017 Aug 25. Epub 2017 Aug 25.
    Department of Biomedical Sciences, University of Padova, Italy. Electronic address:
    During the 60s, the notion that positively charged Ca(2+) ions are rapidly accumulated in energized mitochondria has been first established. In the following decades, mitochondrial Ca(2+) homeostasis was shown to control cell metabolism, cell survival and other cell-specific functions through different mechanism. However, the molecular identity of the molecules controlling this process remained a mystery until just few years ago, when both mitochondrial Ca(2+) uptake and release systems were genetically dissected. Read More

    The regulation of autophagy by calcium signals: Do we have a consensus?
    Cell Calcium 2017 Aug 19. Epub 2017 Aug 19.
    School of Life, Health and Chemical Sciences, The Open University, MK7 6AA, UK.
    Macroautophagy (hereafter called 'autophagy') is a cellular process for degrading and recycling cellular constituents, and for maintenance of cell function. Autophagy initiates via vesicular engulfment of cellular materials and culminates in their degradation via lysosomal hydrolases, with the whole process often being termed 'autophagic flux'. Autophagy is a multi-step pathway requiring the interplay of numerous scaffolding and signalling molecules. Read More

    Mitochondrial Ca(2+)-activated K(+) channels and their role in cell life and death pathways.
    Cell Calcium 2017 Jul 22. Epub 2017 Jul 22.
    Faculty of Science and Engineering, Groningen Research Institute of Pharmacy, Department of Molecular Pharmacology, University of Groningen, 9713 AV Groningen, The Netherlands. Electronic address:
    Ca(2+)-activated K(+) channels (KCa) are expressed at the plasma membrane and in cellular organelles. Expression of all KCa channel subtypes (BK, IK and SK) has been detected at the inner mitochondrial membrane of several cell types. Primary functions of these mitochondrial KCa channels include the regulation of mitochondrial ROS production, maintenance of the mitochondrial membrane potential and preservation of mitochondrial calcium homeostasis. Read More

    Total internal reflectance fluorescence imaging of genetically engineered ryanodine receptor-targeted Ca(2+) probes in rat ventricular myocytes.
    Cell Calcium 2017 Sep 19;66:98-110. Epub 2017 Jul 19.
    Cardiac Signaling Center of University of South Carolina, Clemson University and Medical University of South Carolina, Charleston, SC 29425, USA. Electronic address:
    The details of cardiac Ca(2+) signaling within the dyadic junction remain unclear because of limitations in rapid spatial imaging techniques, and availability of Ca(2+) probes localized to dyadic junctions. To critically monitor ryanodine receptors' (RyR2) Ca(2+) nano-domains, we combined the use of genetically engineered RyR2-targeted pericam probes, (FKBP-YCaMP, Kd=150nM, or FKBP-GCaMP6, Kd=240nM) with rapid total internal reflectance fluorescence (TIRF) microscopy (resolution, ∼80nm). The punctate z-line patterns of FKBP,(2)-targeted probes overlapped those of RyR2 antibodies and sharply contrasted to the images of probes targeted to sarcoplasmic reticulum (SERCA2a/PLB), or cytosolic Fluo-4 images. Read More

    C1q/tumor necrosis factor-related protein-3 enhances the contractility of cardiomyocyte by increasing calcium sensitivity.
    Cell Calcium 2017 Sep 8;66:90-97. Epub 2017 Jul 8.
    Department of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China. Electronic address:
    C1q/tumor necrosis factor-related protein-3 (CTRP3) is an adipokine that protects against myocardial infarction-induced cardiac dysfunction through its pro-angiogenic, anti-apoptotic, and anti-fibrotic effects. However, whether CTRP3 can directly affect the systolic and diastolic function of cardiomyocytes remains unknown. Adult rat cardiomyocytes were isolated and loaded with Fura-2AM. Read More

    Structure of thrombospondin type 3 repeats in bacterial outer membrane protein A reveals its intra-repeat disulfide bond-dependent calcium-binding capability.
    Cell Calcium 2017 Sep 9;66:78-89. Epub 2017 Jun 9.
    National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, People's Republic of China; National Center for Protein Science Shanghai, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201203, People's Republic of China. Electronic address:
    Eukaryotic thrombospondin type 3 repeat (TT3R) is an efficient calcium ion (Ca(2+)) binding motif only found in mammalian thrombospondin family. TT3R has also been found in prokaryotic cellulase Cel5G, which was thought to forfeit the Ca(2+)-binding capability due to the formation of intra-repeat disulfide bonds, instead of the inter-repeat ones possessed by eukaryotic TT3Rs. In this study, we have identified an enormous number of prokaryotic TT3R-containing proteins belonging to several different protein families, including outer membrane protein A (OmpA), an important structural protein connecting the outer membrane and the periplasmic peptidoglycan layer in gram-negative bacteria. Read More

