Impaired mitochondrial function due to familial Alzheimer's disease-causing presenilins mutants via Ca(2+) disruptions.
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[1] Hong Qi,et al. Optimal microdomain crosstalk between endoplasmic reticulum and mitochondria for Ca2+ oscillations , 2015, Scientific Reports.
[2] Hajime Takano,et al. Suppression of InsP3 Receptor-Mediated Ca2+ Signaling Alleviates Mutant Presenilin-Linked Familial Alzheimer's Disease Pathogenesis , 2014, The Journal of Neuroscience.
[3] B. Kazmierczak,et al. Membrane associated complexes in calcium dynamics modelling , 2013, Physical biology.
[4] David Terman,et al. Modeling the neuroprotective role of enhanced astrocyte mitochondrial metabolism during stroke. , 2013, Biophysical journal.
[5] Rosario Rizzuto,et al. Mitochondria as sensors and regulators of calcium signalling , 2012, Nature Reviews Molecular Cell Biology.
[6] David Terman,et al. The low conductance mitochondrial permeability transition pore confers excitability and CICR wave propagation in a computational model. , 2011, Journal of theoretical biology.
[7] I. Bezprozvanny,et al. Neuronal calcium signaling, mitochondrial dysfunction, and Alzheimer's disease. , 2010, Journal of Alzheimer's disease : JAD.
[8] Robert W Buzzeo,et al. Mitochondrial amyloid-beta levels are associated with the extent of mitochondrial dysfunction in different brain regions and the degree of cognitive impairment in Alzheimer's transgenic mice. , 2010, Journal of Alzheimer's disease : JAD.
[9] T. Iwatsubo,et al. Gain-of-Function Enhancement of IP3 Receptor Modal Gating by Familial Alzheimer’s Disease–Linked Presenilin Mutants in Human Cells and Mouse Neurons , 2010, Science Signaling.
[10] Michael J. Berridge,et al. Calcium hypothesis of Alzheimer’s disease , 2010, Pflügers Archiv - European Journal of Physiology.
[11] R. Rizzuto,et al. Modulation of intracellular Ca2+ signalling in HeLa cells by the apoptotic cell death enhancer PK11195. , 2008, Biochemical pharmacology.
[12] V. Lee,et al. Mechanism of Ca2+ Disruption in Alzheimer's Disease by Presenilin Regulation of InsP3 Receptor Channel Gating , 2008, Neuron.
[13] M. Brini,et al. Calcium Homeostasis and Mitochondrial Dysfunction in Striatal Neurons of Huntington Disease* , 2008, Journal of Biological Chemistry.
[14] T. Pozzan,et al. Mitochondrial Ca2+ as a key regulator of cell life and death , 2007, Cell Death and Differentiation.
[15] M. S. Jafri,et al. Effect of Ca2+ on cardiac mitochondrial energy production is modulated by Na+ and H+ dynamics. , 2007, American journal of physiology. Cell physiology.
[16] Don-On Daniel Mak,et al. Inositol trisphosphate receptor Ca2+ release channels. , 2007, Physiological reviews.
[17] M. Saleet Jafri,et al. Modeling the mechanism of metabolic oscillations in ischemic cardiac myocytes. , 2006, Journal of theoretical biology.
[18] M. Beal,et al. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases , 2006, Nature.
[19] John Hardy,et al. A Hundred Years of Alzheimer's Disease Research , 2006, Neuron.
[20] F. LaFerla,et al. Enhanced caffeine‐induced Ca2+ release in the 3xTg‐AD mouse model of Alzheimer's disease , 2005, Journal of neurochemistry.
[21] M. S. Jafri,et al. Mitochondrial Calcium Signaling and Energy Metabolism , 2005, Annals of the New York Academy of Sciences.
[22] F. LaFerla,et al. Alzheimer's disease: Aβ, tau and synaptic dysfunction , 2005 .
[23] Grace E. Stutzmann. Calcium Dysregulation, IP3 Signaling, and Alzheimer’s Disease , 2005, The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry.
[24] Raimond L Winslow,et al. A mitochondrial oscillator dependent on reactive oxygen species. , 2004, Biophysical journal.
[25] Grace E Stutzmann,et al. Dysregulated IP3 Signaling in Cortical Neurons of Knock-In Mice Expressing an Alzheimer's-Linked Mutation in Presenilin1 Results in Exaggerated Ca2+ Signals and Altered Membrane Excitability , 2004, The Journal of Neuroscience.
