Nuclear calcium signaling: a cell within a cell

Rodrigues, Michele Ângela; Gomes, Dawidson Assis; Nathanson, Michael H.; Leite, M. Fátima

doi:10.1590/s0100-879x2008005000050

Cited by 35 publications

(22 citation statements)

References 48 publications

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“…Ca 2+ signals within the nucleus are particularly important in cancer cell progression [50, 59, 60]. Buffering nuclear Ca 2+ arrests adenocarcinoma cells in the early phase of mitosis [61], and sensitizes head and neck cancer cells to radiotherapy [59].…”

Section: Discussionmentioning

confidence: 99%

Angiotensin Converting Enzyme Regulates Cell Proliferation and Migration

et al. 2016

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BackgroundThe angiotensin-I converting enzyme (ACE) plays a central role in the renin-angiotensin system, acting by converting the hormone angiotensin-I to the active peptide angiotensin-II (Ang-II). More recently, ACE was shown to act as a receptor for Ang-II, and its expression level was demonstrated to be higher in melanoma cells compared to their normal counterparts. However, the function that ACE plays as an Ang-II receptor in melanoma cells has not been defined yet.AimTherefore, our aim was to examine the role of ACE in tumor cell proliferation and migration.ResultsWe found that upon binding to ACE, Ang-II internalizes with a faster onset compared to the binding of Ang-II to its classical AT1 receptor. We also found that the complex Ang-II/ACE translocates to the nucleus, through a clathrin-mediated process, triggering a transient nuclear Ca2+ signal. In silico studies revealed a possible interaction site between ACE and phospholipase C (PLC), and experimental results in CHO cells, demonstrated that the β3 isoform of PLC is the one involved in the Ca2+ signals induced by Ang-II/ACE interaction. Further studies in melanoma cells (TM-5) showed that Ang-II induced cell proliferation through ACE activation, an event that could be inhibited either by ACE inhibitor (Lisinopril) or by the silencing of ACE. In addition, we found that stimulation of ACE by Ang-II caused the melanoma cells to migrate, at least in part due to decreased vinculin expression, a focal adhesion structural protein.ConclusionACE activation regulates melanoma cell proliferation and migration.

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Section: Discussionmentioning

confidence: 99%

Angiotensin Converting Enzyme Regulates Cell Proliferation and Migration

et al. 2016

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“…It was indicated that the cell nucleus contains the whole set of enzymes required for the InsR 3 synthesis from diphosphoinositolphosphate of the nuclear membrane, so the regulation of nuclear InsP 3 Rs cannot depend on cytoplasmic processes (Gomes et al, 2006; Klein and Malviya, 2008; Rodrigues et al, 2009). Of course, in small cells InsR 3 can freely penetrate into the nucleus by diffusion through the nuclear pores, but in large cells the distance from the plasma membrane to the nucleus is large enough so it is unlikely that InsP 3 Rs in the nuclear membrane are activated by cytosolic InsP 3 R. This point is proved by the fact that that numerous InsP 3 -activated channels were recorded from the inner nuclear membrane of Purkinje and CA1 pyramidal neurons, which are the largest cells in the brain.…”

Section: Insp3rs In Cell Functionsmentioning

confidence: 99%

Intracellular calcium channels: Inositol-1,4,5-trisphosphate receptors

Fedorenko

Попугаева

Enomoto

et al. 2014

European Journal of Pharmacology

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The inositol-1,4,5-trisphosphate receptors (InsP3Rs) are the major intracellular Ca2+-release channels in cells. Activity of InsP3Rs is essential for elementary and global Ca2+ events in the cell. There are three InsP3Rs isoforms that are present in mammalian cells. In this review review we will focus primarily on InsP3R type 1. The InsP3R1 is a predominant isoform in neurons and it is most extensively studied isoform. Combination of biophysical and structural methods revealed key mechanisms of InsP3R function and modulation. Cell biological and biochemical studies lead to identification of a large number of InsP3R-binding proteins. InsP3Rs are involved in the regulation of numerous physiological processes, including learning and memory, proliferation, differentiation, development and cell death. Malfunction of InsP3R1 play a role in a number of neurodegenerative disorders and other disease states. InsP3Rs represent a potentially valuable drug target for treatment of these disorders and for modulating activity of neurons and other cells. Future studies will provide better understanding of physiological functions of InsP3Rs in health and disease.

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“…Thus, glutamate uptake at the synapse is proposed to give rise to Ca 2þ release from the nuclear lumen directly into the nucleus (O'Malley et al 2003;Jong et al 2005Jong et al , 2007Sheldon and Robinson 2007;Kumar et al 2008). This model is bolstered by data documenting the presence and functional responsiveness of EAATs, mGluRs, and IP 3 Rs on the inner nuclear membranes of a variety of cell types including dissociated neurons (Humbert et al 1996;Echevarria et al 2003;Gerasimenko et al 2003;O'Malley et al 2003;Jong et al 2005Jong et al , 2007Marchenko et al 2005;Quesada and Verdugo 2005;Marchenko and Thomas 2006;Sheldon and Robinson 2007;Kumar et al 2008;Bootman et al 2009;Rodrigues et al 2009). It remains to be seen, however, whether and under which conditions internal Ca 2þ release mediated by intranuclear mGluRs and IP 3 Rs can be evoked in intact brain tissue.…”

Section: Generating Nuclear Ca 2þ Signalsmentioning

confidence: 99%

Calcium Signaling in Synapse-to-Nucleus Communication

Hagenston

Bading

2011

Cold Spring Harbor Perspectives in Biology

115

113

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Changes in the intracellular concentration of calcium ions in neurons are involved in neurite growth, development, and remodeling, regulation of neuronal excitability, increases and decreases in the strength of synaptic connections, and the activation of survival and programmed cell death pathways. An important aspect of the signals that trigger these processes is that they are frequently initiated in the form of glutamatergic neurotransmission within dendritic trees, while their completion involves specific changes in the patterns of genes expressed within neuronal nuclei. Accordingly, two prominent aims of research concerned with calcium signaling in neurons are determination of the mechanisms governing information conveyance between synapse and nucleus, and discovery of the rules dictating translation of specific patterns of inputs into appropriate and specific transcriptional responses. In this article, we present an overview of the avenues by which glutamatergic excitation of dendrites may be communicated to the neuronal nucleus and the primary calcium-dependent signaling pathways by which synaptic activity can invoke changes in neuronal gene expression programs.

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Nuclear calcium signaling: a cell within a cell

Cited by 35 publications

References 48 publications

Angiotensin Converting Enzyme Regulates Cell Proliferation and Migration

Angiotensin Converting Enzyme Regulates Cell Proliferation and Migration

Intracellular calcium channels: Inositol-1,4,5-trisphosphate receptors

Calcium Signaling in Synapse-to-Nucleus Communication

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