    Exocytotic fusion pores as a target for therapy.
    Cell Calcium 2017 Sep 19;66:71-77. Epub 2017 Jun 19.
    Laboratory of Neuroendocrinology-Molecular Cell Physiology, Faculty of Medicine, University of Ljubljana, Zaloška 4, 1000 Ljubljana, Slovenia; Celica Biomedical Center, Tehnološki park 24, 1000 Ljubljana, Slovenia. Electronic address:
    Regulated exocytosis can be split into a sequence of steps ending with the formation and the dilation of a fusion pore, a neck-like connection between the vesicle and the plasma membrane. Each of these steps is precisely controlled to achieve the optimal spatial and temporal profile of the release of signalling molecules. At the level of the fusion pore, tuning of the exocytosis can be achieved by preventing its formation, by stabilizing the unproductive narrow fusion pore, by altering the speed of fusion pore expansion and by completely closing the fusion pore. Read More

    Two EF-hand motifs in ryanodine receptor calcium release channels contribute to isoform-specific regulation by calmodulin.
    Cell Calcium 2017 Sep 6;66:62-70. Epub 2017 Jun 6.
    Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, United States; Cardiac Signaling Center, University of South Carolina, Medical University of South Carolina and Clemson University, Charleston, SC 29425, United States. Electronic address:
    The mammalian ryanodine receptor Ca(2+) release channel (RyR) has a single conserved high affinity calmodulin (CaM) binding domain. However, the skeletal muscle RyR1 is activated and cardiac muscle RyR2 is inhibited by CaM at submicromolar Ca(2+). This suggests isoform-specific domains are involved in RyR regulation by CaM. Read More

    Muscling in on TRP channels in vascular smooth muscle cells and cardiomyocytes.
    Cell Calcium 2017 Sep 15;66:48-61. Epub 2017 Jun 15.
    Laboratory of Ion Channel Research, TRP Research Platform Leuven (TRPLe), Department of Cellular and Molecular Medicine, KU Leuven, 3000 Leuven, Belgium. Electronic address:
    The human TRP protein family comprises a family of 27 cation channels with diverse permeation and gating properties. The common theme is that they are very important regulators of intracellular Ca(2+) signaling in diverse cell types, either by providing a Ca(2+) influx pathway, or by depolarising the membrane potential, which on one hand triggers the activation of voltage-gated Ca(2+) channels, and on the other limits the driving force for Ca(2+) entry. Here we focus on the role of these TRP channels in vascular smooth muscle and cardiac striated muscle. Read More

    Acetylcholine induces intracellular Ca(2+) oscillations and nitric oxide release in mouse brain endothelial cells.
    Cell Calcium 2017 Sep 12;66:33-47. Epub 2017 Jun 12.
    Laboratory of General Physiology, Department of Biology and Biotechnology "Lazzaro Spallanzani", University of Pavia, Pavia, Italy. Electronic address:
    Basal forebrain neurons increase cortical blood flow by releasing acetylcholine (Ach), which stimulates endothelial cells (ECs) to produce the vasodilating gasotransmitter, nitric oxide (NO). Surprisingly, the mechanism whereby Ach induces NO synthesis in brain microvascular ECs is unknown. An increase in intracellular Ca(2+) concentration recruits a multitude of endothelial Ca(2+)-dependent pathways, such as Ca(2+)/calmodulin endothelial NO synthase (eNOS). Read More

    TRPP2 ion channels: Critical regulators of organ morphogenesis in health and disease.
    Cell Calcium 2017 Sep 1;66:25-32. Epub 2017 Jun 1.
    Renal Division, Department of Medicine, Faculty of Medicine, University of Freiburg, Hugstetter Straße 55, 79106 Freiburg, Germany. Electronic address:
    Ion channels control the membrane potential and mediate transport of ions across membranes. Archetypical physiological functions of ion channels include processes such as regulation of neuronal excitability, muscle contraction, or transepithelial ion transport. In that regard, transient receptor potential ion channel polycystin 2 (TRPP2) is remarkable, because it controls complex morphogenetic processes such as the establishment of properly shaped epithelial tubules and left-right-asymmetry of organs. Read More

