Disease relevance of Calcium Signaling

• HIV-1 pathogenicity factor Nef has been shown to modulate calcium signaling in host cells, but the underlying molecular mechanisms have remained unclear [1].
• The inhibitory action of PYY and related peptides on gastrin-stimulated histamine release and calcium signaling was eliminated by pretreatment with 200 ng/mL pertussis toxin [2].
• Tamoxifen-induced enhancement of calcium signaling in glioma and MCF-7 breast cancer cells [3].
• Does AMP-activated protein kinase couple inhibition of mitochondrial oxidative phosphorylation by hypoxia to calcium signaling in O2-sensing cells [4]?
• This ability of Nef to substitute for triggering of the calcium pathway in induction of NFAT could promote activation of human immunodeficiency virus (HIV)-infected T cells in response to stimuli mediated via TCR or other cell surface receptors under conditions when activation of Ras rather than calcium signaling would otherwise predominate [5].

Psychiatry related information on Calcium Signaling

• Mutations in the presenilin genes (PS1, PS2), the leading cause of autosomal dominant familial Alzheimer's disease (FAD), cause highly specific alterations in intracellular calcium signaling pathways that may contribute to the neurodegenerative and pathological lesions of the disease [6].
• Epidermal growth factor induced cytosolic free calcium oscillations consisting of periodic trains of spikes with a latency period of up to several minutes [7].

High impact information on Calcium Signaling

• Evidence that the Wingless/calcium signaling pathway is a strong ventralizing signal in Xenopus, mediated by phosphoinositide signaling, is adumbrated [8].
• Gap junction channels are responsible for direct intercellular transfer of ions and small molecules including propagation of inositol trisphosphate-dependent calcium waves [9].
• Mechanisms of calcium signaling by cyclic ADP-ribose and NAADP [10].
• Calcium signaling activates the phosphatase calcineurin and induces movement of NFATc proteins into the nucleus, where they cooperate with other proteins to form complexes on DNA [11].
• This interaction induces str-2 expression by reducing calcium signaling through a voltage-dependent Ca2+ channel and the CaM kinase II UNC-43 [12].

Chemical compound and disease context of Calcium Signaling

• In this study, the effects and interactions of endothelin-1 (25 nM), alpha-thrombin (0.9 microM), epidermal growth factor (40 nM), prostaglandin E1 (5 microM), and prostaglandin F1 alpha (5 microM) were examined on calcium signaling in UMR-106 rat osteoblastic osteosarcoma cells [13].
• These findings report for the first time the cardiac cell-specific implication of Ang II and the intracellular calcium signaling pathway stimulated by the AT1 receptor in cardiac hypertrophy in DOCA-salt-hypertensive rats [14].
• Our study unequivocally shows that the hLH receptor is coupled to the inositol phosphate/calcium signaling pathway via a pertussis toxin-sensitive G protein-coupled receptor [15].
• Agonist-specific calcium signaling and phosphoinositide hydrolysis in human SK-N-MCIXC neuroepithelioma cells [16].
• Our results point towards increased inositol triphospate (IP3)-mediated calcium signaling in Alzheimer's disease [17].

Biological context of Calcium Signaling

• Control of calcium oscillations by phosphorylation of metabotropic glutamate receptors [18].
• Rhythmic exocytosis stimulated by GnRH-induced calcium oscillations in rat gonadotropes [19].
• HBx activation of HBV DNA replication was blocked by inhibiting Pyk2 or calcium signaling mediated by mitochondrial calcium channels, which suggests that HBx targets mitochondrial calcium regulation [20].
• Nur77 expression is controlled by the transcription factor myocyte enhancer factor 2 (MEF2), but how MEF2 is activated by calcium signaling is still obscure [21].
• Environmental sensing is the focus of the fifth section with a treatment of two-component systems; GTP-binding proteins; mitogen-activated protein, p21-activated, and germinal center kinases; calcium signaling; protein phosphatases; photobiology; circadian rhythms; and heat shock and stress responses [22].

