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Relevant bibliographies by topics / Intracellular calcium homeostasis / Dissertations / Theses

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Dissertations / Theses on the topic 'Intracellular calcium homeostasis'

Author: Grafiati

Published: 25 May 2024

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1

Vasilev, Filip. "New roles for actin-binding proteins and PIP2 in intracellular calcium homeostasis." Thesis, Open University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.582807.

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Spatiotemporal increase of the intracellular Ca2+ is the most universal way to regulate the function of a eukaryotic cell. Owing to a host of actin-binding proteins and enzymes whose activities are modulated by the local concentration of Ca2+, free Ca2+ in cytosol serves as a pivotal second messenger in a variety of cell functions. The rise and fall of intracellular Ca2+ wave has been best illustrated in eggs at fertilization. However, the molecular mechanism by which intracellular Ca2+ is increased in the fertilized egg is largely unknown despite the discoveries of the distinct Ca2+-mobilizin

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2

Thor, Der. "The effect of estrogen on intracellular calcium homeostasis in human endothelial cells." Scholarly Commons, 2009. https://scholarlycommons.pacific.edu/uop_etds/2397.

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The effect of estrogen on the vasculature is mediated in part by influences on NO bioavailability. Nitric oxide (NO) is a potent vasodilator which is synthesized in endothelial cell by endothelial nitric oxide synthase (eNOS) catalyzed conversion of L-arginine to L-citrulline. Although estrogen has been shown to increase eNOS expression and/or activity, the mechanism of estrogen-mediated increased eNOS activity in endothelial cells remains elusive. The Ca 2+ /calmodulin complex is known to aid in eNOS activation by dissociating eNOS from the membrane bound protein, caveolin-1. We investigated

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3

Kipanyula, Maulilio. "Ca2+ homeostasis in familial Alzheimer's disease: a view from intracellular Ca2+ stores." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3421718.

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Familial Alzheimer's disease (FAD) -linked mutations in presenilin 1 and 2 (PS1, PS2) have been causally implicated in neurodegeneration and eventually neuronal cell death by amyloid toxicity and perturbation of cellular Ca2+ homeostasis. The mechanism governing this latter phenomenon remains unclear. In the cytosol, upon stimulation, both exaggerated and reduced Ca2+ release have been reported in different cell lines and neurons expressing PS1 and PS2 mutants. Despite the contradicting data yet available, it is undisputable that FAD-linked PS mutants cause imbalances of cellular Ca2+ homeosta

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4

Leustik, Martin [Verfasser]. "Listeriolysin O and Pneumolysin: Effects on intracellular calcium homeostasis and epithelial barrier integrity / Martin Leustik." Gießen : Universitätsbibliothek, 2013. http://d-nb.info/106499170X/34.

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5

Allan, Laura Elizabeth. "Investigating the effects of the Alzheimer's disease-associated amyloid β-peptide on intracellular calcium homeostasis". Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/283857.

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I investigated the effects of Aβ<sub>42</sub> on the Ca<sup>2+</sup> signalling capacity of human neuroblastoma SH-SY5Y cells and primary hippocampal cultures. I developed an <i>in vitro</i> model system of dissociated hippocampal neurons and glial cells in order to reflect as closely as possible the mature hippocampus. Extensive characterisation of the culture revealed that functional neuronal networks were established by day <i>in vitro </i>11, as demonstrated by the occurrence of spontaneous oscillations in both membrane potential and intracellular Ca<sup>2+</sup> levels. Neurons exhibited

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6

Brusich, Douglas J. "Dual roles for an intracellular calcium-signaling pathway in regulating synaptic homeostasis and neuronal excitability." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1830.

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Neurons are specialized cells that communicate via electrical and chemical signaling. It is well-known that homeostatic mechanisms exist to potentiate neuronal output when activity falls. Likewise, while neurons rely on excitable states to function, these same excitable states must be kept in check for stable function. However, the identity of molecular factors and pathways regulating these pathways remain elusive. Chapter 2 of this thesis reports the findings from an RNA interference- and electrophysiology-based screen to identify factors necessary for the long-term maintenance of homeostatic

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7

Campion, Katherine. "Characterisation of calcium-sensing receptor extracellular pH sensitivity and intracellular signal integration." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-calciumsensing-receptor-extracellular-ph-sensitivity-and-intracellular-signal-integration(e11adf01-4748-42ed-8679-f8b990d79dea).html.

