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Relevant bibliographies by topics / Unipore calcique mitochondrial

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Academic literature on the topic 'Unipore calcique mitochondrial'

Author: Grafiati

Published: 24 May 2025

Last updated: 29 May 2025

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Journal articles on the topic "Unipore calcique mitochondrial"

1

Wang, Guang Jian, and Stanley A. Thayer. "NMDA-Induced Calcium Loads Recycle Across the Mitochondrial Inner Membrane of Hippocampal Neurons in Culture." Journal of Neurophysiology 87, no. 2 (2002): 740–49. http://dx.doi.org/10.1152/jn.00345.2001.

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Mitochondria sequester N-methyl-d-aspartate (NMDA)-induced Ca2+ loads and regulate the shape of intracellular Ca2+ concentration ([Ca2+]i) responses in neurons. When isolated mitochondria are exposed to high [Ca2+],Ca2+ enters the matrix via the uniporter and returns to the cytosol by Na+/Ca2+ exchange. Released Ca2+ may re-enter the mitochondrion recycling across the inner membrane dissipating respiratory energy. Ca2+ recycling, the continuous uptake and release of Ca2+ by mitochondria, has not been described in intact neurons. Here we used single-cell microfluorimetry to measure [Ca2+]i and

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2

Dubinin, Mikhail V., Eugeny Yu Talanov, Kirill S. Tenkov, Vlada S. Starinets, Natalia V. Belosludtseva, and Konstantin N. Belosludtsev. "The Effect of Deflazacort Treatment on the Functioning of Skeletal Muscle Mitochondria in Duchenne Muscular Dystrophy." International Journal of Molecular Sciences 21, no. 22 (2020): 8763. http://dx.doi.org/10.3390/ijms21228763.

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Duchenne muscular dystrophy (DMD) is a severe hereditary disease caused by a lack of dystrophin, a protein essential for myocyte integrity. Mitochondrial dysfunction is reportedly responsible for DMD. This study examines the effect of glucocorticoid deflazacort on the functioning of the skeletal-muscle mitochondria of dystrophin-deficient mdx mice and WT animals. Deflazacort administration was found to improve mitochondrial respiration of mdx mice due to an increase in the level of ETC complexes (complexes III and IV and ATP synthase), which may contribute to the normalization of ATP levels in

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3

Rimessi, Alessandro, Chiara Pozzato, Lorenzo Carparelli, et al. "Pharmacological modulation of mitochondrial calcium uniporter controls lung inflammation in cystic fibrosis." Science Advances 6, no. 19 (2020): eaax9093. http://dx.doi.org/10.1126/sciadv.aax9093.

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Mitochondria physically associate with the endoplasmic reticulum to coordinate interorganelle calcium transfer and regulate fundamental cellular processes, including inflammation. Deregulated endoplasmic reticulum–mitochondria cross-talk can occur in cystic fibrosis, contributing to hyperinflammation and disease progression. We demonstrate that Pseudomonas aeruginosa infection increases endoplasmic reticulum–mitochondria associations in cystic fibrosis bronchial cells by stabilizing VAPB-PTPIP51 (vesicle-associated membrane protein–associated protein B–protein tyrosine phosphatase interacting

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4

Naon, Deborah, Marta Zaninello, Marta Giacomello, et al. "Critical reappraisal confirms that Mitofusin 2 is an endoplasmic reticulum–mitochondria tether." Proceedings of the National Academy of Sciences 113, no. 40 (2016): 11249–54. http://dx.doi.org/10.1073/pnas.1606786113.

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The discovery of the multiple roles of mitochondria–endoplasmic reticulum (ER) juxtaposition in cell biology often relied upon the exploitation of Mitofusin (Mfn) 2 as an ER–mitochondria tether. However, this established Mfn2 function was recently questioned, calling for a critical re-evaluation of Mfn2’s role in ER–mitochondria cross-talk. Electron microscopy and fluorescence-based probes of organelle proximity confirmed that ER–mitochondria juxtaposition was reduced by constitutive or acute Mfn2 deletion. Functionally, mitochondrial uptake of Ca2+ released from the ER was reduced following a

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5

Tedesco, Scattolini, Albiero, et al. "Mitochondrial Calcium Uptake Is Instrumental to Alternative Macrophage Polarization and Phagocytic Activity." International Journal of Molecular Sciences 20, no. 19 (2019): 4966. http://dx.doi.org/10.3390/ijms20194966.