    TRP channel pores and local calcium signals.
    Cell Calcium 2017 Sep 30;66:19-24. Epub 2017 May 30.
    Lab of Ion Channel Research (LICR), KU Leuven, Herestraat 49, Box 802, B-3000 Leuven, Belgium. Electronic address:
    Calcium signals control a plethora of essential cellular functions ranging from secretion and contraction to gene expression and sensory signaling cascades. An essential part of intracellular calcium signals originates from the transmembrane flux of calcium ions, which is mainly mediated through different calcium-permeable cation channels with variable calcium selectivity. Opening of individual calcium permeable channels induces a local cytosolic calcium rise that can be highly restricted in time and space. Read More

    A benzothiadiazine derivative and methylprednisolone are novel and selective activators of transient receptor potential canonical 5 (TRPC5) channels.
    Cell Calcium 2017 Sep 2;66:10-18. Epub 2017 Jun 2.
    Rudolf-Boehm-Institute of Pharmacology and Toxicology, Leipzig University, Härtelstraße 16-18, 04107 Leipzig, Germany. Electronic address:
    The transient receptor potential canonical channel 5 (TRPC5) is a Ca(2+)-permeable ion channel, which is predominantly expressed in the brain. TRPC5-deficient mice exhibit a reduced innate fear response and impaired motor control. In addition, outgrowth of hippocampal and cerebellar neurons is retarded by TRPC5. Read More

    Regulation of L-type CaV1.3 channel activity and insulin secretion by the cGMP-PKG signaling pathway.
    Cell Calcium 2017 Sep 15;66:1-9. Epub 2017 May 15.
    Departamento de Biología Celular, Cinvestav-IPN, Ciudad de México, Mexico. Electronic address:
    cGMP is a second messenger widely used in the nervous system and other tissues. One of the major effectors for cGMP is the serine/threonine protein kinase, cGMP-dependent protein kinase (PKG), which catalyzes the phosphorylation of a variety of proteins including ion channels. Previously, it has been shown that the cGMP-PKG signaling pathway inhibits Ca(2+) currents in rat vestibular hair cells and chromaffin cells. Read More

    Calcium signaling and cell cycle: Progression or death.
    Cell Calcium 2017 Jul 25. Epub 2017 Jul 25.
    Université Paris Descartes, Sorbonne Paris Cité, Paris, France; Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France; Institut National de la Santé et de la Recherche Médicale, U1138, Paris, France; Université Pierre et Marie Curie, Paris, France; Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus, Villejuif, France. Electronic address:
    Cytosolic Ca(2+) concentration levels fluctuate in an ordered manner along the cell cycle, in line with the fact that Ca(2+) is involved in the regulation of cell proliferation. Cell proliferation should be an error-free process, yet is endangered by mistakes. In fact, a complex network of proteins ensures that cell cycle does not progress until the previous phase has been successfully completed. Read More

    TRPs and Ca(2+) in cell death and survival.
    Cell Calcium 2017 Jul 15. Epub 2017 Jul 15.
    Inserm U1003, Laboratory of Excellence, Ion Channels Science and Therapeutics, Equipe Labellisée par la Ligue Nationale Contre le Cancer, SIRIC ONCOLille, Université de Lille 1-Sciences et Technologies, Villeneuve d'Ascq 59656, France. Electronic address:
    Transient Receptor Potential (TRP) family mediate the influx of monovalent and/or divalent cations into cells in response to environmental stimuli. Pharmacological or genetic manipulations of TRP channels demonstrate that TRP channels influence cell death rates, prolonging or shortening of cell survival. Due to their diverse cellular localization, TRP channels mediated Ca(2+) influx generates distinct intracellular Ca(2+) signals that regulate downstream pathways converging to apoptosis or survival. Read More

    SERCA control of cell death and survival.
    Cell Calcium 2017 Jul 12. Epub 2017 Jul 12.
    Cardiovascular Research Institute, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA; Diabetes, Obesity and Metabolism Institute, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA; Graduate School of Biological Sciences, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Electronic address:
    Intracellular calcium (Ca(2+)) is a critical coordinator of various aspects of cellular physiology. It is increasingly apparent that changes in cellular Ca(2+) dynamics contribute to the regulation of normal and pathological signal transduction that controls cell growth and survival. Aberrant perturbations in Ca(2+) homeostasis have been implicated in a range of pathological conditions, such as cardiovascular diseases, diabetes, tumorigenesis and steatosis hepatitis. Read More