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Parathyroid hormone (PTH) secretion maintains free-ionised extracellular calcium (Ca2+o) homeostasis under the control of the calcium-sensing receptor (CaR). In humans and dogs, blood acidosis and alkalosis is associated with increased or suppressed PTH secretion respectively. Furthermore, large (1.0 pH unit) changes in extracellular pH (pHo) alter Ca2+o sensitivity of the CaR in CaR-transfected HEK-293 cells (CaR-HEK). Indeed, it has been found in this laboratory that even pathophysiological acidosis (pH 7.2) renders CaR less sensitive to Ca2+o while pathophysiological alkalosis (pH 7.6) incr

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8

Rintoul, Gordon Leslie. "Functional studies of calbindin-D¦2¦8[subscript]k and its role in intracellular calcium homeostasis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61165.pdf.

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9

Hung, Chun-hin, and 孔進軒. "Effect of novel Chinese specific presenilin-1 V97L mutation on intracellular calcium homeostasis in human neuroblastoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193533.

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Presenilin-1 (PS1) mutations caused by the PSEN1 gene mutations are the major cause of early onset familial Alzheimer’s disease (EOFAD). Two Chinesespecific EOFAD related PS1 mutations, V97L and A136G, have been found. Studies suggested that V97L mutation lead to the overexpression of Aβ42 and tau hyperphosphorylation, which are the major hallmarks of Alzheimer’s disease (AD), while properties of A136G were unclear. Since calcium dysregulation was suggested to play an important role in AD, the research project investigated if V97L and A136G mutations also lead to altered endoplasmic reticulum

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10

Gupta, Paul. "The control of intracellular calcium homeostasis by aspirin-like drugs and its relationship to mediator function." Thesis, University of Sunderland, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237813.

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11

wong, andrea kuan cie. "Single organelle fret-based analysis of intracellular calcium: different effects of presinilis carrying Familial Alzheimer's Disease mutations." Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423762.

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Calcium (Ca2+) is one of the major intracellular messengers that impacts nearly every aspect of cell life. In particular, it plays essential roles in neuronal development, synaptic transmission and plasticity, as well as in the regulation of metabolic pathways and cell fate decisions. The first goal of my work was to study more in details the Golgi apparatus (GA), as an intracellular Ca2+ store. The Golgi complex may store up to 5% of the total cellular Ca2+ at higher concentrations and contains several different luminal Ca2+-binding proteins and Ca2+-release channels. The use of a specific

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12

Kam, Wan-lung Kenneth. "Effect of ovariectomy and estrogen replacement on the [beta]-Adrenergic receptor signaling pathway and intracellular Ca2+ homeostasis in the rat heart." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31473143.

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13

CORRICELLI, Mariangela. "Two different points of view on signal transduction: defective autophagy as a key feature of Cerebral Cavernous Malformations and c-Src as modulator of intracellular Ca2+ homeostasis." Doctoral thesis, Università degli studi di Ferrara, 2018. http://hdl.handle.net/11392/2478764.

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Nel primo progetto abbiamo indagato il coinvolgimento dell’autofagia nella patogenesi delle Malformazioni Cavernose Cerebrali (CCM). CCM è una grave malattia cerebrovascolare che colpisce circa lo 0.3-0.5% della popolazione ed è caratterizzata da capillari dilatati e fragili che predispongono a convulsioni, deficit neurologici e fatali emorragie intracerebrali. CCM è una malattia genetica che può insorgere in modo sporadico o essere ereditata con modalità di trasmissione autosomica dominante. La causa è stata identificata in mutazioni che determinano la perdita di tre geni, KRIT1 (CCM1), CCM2

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14

Lallet-Daher, Hélène. "Implication du canal potassique calcium dépendant à conductance intermédiaire IKca1 dans la cancerogenèse humaine." Electronic Thesis or Diss., Lille 1, 2008. http://www.theses.fr/2008LIL10135.