Anatomical context of Calcium Signaling

• We find that anandamide blocks the propagation of astrocyte calcium waves generated by either mechanical stimulation or local glutamate application [23].
• Internal calcium oscillations induced by alpha-haemolysin in a renal epithelial cell line stimulated production of cytokines interleukin (IL)-6 and IL-8 [24].
• Larval muscle fibers of a beetle, Xylotrupes dichotomus, produce calcium spikes that are maintained when the fibers are bathed in saline solutions containing manganese, cadmium, zinc, or beryllium instead of calcium [25].
• We now show that human dendritic cells (DC) pulsed with peptide-loaded mycobacterial HSP70 complexes generate potent antigen-specific cytotoxic lymphocyte (CTL) responses, which are dependent on an HSP70-stimulated calcium signaling cascade [26].
• Self-reactive B cells lacking the phosphatase CD45 did not exhibit calcium oscillations or ERK/pp90rsk activation, nor did they repond negatively to self-antigen [27].

Associations of Calcium Signaling with chemical compounds

• In contrast to conventional sodium or calcium spikes, these spikes were mediated mostly by NMDA (N-methyl-D-aspartate) receptor channels, which contributed at least 80% of the total charge [28].
• Norepinephrine inhibits the development of a shoulder on the aciton potential, the magnitude of the hyperpolarizing afterpotential, and the rate of rise and amplitude of the calcium spike [29].
• Ethanol augmented the hyperpolarization that followed repetitive firing or that followed the eliciting of calcium spikes in the presence of tetrodotoxin, but not the rapid afterhyperpolarization in calcium-free medium [30].
• Conversely, cold and abscisic acid elicited calcium oscillations in det3, and stomatal closure occurred normally [31].
• Calcium imaging of single cells has begun to reveal that this inositol 1,4,5-trisphosphate/calcium signaling system is organized in complex patterns, which include localization of calcium signals to discrete regions of cells and the generation of both calcium waves and calcium oscillations [32].

Gene context of Calcium Signaling

• Huntingtin and huntingtin-associated protein 1 influence neuronal calcium signaling mediated by inositol-(1,4,5) triphosphate receptor type 1 [33].
• Collectively, our findings suggest that the overfilling of calcium stores represents the fundamental cellular defect underlying the alterations in calcium signaling conferred by presenilin mutations [6].
• The single chain Fvs (scFv) generated by this step-back selection procedure also inhibited MIP-1 alpha-mediated calcium signaling [34].
• Calsenilin reverses presenilin-mediated enhancement of calcium signaling [35].
• Notably, expression of calsenilin alone had no discernable effects on calcium signaling, suggesting that calsenilin modulates these signals by a mechanism independent of simple calcium buffering [35].

Analytical, diagnostic and therapeutic context of Calcium Signaling

• Altered expression of genes of the Bmp/Smad and Wnt/calcium signaling pathways in the cone-only Nrl-/- mouse retina, revealed by gene profiling using custom cDNA microarrays [36].
• Our working hypothesis is that disruption of the ontogenetically defined pattern of NMDAR subunit expression and NMDAR-mediated calcium signaling in glutamatergic synapses is a principal mechanism for Pb(2+)-induced deficits in synaptic plasticity and in learning and memory documented in animal models of Pb(2+) neurotoxicity [37].
• Western blotting of tubule preparations from trp and trpl mutants revealed a correlation between TRPL levels and CAP(2b)-stimulated fluid transport and calcium signaling [38].
• In the absence of extracellular calcium, perfusion of pancreatic acinar cells with 1 nM CCK-8 and 1 mM vanadate did not significantly affect the typical transient calcium spike induced by CCK-8, but the plateau phase of calcium in response to CCK-8 remained elevated [39].
• Microinjection of the selective cADPR antagonist 8NH2-cADPR completely abolished subsequent stimulation of Ca2+ signaling via ETA and ETB receptors. cADPR therefore appears to have an obligatory role for ETA-R and ETB-R-mediated calcium signaling in PSMC [40].

References