    Calcium signaling and molecular mechanisms underlying neurodegenerative diseases.
    Cell Calcium 2017 Jun 30. Epub 2017 Jun 30.
    Laboratory of Molecular Neurodegeneration, Department of Medical Physics, Peter The Great St. Petersburg Polytechnic University, St. Petersburg, Russian Federation; Department of Physiology, UT Southwestern Medical Center at Dallas, Dallas, TX, USA. Electronic address:
    Calcium (Ca(2+)) is a ubiquitous second messenger that regulates various activities in eukaryotic cells. Especially important role calcium plays in excitable cells. Neurons require extremely precise spatial-temporal control of calcium-dependent processes because they regulate such vital functions as synaptic plasticity. Read More

    VDAC1 functions in Ca(2+) homeostasis and cell life and death in health and disease.
    Cell Calcium 2017 Jun 23. Epub 2017 Jun 23.
    Department of Life Sciences and the National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.
    In the outer mitochondrial membrane (OMM), the voltage-dependent anion channel 1 (VDAC1) serves as a mitochondrial gatekeeper, controlling the metabolic and energy cross-talk between mitochondria and the rest of the cell. VDAC1 also functions in cellular Ca(2+) homeostasis by transporting Ca(2+) in and out of mitochondria. VDAC1 has also been recognized as a key protein in mitochondria-mediated apoptosis, contributing to the release of apoptotic proteins located in the inter-membranal space (IMS) and regulating apoptosis via association with pro- and anti-apoptotic members of the Bcl-2 family of proteins and hexokinase. Read More

    Bcl-2 inhibitors as anti-cancer therapeutics: The impact of and on calcium signaling.
    Cell Calcium 2017 Jun 4. Epub 2017 Jun 4.
    KU Leuven, Laboratory of Molecular and Cellular Signaling, Campus Gasthuisberg O/N-I bus 802, Herestraat 49, B-3000 Leuven, Belgium; Leuven Kanker Instituut (LKI), Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. Electronic address:
    Bcl-2-protein family members are essential regulators of apoptosis. Anti-apoptotic Bcl-2 proteins ensure cell survival via different mechanisms, including via binding of pro-apoptotic Bcl-2-family members and the modulation of intracellular Ca(2+)-transport systems. Many cancer cells upregulate these proteins to overcome the consequences of ongoing oncogenic stress. Read More

    TRPML1: The Ca((2+))retaker of the lysosome.
    Cell Calcium 2017 Jun 24. Epub 2017 Jun 24.
    Telethon Institute of Genetics and Medicine (TIGEM), Via Campi Flegrei 34, 80078 Pozzuoli ,NA, Italy. Electronic address:
    Efficient functioning of lysosome is necessary to ensure the correct performance of a variety of intracellular processes such as degradation of cargoes coming from the endocytic and autophagic pathways, recycling of organelles, and signaling mechanisms involved in cellular adaptation to nutrient availability. Mutations in lysosomal genes lead to more than 50 lysosomal storage disorders (LSDs). Among them, mutations in the gene encoding TRPML1 (MCOLN1) cause Mucolipidosis type IV (MLIV), a recessive LSD characterized by neurodegeneration, psychomotor retardation, ophthalmologic defects and achlorhydria. Read More

    Role of SOCE architects STIM and Orai proteins in Cell Death.
    Cell Calcium 2017 Jun 9. Epub 2017 Jun 9.
    Systems Biology Group, CSIR-Institute of Genomics and Integrative Biology, Mathura Road, New Delhi 110025, India. Electronic address:
    Calcium (Ca(2+)) signaling plays a critical role in regulating plethora of cellular functions including cell survival, proliferation and migration. The perturbations in cellular Ca(2+) homeostasis can lead to cell death either by activating autophagic pathways or through induction of apoptosis. Endoplasmic reticulum (ER) is the major storehouse of Ca(2+) within cells and a number of physiological agonists mediate ER Ca(2+) release by activating IP3 receptors (IP3R). Read More

    Metabolic regulation of the PMCA: Role in cell death and survival.
    Cell Calcium 2017 Jun 8. Epub 2017 Jun 8.
    Division of Molecular & Clinical Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, United Kingdom. Electronic address:
    The plasma membrane Ca(2+)-ATPase (PMCA) is a ubiquitously expressed, ATP-driven Ca(2+) pump that is critical for maintaining low resting cytosolic Ca(2+) ([Ca(2+)]i) in all eukaryotic cells. Since cytotoxic Ca(2+) overload has such a central role in cell death, the PMCA represents an essential "linchpin" for the delicate balance between cell survival and cell death. In general, impaired PMCA activity and reduced PMCA expression leads to cytotoxic Ca(2+) overload and Ca(2+) dependent cell death, both apoptosis and necrosis, whereas maintenance of PMCA activity or PMCA overexpression is generally accepted as being cytoprotective. Read More

