Showing papers in "Cell Calcium in 2010"

TL;DR: It is suggested that blocking certain receptors and ion channels is unlikely to be a useful therapeutic strategy due to potential deleterious side effects, however, identifying those that are most responsible for cell death and their downstream signalling pathways may lead to improved strategies for treating ischemic and excitotoxic disorders.

TL;DR: Results indicate that overactivation of NMDA and AMPA receptor, mitochondrial Ca2+ overload and mitochondrial damage underlie the neurotoxicity induced by Abeta oligomers, and drugs that modulate these events can prevent from Abeta damage to neurons in Alzheimer's disease.

TL;DR: There is growing evidence to suggest that not all forms of Ca2+ dysregulation in AD neurons are harmful and some of them instead may be compensatory, which may help modulate neuronal excitability and slow AD pathology, especially in the early stages of the disease.

TL;DR: The hypothesis of a "toxic shift of Ca2+" within the endoplasmic reticulum-mitochondria Ca 2+ cycle (ERMCC) as a key mechanism in motor neuron degeneration is introduced, and molecular targets which may be of interest for future ERMCC modulating neuroprotective therapies are discussed.

TL;DR: The hypothesis that the primary factor driving neurodegenerative changes in PD is the metabolic stress created by sustained Ca2+ entry is examined, particularly in the face of genetic or environmental factors that compromise oxidative defenses or proteostatic competence.

TL;DR: An overview of the current knowledge of the (short-term) regulatory mechanisms that affect Ca2+-release and Ca2-leak pathways and of the long-term adaptations in ER size and capacity is given.

TL;DR: The role of glial calcium signalling in various forms of pathological processes including neurological and psychiatric disorders and neurodegeneration is summarised.

TL;DR: It is concluded that ionotropic receptors contribute to astroglial Ca(2+) signalling and may provide a specific mechanism for fast neuronal-glial signalling at the synaptic level.

TL;DR: It is suggested that Ca(2+) influx is required for the migration of human nasopharyngeal carcinoma 5-8F cells and identified TRPM7 as a novel potential-regulator of the Ca( 2+) influx that allows migration of 5- 8F cells.

TL;DR: It is suggested that TNF-α and IL-1β increase the SR Ca2+ leak from the SR, which contributes to the depressed Ca2- transient and contractility, and may contribute to arrhythmias in sepsis as the resultingCa2+ extrusion via NCX is electrogenic, leading to cell depolarisation.

TL;DR: The accumulating evidence implicating Ca2+ dysregulation in both painful and degenerative neuropathies, along with recent advances in understanding of regional variations in Ca2+.

TL;DR: The results strongly suggest that not only proteins but lipids also may be part or active players in the modulation of the store-operated calcium entry (SOCE), and highlight the evidence showing novel members from SOCIC.

TL;DR: A previously unrecognized role for Ca(2+) signaling via this InsP3R isoform in colon cancer is suggested, and its expression level is directly related to aggressiveness of the tumor, which may reflect inhibition of apoptosis by the receptor.

TL;DR: This review covers the significant discoveries on the physiological function and regulatory mechanism of the TRPM1 channel in retinal ON bipolar cells and the association of human TR PM1 mutations with congenital stationary night blindness.

TL;DR: It is proposed here that excess Orai1 uncouples SERCA from Ca(2+) entry in the intact cell by disturbing the fine topology of Ca( 2+) pumping complexes within the ER-plasma membrane junctions.

TL;DR: The data reveal that that the T-tubules in atrial cells impart significant functional properties, but loss of these tubular membranes does not affect Ca2+ signalling as dramatically as detubulation in ventricular myocytes.

TL;DR: The results suggest that inhibition and activation of SOCE/I(CRAC) by the 2-APB analogues is mediated by STIM.

TL;DR: It is suggested that two-pore channels may physically interact with ryanodine receptors to account for more direct release of calcium from the endoplasmic reticulum in analogy with the conformational coupling of voltage-sensitive calcium channels and ryanODine receptors in skeletal muscle.

TL;DR: This review revisits the basic tenets of the Ca2+ hypothesis of neuronal ageing and stress the major conceptual changes that occurred between the time of its original proposal and now, in particular in respect to the extent of neuronal loss in normal ageing.

TL;DR: Recent studies which have used a similar approach to investigate key residues underlying the in vivo modulation by select regulatory factors are evaluated and structural requirements in the channel domain which comprise the conduction pathway and are suggested to be involved in the gating of the channel are reviewed.

TL;DR: Emerging evidence that excessive calcium-induced NO production can contribute to the accumulation of misfolded proteins, specifically by S-nitrosylation of the ubiquitin E3 ligase, parkin, and the chaperone enzyme for nascent protein folding, protein-disulfide isomerase is discussed.

TL;DR: Changes in the concentration and spatial distribution of Ca(2+) ions in the cytoplasm constitute a ubiquitous intracellular signaling module in cellular physiology and have been implicated in practically every aspect of cellular physiology, including cellular proliferation.

TL;DR: The data suggest that chronic low-grade inflammation produces circulating cytokine levels that are sufficient to induce beta- cell dysfunction and may play a contributing role in beta-cell failure in early T2D.

TL;DR: Recent advances in the understanding of white matter Ca2+ dyshomeostasis in experimental paradigms which are relevant to stroke, perinatal ischemia, multiple sclerosis, psychiatric disorders, Alzheimer's disease and traumatic injury are summarized.

TL;DR: Interestingly, dl-2-amino-5-phosphopentanoic acid (AP5) and [(+)-dizocilpine] (MK801), two inhibitors of animal and plant ionotropic glutamate receptors, suppress DHS-induced cell death symptoms by selectively inhibiting the variations of nuclear calcium concentration.

TL;DR: It is suggested that H2O2 can activate Ca(2+) entry through TRPM2 as well as store-operated CRAC channels, thereby adding a new facet to ROS-induced Ca( 2+) signaling.

TL;DR: Observations show that succinate acts as a signaling molecule in cardiomyocytes, modulating global Ca(2+) transient and cell viability through a PKA-dependent pathway.

TL;DR: Fluorescent dyes failed to follow Ca(2+) changes adequately, especially during repetitive stimulation, and cells loaded with low concentrations of rhod-2 suffered large changes in mitochondrial morphology after light excitation, which was small and reversible at low concentrations, but produced large and prolonged damage at higher concentrations.

TL;DR: This work shows for the first time millisecond activation and deactivation of SOCE during low amplitude [Ca(2+)](SR) oscillations at low [Ca-2+](SR), and proposes the SOCE complex forms during the progressive depletion of [Ca (2+)], prior to reaching the activation threshold of SOCe.

TL;DR: The biosynthesis of the zinc finger transcription factor Egr-1 is stimulated by many extracellular signaling molecules including hormones, neurotransmitters, growth and differentiation factors, and is thus a Ca(2+) regulated transcription factor - similar to CREB, NFAT, NF-kappaB and others.