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Des études récentes montrent que l'homéostasie calcique intracellulaire, ainsi que l'expression et l'activité de canaux ioniques jouent un rôle essentiel dans le contrôle de la prolifération cellulaire aussi bien dans un contexte physiologique que dans certains cancers. Cependant, aucune approche proposant les canaux ioniques comme cible thérapeutique n'est actuellement envisagée dans le cadre des traitements des cancers de la prostate. Dans ce travail nous avons mis en évidence l'expression, la fonctionnalité et l'implication des canaux potassiques calcium-activés (IKca1) dans la prolifératio

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15

Yu-Fan and 謝雨帆. "RAP1GDS1 is the substrate of TG2 for modulating intracellular calcium homeostasis." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/e8wt2a.

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博士<br>中山醫學大學<br>微生物免疫研究所<br>100<br>Background: Type 2 transglutaminase (TG2) is a multifunctional protein, which catalyzes Ca2+-dependent protein modifications, acts as a G protein in transmembrane signaling and cell surface adhesion mediator. It not only has a pro-apoptotic function but also presences in the mitochondria and participates in the molecular events of apoptosis. Modulating calcium signaling from the endoplasmic reticulum (ER) to mitochondria can be critical in the induction of mitochondrial dependent cell death pathway; however, the mechanism of action of TG2 is unknown. Accordin

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16

Rintoul, Gordon Leslie. "Functional studies of Calbindin-D28K and its role in intracellular calcium homeostasis." Thesis, 2000. http://hdl.handle.net/2429/13171.

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Calbindin-D28k (CaBP) is a 28 kD calcium-binding protein found in specific neuronal populations in the mammalian brain. The hypothesized Ca²⁺-buffering action of CaBP is the basis of suggestions that this protein may serve to protect neurons against cell death mediated by large or prolonged increases in intracellular free Ca²⁺ concentration. However, to date, there is little direct evidence to support this hypothesis. To address this question directly, we have examined Ca²⁺-buffering by CaBP in stably transfected HEK 293 and HeLa cell lines. A variety of methods were employed to induce calcium

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17

Chen, Jie-Shin, and 陳潔心. "MicroRNA-3906 Maintains Fast Muscle Intracellular Calcium Homeostasis through Fine Tuning the Homer-1b in Zebrafish." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/64522332422830888509.

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碩士<br>國立臺灣大學<br>分子與細胞生物學研究所<br>101<br>Previously we reported an intronic microRNA (miR), miR-In300 or miR-3906, which locates at the first intron of zebrafish myf5 gene, suppresses the transcription of myf5 through silencing dickkopf-related protein 3 (dkk3r/dkk3a) during early development such as 16 hpf when myf5 is highly transcribed. However, when myf5 mRNAs are gradually reduced to undetectable level in mature somites at late developmental stage, miR-3906 is still predominant. We had been performed LAMP assay and in vitro/in vivo luciferase reporter assay, and found that miR-3906 enabled t

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18

Tintinger, Gregory Ronald. "Membrane potential and intracellular cyclic AMP as regulators of calcium homeostasis in formyl peptide-activated human neutrophils : lessons from chronic granulomatous disease." Thesis, 2002. http://hdl.handle.net/2263/29223.

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Neutrophils playa key role in the systemic inflammatory response which may lead to serious tissue injury and multiple organ dysfunction. In this setting, activated neutrophils, largely in response to tumour necrosis factor-alpha (TNF-α), secrete reactive oxidants, granule proteases and bioactive lipids, as well as pro-inflammatory cytokines, emphasising the importance of these cells as targets for anti-inflammatory therapies. There are, however, only a few currently available agents that directly modulate neutrophil pro-inflammatory responses in clinical practice, with corticosteroids being re

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19

Kwan, Melodie. "Effect of the mood stabilizer valproate on intracellular calcium homeostatis in bipolar I disorder." 2004. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=95225&T=F.

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