    Endoplasmic reticulum chaperones tweak the mitochondrial calcium rheostat to control metabolism and cell death.
    Cell Calcium 2017 May 31. Epub 2017 May 31.
    Faculty of Medicine and Dentistry, Department of Cell Biology, University of Alberta, Edmonton, T6G2H7, Canada,. Electronic address:
    The folding of secretory proteins is a well-understood mechanism, based on decades of research on endoplasmic reticulum (ER) chaperones. These chaperones interact with newly imported polypeptides close to the ER translocon. Classic examples for these proteins include the immunoglobulin binding protein (BiP/GRP78), and the lectins calnexin and calreticulin. Read More

    Polycystin and calcium signaling in cell death and survival.
    Cell Calcium 2017 May 24. Epub 2017 May 24.
    Department of Pharmacology, Yale University, 333 Cedar St, New Haven, CT, 06520, USA; Department of Cellular and Molecular Physiology, Yale University, 333 Cedar St, New Haven, CT, 06520, USA. Electronic address:
    Mutations in polycystin-1 (PC1) and polycystin-2 (PC2) result in a commonly occurring genetic disorder, called Autosomal Dominant Polycystic Kidney Disease (ADPKD), that is characterized by the formation and development of kidney cysts. Epithelial cells with loss-of-function of PC1 or PC2 show higher rates of proliferation and apoptosis and reduced autophagy. PC1 is a large multifunctional transmembrane protein that serves as a sensor that is usually found in complex with PC2, a calcium (Ca(2+))-permeable cation channel. Read More

    Ca(2+) signaling, apoptosis and autophagy in the developing cochlea: Milestones to hearing acquisition.
    Cell Calcium 2017 May 11. Epub 2017 May 11.
    Department of Physics and Astronomy "G. Galilei", University of Padua, 35131 Padua, Italy; Venetian Institute of Molecular Medicine (VIMM), Foundation for Advanced Biomedical Research, 35129 Padua, Italy; Department of Biomedical Sciences, Institute of Protein Biochemistry, Italian National Research Council, 80131 Naples (NA), Italy.
    In mammals, the sense of hearing arises through a complex sequence of morphogenetic events that drive the sculpting of the auditory sensory epithelium into its terminally functional three-dimensional shape. While the majority of the underlying mechanisms remain unknown, it has become increasingly clear that Ca(2+) signaling is at center stage and plays numerous fundamental roles both in the sensory hair cells and in the matrix of non-sensory, epithelial and supporting cells, which embed them and are tightly interconnected by a dense network of gap junctions formed by connexin 26 (Cx26) and connexin 30 (Cx30) protein subunits. In this review, we discuss the intricate interplay between Ca(2+) signaling, connexin expression and function, apoptosis and autophagy in the crucial steps that lead to hearing acquisition. Read More

    Genetic strategies to analyze primary TRP channel-expressing cells in mice.
    Cell Calcium 2017 May 17. Epub 2017 May 17.
    Pharmacology and Toxicology, Center for Molecular Signaling (PZMS), Saarland University School of Medicine, Homburg, Germany. Electronic address:
    Transient receptor potential (TRP) ion channels regulate fundamental biological processes throughout the body. TRP channel dysfunction has been causally linked to a number of disease states and thus establishes these channels as promising therapeutic targets. In order to dissect the physiological role of individual TRP channels in specific tissues, a detailed understanding of the expression pattern of the different TRP channels throughout the organism is essential. Read More

    Ca(2+) signalling underlying pancreatitis.
    Cell Calcium 2017 May 18. Epub 2017 May 18.
    Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. Electronic address:
    In spite of significant scientific progress in recent years, acute pancreatitis (AP) is still a dangerous and in up to 5% of cases deadly disease with no specific cure. It is self-resolved in the majority of cases, but could result in chronic pancreatitis (CP) and increased risk of pancreatic cancer (PC). One of the early events in AP is premature activation of digestive pro-enzymes, including trypsinogen, inside pancreatic acinar cells (PACs) due to an excessive rise in the cytosolic Ca(2+) concentration, which is the result of Ca(2+) release from internal stores followed by Ca(2+) entry through the store operated Ca(2+) channels in the plasma membrane. Read More