[26] M. Hayden,et al. Huntingtin and Huntingtin-Associated Protein 1 Influence Neuronal Calcium Signaling Mediated by Inositol-(1,4,5) Triphosphate Receptor Type 1 , 2003, Neuron.
[27] R. Winslow,et al. An integrated model of cardiac mitochondrial energy metabolism and calcium dynamics. , 2003, Biophysical journal.
[28] H. Kretzschmar,et al. Capacitive Calcium Entry Is Directly Attenuated by Mutant Presenilin-1, Independent of the Expression of the Amyloid Precursor Protein* , 2003, The Journal of Biological Chemistry.
[29] F. LaFerla. Calcium dyshomeostasis and intracellular signalling in alzheimer's disease , 2002, Nature Reviews Neuroscience.
[30] R. Balaban,et al. Simulation of cardiac work transitions, in vitro: effects of simultaneous Ca2+ and ATPase additions on isolated porcine heart mitochondria. , 2001, Cell calcium.
[31] J. Keizer,et al. Mitochondrial modulation of intracellular Ca(2+) signaling. , 2001, Journal of theoretical biology.
[32] E. Barrett,et al. Stimulation-Evoked Increases in Cytosolic [Ca2+] in Mouse Motor Nerve Terminals Are Limited by Mitochondrial Uptake and Are Temperature-Dependent , 2000, The Journal of Neuroscience.
[33] R. Empson,et al. Functional Phenotype in Transgenic Mice Expressing Mutant Human Presenilin-1 , 2000, Neurobiology of Disease.
[34] M. Mattson,et al. Presenilin-1 Mutation Increases Neuronal Vulnerability to Focal Ischemia In Vivo and to Hypoxia and Glucose Deprivation in Cell Culture: Involvement of Perturbed Calcium Homeostasis , 2000, The Journal of Neuroscience.
[35] B. de Strooper,et al. Presenilin 1 Controls γ-Secretase Processing of Amyloid Precursor Protein in Pre-Golgi Compartments of Hippocampal Neurons , 1999, The Journal of cell biology.
[36] C. Cotman,et al. Alzheimer's Presenilin-1 Mutation Potentiates Inositol 1,4,5-Trisphosphate-Mediated Calcium Signaling in Xenopus , 1999 .
[37] Michael R. Duchen,et al. Transient Mitochondrial Depolarizations Reflect Focal Sarcoplasmic Reticular Calcium Release in Single Rat Cardiomyocytes , 1998, The Journal of cell biology.
[38] M. Beal,et al. Mitochondrial dysfunction in neurodegenerative diseases. , 1998, Biochimica et biophysica acta.
[39] Lawrence M. Lifshitz,et al. Close contacts with the endoplasmic reticulum as determinants of mitochondrial Ca2+ responses. , 1998, Science.
[40] Hugo Vanderstichele,et al. Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein , 1998, Nature.
[41] J. Hardy,et al. The presenilins and Alzheimer's disease. , 1997, Human molecular genetics.
[42] J. Keizer,et al. Minimal model of beta-cell mitochondrial Ca2+ handling. , 1997, The American journal of physiology.
[43] A. Vercesi,et al. The Role of Reactive Oxygen Species in Mitochondrial Permeability Transition , 1997, Bioscience reports.
[44] J. Keizer,et al. A single-pool inositol 1,4,5-trisphosphate-receptor-based model for agonist-stimulated oscillations in Ca2+ concentration. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[45] J. Mccormack,et al. Role of calcium ions in regulation of mammalian intramitochondrial metabolism. , 1990, Physiological reviews.
[46] Z. Khachaturian. Introduction and Overview , 1989, Annals of the New York Academy of Sciences.
[47] R. Denton,et al. Ca2+ transport by mammalian mitochondria and its role in hormone action. , 1985, The American journal of physiology.
[48] R. Bohnensack. The role of the adenine nucleotide translocator in oxidative phosphorylation. A theoretical investigation on the basis of a comprehensive rate law of the translocator , 1982, Journal of bioenergetics and biomembranes.
[49] E. Melamed,et al. Apoptosis as a general cell death pathway in neurodegenerative diseases. , 2000, Journal of neural transmission. Supplementum.