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Relevant bibliographies by topics / Intracellular calcium homeostasis

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Dissertations / Theses

Academic literature on the topic 'Intracellular calcium homeostasis'

Author: Grafiati

Published: 25 May 2024

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Dissertations / Theses on the topic "Intracellular calcium homeostasis"

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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