    TRPM channels as potential therapeutic targets against pro-inflammatory diseases.
    Cell Calcium 2017 May 3. Epub 2017 May 3.
    Walther Straub Institute of Pharmacology and Toxicology, LMU Munich, Germany.
    The immune system protects our body against foreign pathogens. However, if it overshoots or turns against itself, pro-inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease, or diabetes develop. Ions, the most basic signaling molecules, shape intracellular signaling cascades resulting in immune cell activation and subsequent immune responses. Read More

    The role of Ca(2+) in cell death caused by oxidative glutamate toxicity and ferroptosis.
    Cell Calcium 2017 May 12. Epub 2017 May 12.
    University Medical Center and Focus Program Translational Neuroscience (FTN) of the Johannes Gutenberg University Mainz, Department of Neurology, Mainz, Germany. Electronic address:
    Ca(2+) ions play a fundamental role in cell death mediated by oxidative glutamate toxicity or oxytosis, a form of programmed cell death similar and possibly identical to other forms of cell death like ferroptosis. Ca(2+) influx from the extracellular space occurs late in a cascade characterized by depletion of the intracellular antioxidant glutathione, increases in cytosolic reactive oxygen species and mitochondrial dysfunction. Here, we aim to compare oxidative glutamate toxicity with ferroptosis, address the signaling pathways that culminate in Ca(2+) influx and cell death and discuss the proteins that mediate this. Read More

    Calcium and regulation of the mitochondrial permeability transition.
    Cell Calcium 2017 May 10. Epub 2017 May 10.
    Department of Biomedical Sciences and CNR Neuroscience Institute, University of Padova, Italy. Electronic address:
    Recent years have seen renewed interest in the permeability transition pore, a high conductance channel responsible for permeabilization of the inner mitochondrial membrane, a process that leads to depolarization and Ca(2+) release. Transient openings may be involved in physiological Ca(2+) homeostasis while long-lasting openings may trigger and/or execute cell death. In this review we specifically focus (i) on the hypothesis that the PTP forms from the F-ATP synthase and (ii) on the mechanisms through which Ca(2+) can reversibly switch this energy-conserving nanomachine into an energy-dissipating device. Read More

    Transient receptor potential (TRP) channel function in the reproductive axis.
    Cell Calcium 2017 May 3. Epub 2017 May 3.
    Pharmacology and Toxicology, Center for Molecular Signaling (PZMS), Saarland University School of Medicine, Homburg, Germany. Electronic address:
    Transient receptor potential (TRP) channels play important functional roles in the signal transduction machinery of hormone-secreting cells and have recently been implicated in reproductive physiology. While expression studies have demonstrated TRP channel expression at all levels of the hypothalamic-pituitary-gonadal (hpg) axis, functional details about TRP channel action at the level of the individual cells controlling reproduction are just beginning to emerge. Canonical TRP (TRPC) channels are prominently expressed in the reproductive center of the neuroendocrine brain, i. Read More

    Mitochondrial and endoplasmic reticulum calcium homeostasis and cell death.
    Cell Calcium 2017 May 5. Epub 2017 May 5.
    Dept. of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy. Electronic address:
    The endoplasmic reticulum (ER) and mitochondria cannot be considered as static structures, as they intimately communicate, forming very dynamic platforms termed mitochondria-associated membranes (MAMs). In particular, the ER transmits proper Ca(2+) signals to mitochondria, which decode them into specific inputs to regulate essential functions, including metabolism, energy production and apoptosis. Here, we will describe the different molecular players involved in the transfer of Ca(2+) ions from the ER lumen to the mitochondrial matrix and how modifications in both ER-mitochondria contact sites and Ca(2+) signaling can alter the cell death execution program. Read More

    Endoplasmic reticulum-resident selenoproteins as regulators of calcium signaling and homeostasis.
    Cell Calcium 2017 May 4. Epub 2017 May 4.
    Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA. Electronic address:
    The human selenoprotein family contains 25 members that share the common feature of containing the amino acid, selenocysteine (Sec). Seven selenoproteins are localized to the endoplasmic reticulum (ER) and exhibit different structural features contributing to a range of cellular functions. Some of these functions are either directly or indirectly related to calcium (Ca(2+)) flux or homeostasis. Read More

    Transient receptor potential (TRP) channels as molecular targets in lung toxicology and associated diseases.
    Cell Calcium 2017 Apr 26. Epub 2017 Apr 26.
    Walther-Straub-Institute of Pharmacology and Toxicology, Member of the German Center for Lung Research (DZL), LMU Munich, Germany.
    The lungs as the gateways of our body to the external environment are essential for gas exchange. They are also exposed to toxicants from two sides, the airways and the vasculature. Apart from naturally produced toxic agents, millions of human made chemicals were produced since the beginning of the industrial revolution whose toxicity still needs to be determined. Read More