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Macrophages are highly plastic and dynamic cells that exert much of their function through phagocytosis. Phagocytosis depends on a coordinated, finely tuned, and compartmentalized regulation of calcium concentrations. We examined the role of mitochondrial calcium uptake and mitochondrial calcium uniporter (MCU) in macrophage polarization and function. In primary cultures of human monocyte-derived macrophages, calcium uptake in mitochondria was instrumental for alternative (M2) macrophage polarization. Mitochondrial calcium uniporter inhibition with KB-R7943 or MCU knockdown, which prevented mi

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6

Zhang, Linlin, Jingyi Qi, Xu Zhang, et al. "The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells." International Journal of Molecular Sciences 23, no. 12 (2022): 6667. http://dx.doi.org/10.3390/ijms23126667.

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Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca2+ is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca2+ participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca2+ through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca2+ in both mitochondria

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7

MONTERO, Mayte, Carmen D. LOBATÓN, Esther HERNÁNDEZ-SANMIGUEL, et al. "Direct activation of the mitochondrial calcium uniporter by natural plant flavonoids." Biochemical Journal 384, no. 1 (2004): 19–24. http://dx.doi.org/10.1042/bj20040990.

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During cell activation, mitochondria play an important role in Ca2+ homoeostasis due to the presence of a fast and specific Ca2+ channel in its inner membrane, the mitochondrial Ca2+ uniporter. This channel allows mitochondria to buffer local cytosolic [Ca2+] changes and controls the intramitochondrial Ca2+ levels, thus modulating a variety of phenomena from respiratory rate to apoptosis. We have described recently that SB202190, an inhibitor of p38 MAPK (mitogen-activated protein kinase), strongly activated the uniporter. We show in the present study that a series of natural plant flavonoids,

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8

Satrústegui, Jorgina, Beatriz Pardo, and Araceli del Arco. "Mitochondrial Transporters as Novel Targets for Intracellular Calcium Signaling." Physiological Reviews 87, no. 1 (2007): 29–67. http://dx.doi.org/10.1152/physrev.00005.2006.

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Ca2+signaling in mitochondria is important to tune mitochondrial function to a variety of extracellular stimuli. The main mechanism is Ca2+entry in mitochondria via the Ca2+uniporter followed by Ca2+activation of three dehydrogenases in the mitochondrial matrix. This results in increases in mitochondrial NADH/NAD ratios and ATP levels and increased substrate uptake by mitochondria. We review evidence gathered more than 20 years ago and recent work indicating that substrate uptake, mitochondrial NADH/NAD ratios, and ATP levels may be also activated in response to cytosolic Ca2+signals via a mec

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9

Tsai, Chen-Wei, Yujiao Wu, Ping-Chieh Pao, et al. "Proteolytic control of the mitochondrial calcium uniporter complex." Proceedings of the National Academy of Sciences 114, no. 17 (2017): 4388–93. http://dx.doi.org/10.1073/pnas.1702938114.

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The mitochondrial calcium uniporter is a Ca2+-activated Ca2+ channel complex mediating mitochondrial Ca2+ uptake, a process crucial for Ca2+ signaling, bioenergetics, and cell death. The uniporter is composed of the pore-forming MCU protein, the gatekeeping MICU1 and MICU2 subunits, and EMRE, a single-pass membrane protein that links MCU and MICU1 together. As a bridging subunit required for channel function, EMRE could paradoxically inhibit uniporter complex formation if expressed in excess. Here, we show that mitochondrial mAAA proteases AFG3L2 and SPG7 rapidly degrade unassembled EMRE using

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10

Zavodnik, I. B. "Mitochondria, calcium homeostasis and calcium signaling." Biomeditsinskaya Khimiya 62, no. 3 (2016): 311–17. http://dx.doi.org/10.18097/pbmc20166203311.

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Са2+ is a very important and versatile intracellular signal which controls numerous biochemical and physiological (pathophysiological) processes in the cell. Good evidence exists that mitochondria are sensors, decoders and regulators of calcium signaling. Precise regulation of calcium signaling in the cell involves numerous molecular targets, which induce and decode changes of Са2+ concentrations in the cell (pumps, channels, Са2+-binding proteins, Са2+-dependent enzymes, localized in the cytoplasm and organelles). Mitochondrial Са2+ uniporter accumulates excess of Са2+ in mitochondria, while

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