    Monitoring single-synapse glutamate release and presynaptic calcium concentration in organised brain tissue.
    Cell Calcium 2017 Jun 30;64:102-108. Epub 2017 Mar 30.
    UCL Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK. Electronic address:
    Brain function relies in large part on Ca(2+)-dependent release of the excitatory neurotransmitter glutamate from neuronal axons. Establishing the causal relationship between presynaptic Ca(2+) dynamics and probabilistic glutamate release is therefore a fundamental quest across neurosciences. Its progress, however, has hitherto depended primarily on the exploration of either cultured nerve cells or giant central synapses accessible to direct experimental probing in situ. Read More

    From mucolipidosis type IV to Ebola: TRPML and two-pore channels at the crossroads of endo-lysosomal trafficking and disease.
    Cell Calcium 2017 Apr 23. Epub 2017 Apr 23.
    Munich Center for Integrated Protein Science CIPSM, Center for Drug Research, Ludwig-Maximilians-Universität, München, Germany; Department of Pharmacy, Center for Drug Research, Ludwig-Maximilians-Universität München, Germany. Electronic address:
    What do lysosomal storage disorders such as mucolipidosis type IV have in common with Ebola, cancer cell migration, or LDL-cholesterol trafficking? LDL-cholesterol, certain bacterial toxins and viruses, growth factors, receptors, integrins, macromolecules destined for degradation or secretion are all sorted and transported via the endolysosomal system (ES). There are several pathways known in the ES, e.g. Read More

    The S4---S5 linker - gearbox of TRP channel gating.
    Cell Calcium 2017 Apr 4. Epub 2017 Apr 4.
    Institut für Experimentelle und Klinische Pharmakologie und Toxikologie, Universität des Saarlandes, 66421 Homburg, Germany. Electronic address:
    Transient receptor potential (TRP) channels are cation channels which participate in a wide variety of physiological processes in organisms ranging from fungi to humans. They fulfill roles in body homeostasis, are sensors for noxious chemicals and temperature in the mammalian somatosensory system and are activated by light stimulated phospholipase C activity in Drosophila or by hypertonicity in yeast. The transmembrane topology of TRP channels is similar to that of voltage-gated cation channels. Read More

    Calcium signaling and cellular senescence.
    Cell Calcium 2017 Apr 5. Epub 2017 Apr 5.
    Inserm U1052, Centre de Recherche en Cancérologie de Lyon, F-69373 Lyon, France; CNRS UMR 5286, F-69373 Lyon, France; Centre Léon Bérard, F-69373 Lyon, France; Université de Lyon, F-69373 Lyon, France. Electronic address:
    Cellular senescence is a stable cell proliferation arrest induced by a variety of stresses including telomere shortening, oncogene activation and oxidative stress. This process plays a crucial role in many physiopathological contexts, especially during aging when cellular senescence favors development of age-related diseases, shortening lifespan. However, the molecular and cellular mechanisms controlling senescence are still a matter of active research. Read More

    Enamel: Molecular identity of its transepithelial ion transport system.
    Cell Calcium 2017 Jul 29;65:1-7. Epub 2017 Mar 29.
    Dept. Basic Science and Craniofacial Biology, New York University College of Dentistry, 345 East 24th Street, New York, NY 10010, United States. Electronic address:
    Enamel is the most calcified tissue in vertebrates. It differs from bone in a number of characteristics including its origin from ectodermal epithelium, lack of remodeling capacity by the enamel forming cells, and absence of collagen. The enamel-forming cells known as ameloblasts, choreograph first the synthesis of a unique protein-rich matrix, followed by the mineralization of this matrix into a tissue that is ∼95% mineral. Read More

    The role of STIM1 and SOCE in smooth muscle contractility.
    Cell Calcium 2017 May 10;63:60-65. Epub 2017 Mar 10.
    Department of Medicine, Duke University School of Medicine, Durham, NC, 27704, United States. Electronic address:
    Contraction is a central feature for skeletal, cardiac and smooth muscle; this unique feature is largely dependent on calcium (Ca(2+)) signaling and therefore maintenance of internal Ca(2+) stores. Stromal interaction molecule 1 (STIM1) is a single-pass transmembrane protein that functions as a Ca(2+) sensor for the activation store-operated calcium channels (SOCCs) on the plasma membrane in response to depleted internal sarco(endo)plasmic (S/ER) reticulum Ca(2+) stores. STIM1 was initially characterized in non-excitable cells; however, evidence from both animal models and human mutations suggests a role for STIM1 in modulating Ca(2+) homeostasis in excitable tissues as well. Read More

    Meprin β and BMP-1 are differentially regulated by CaCl2.
    Cell Calcium 2017 Jul 19;65:8-13. Epub 2017 Mar 19.
    Anatomical Institute, Otto-Hahn-Platz 8, 24118 Kiel, Germany. Electronic address:
    The two metalloproteases meprin β and bone morphogenetic protein 1 (BMP-1) are both members of the astacin protease family. They share specificity for negatively charged residues around the scissile bond and they are expressed in overlapping compartments of the human body. One important proteolytic substrate they share is pro-collagen I. Read More

    Monitoring in vivo function of cortical microglia.
    Cell Calcium 2017 Jun 14;64:109-117. Epub 2017 Mar 14.
    Institute of Physiology, Department of Neurophysiology, Eberhard Karls University Tübingen, Keplerstraße 15, 72074 Tübingen, Germany. Electronic address:
    Microglia, the innate immune cells of the brain, are becoming increasingly recognized as an important player both in the context of physiological brain function and brain pathology. To fulfill their executive functions microglia can modify their morphology, migrate or move their processes in a directed fashion, and modify the intracellular Ca(2+) dynamics leading to modifications in gene expression, phagocytosis, release of cytokines and other inflammation markers, etc. Here we describe the recently developed tools enabling in vivo monitoring of morphology and Ca(2+) signaling of microglia and show how these techniques may be used for examining microglial function in healthy and diseased brain. Read More

    Assessment of TRPM7 functions by drug-like small molecules.
    Cell Calcium 2017 Mar 14. Epub 2017 Mar 14.
    Walther-Straub Institute of Pharmacology and Toxicology, LMU, Munich, Germany. Electronic address:
    Transient receptor potential cation channel subfamily M member 7 (TRPM7) is a plasma membrane ion channel linked to a cytosolic protein kinase domain. Genetic inactivation of this bi-functional protein revealed its crucial role in Ca(2+) signalling, Mg(2+) metabolism, immune responses, cell motility, proliferation and differentiation. Malfunctions of TRPM7 are associated with anoxic neuronal death, cardiac fibrosis, tumour progression and macrothrombocytopenia. Read More

    One nuclear calcium transient induced by a single burst of action potentials represents the minimum signal strength in activity-dependent transcription in hippocampal neurons.
    Cell Calcium 2017 Jul 6;65:14-21. Epub 2017 Mar 6.
    Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University, 69120 Heidelberg, Germany. Electronic address:
    Neurons undergo dramatic changes in their gene expression profiles in response to synaptic stimulation. The coupling of neuronal excitation to gene transcription is well studied and is mediated by signaling pathways activated by cytoplasmic and nuclear calcium transients. Despite this, the minimum synaptic activity required to induce gene expression remains unknown. Read More

    The establishment of appropriate methods for egg-activation by human PLCZ1 RNA injection into human oocyte.
    Cell Calcium 2017 Jul 6;65:22-30. Epub 2017 Mar 6.
    Saint Mother Obstetrics and Gynecology Clinic, Institute for ART, Fukuoka 807-0825, Japan.
    Phospholipase C-zeta (PLCZ1), a strong candidate of egg-activating sperm factor, can induce Ca(2+) oscillations and cause egg activation. For the application of PLCZ1 to clinical use, we examined the pattern of Ca(2+) responses and developmental rate by comparing PLCZ1 RNA injection methods with the other current methods, such as cytosolic aspiration, electrical stimulation and ionomycin treatment in human oocytes. We found that the pattern of Ca(2+) oscillations after PLCZ1 RNA injection exhibited similar characteristics to that after ICSI treatment. Read More

    Interrogating cyclic AMP signaling using optical approaches.
    Cell Calcium 2017 Jun 1;64:47-56. Epub 2017 Mar 1.
    VA Boston Healthcare System and the Dept. of Surgery, Brigham & Women's Hospital and Harvard Medical School, 1400 VFW PKW, West Roxbury, MA 02132, USA. Electronic address:
    Optical reporters for cAMP represent a fundamental advancement in our ability to investigate the dynamics of cAMP signaling. These fluorescent sensors can measure changes in cAMP in single cells or in microdomains within cells as opposed to whole populations of cells required for other methods of measuring cAMP. The first optical cAMP reporters were FRET-based sensors utilizing dissociation of purified regulatory and catalytic subunits of PKA, introduced by Roger Tsien in the early 1990s. Read More

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