Academic literature on the topic 'Mitochondrial movement'
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Journal articles on the topic "Mitochondrial movement":
Elizaveta, Bon. "Mitochondrial Movement: A Review." Clinical Research Notes 3, no. 3 (April 30, 2022): 01–06. http://dx.doi.org/10.31579/2690-8816/059.
Delmotte, Philippe, Vanessa A. Zavaletta, Michael A. Thompson, Y. S. Prakash, and Gary C. Sieck. "TNFα decreases mitochondrial movement in human airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 1 (July 1, 2017): L166—L176. http://dx.doi.org/10.1152/ajplung.00538.2016.
Gurdon, Csanad, Zora Svab, Yaping Feng, Dibyendu Kumar, and Pal Maliga. "Cell-to-cell movement of mitochondria in plants." Proceedings of the National Academy of Sciences 113, no. 12 (March 7, 2016): 3395–400. http://dx.doi.org/10.1073/pnas.1518644113.
E.I,, Bon. "Mechanisms of Movement of Mitochondria in the Cell." Clinical Endocrinology and Metabolism 1, no. 1 (October 26, 2022): 01–06. http://dx.doi.org/10.31579/2834-8761/005.
Yi, Muqing, David Weaver, and György Hajnóczky. "Control of mitochondrial motility and distribution by the calcium signal." Journal of Cell Biology 167, no. 4 (November 15, 2004): 661–72. http://dx.doi.org/10.1083/jcb.200406038.
Kaasik, Allen, Dzhamilja Safiulina, Alexander Zharkovsky, and Vladimir Veksler. "Regulation of mitochondrial matrix volume." American Journal of Physiology-Cell Physiology 292, no. 1 (January 2007): C157—C163. http://dx.doi.org/10.1152/ajpcell.00272.2006.
Simon, V. R., T. C. Swayne, and L. A. Pon. "Actin-dependent mitochondrial motility in mitotic yeast and cell-free systems: identification of a motor activity on the mitochondrial surface." Journal of Cell Biology 130, no. 2 (July 15, 1995): 345–54. http://dx.doi.org/10.1083/jcb.130.2.345.
Förtsch, Johannes, Eric Hummel, Melanie Krist, and Benedikt Westermann. "The myosin-related motor protein Myo2 is an essential mediator of bud-directed mitochondrial movement in yeast." Journal of Cell Biology 194, no. 3 (August 1, 2011): 473–88. http://dx.doi.org/10.1083/jcb.201012088.
Finsterer, J., and S. Zarrouk-Mahjoub. "Mitochondrial movement disorders." Revue Neurologique 172, no. 11 (November 2016): 716–17. http://dx.doi.org/10.1016/j.neurol.2016.09.002.
Beltran-Parrazal, Luis, Héctor E. López-Valdés, K. C. Brennan, Mauricio Díaz-Muñoz, Jean de Vellis, and Andrew C. Charles. "Mitochondrial transport in processes of cortical neurons is independent of intracellular calcium." American Journal of Physiology-Cell Physiology 291, no. 6 (December 2006): C1193—C1197. http://dx.doi.org/10.1152/ajpcell.00230.2006.
Dissertations / Theses on the topic "Mitochondrial movement":
Shchepinova, Maria M. "Molecular probes for monitoring mitochondrial movement and function." Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7835/.
Vaillant-Beuchot, Loan. "Étude des mécanismes liés aux dysfonctions mitochondriales, à l'altération de la mitophagie et aux défauts du transport mitochondrial dans la maladie d'Alzheimer." Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6019.
Mitochondria are essential organelles in cells, ensuring energy production with ATP synthesis, calcium buffering, apoptosis regulation. These functions are altered at early stages of Alzheimer's disease (AD) and are essentially induced by the Amyloid (Aβ), produced after the sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretase. Aβ is a major actor of AD development but all the treatments targeting this peptide remain ineffective. C-terminal APP fragments (APP-CTFs: C83 and C99 (Aβ precursor) are other fragments presenting specific toxicity in AD and new potential therapeutic targets. My project is focus on the study of APP-CTFs toxicity, independently of Aβ, on the structure, function of mitochondria, their degradation by mitophagy and on mitochondrial transport proteins. They constitute the complex allowing mitochondrial transport in cells, especially in neurons, closely linked to mitochondrial renewal, particularly in neurons.First axe: APP-CTFs impact on mitochondrial structure, function and mitophagy. We described APP-CTFs accumulation in mitochondrial fraction in vitro (human neuroblastoma cells expressing APP Swedish double mutation (SH-SY5Y-APPswe) or C99 fragment (SH-SY5Y-C99)) and in vivo (3xTgAD mice expressing APPswe, TauP301L, PS1 (M146V) or C99 fragment after viral injection). We inhibit the cleavage of APP-CTFs and the production of Aβ by pharmacological approaches, to abolish γ-secretase activity. Ours results show for the first time in vitro and in vivo, that high concentration of APP-CTFs independently of Aβ, impact mitochondrial structure, function and alter mitophagy process, resulting in an accumulation of altered mitochondria producing high levels of toxic reactive oxygen species. In addition, our results in patient brains of sporadic AD (SAD) patients show altered mitophagic protein levels correlating with APP-CTFs accumulation (1-2).Second axe: study of the effects of APP, APP-CTFs and Aβ peptide on mitochondrial transport machinery. I reported the specific regulation of mitochondrial transport protein by endogenous APP (Mice fibroblasts APP WT and KO) and the overexpression of APPswe (and in SH-SY-5Y-APPswe cells). APP-CTFs and Aβ differentially regulate mitochondrial transport protein levels in treated SH-SY-5Y-APPswe cells with γ-secretase inhibitor. These results were validated in mice fibroblasts KO for presenilins (catalytic compounds of γ-secretase) avoiding APP-CTFs degradation. APP-CTFs and Aβ impair the recruitment of mitochondria to its transport machinery in differentiated SHSY-5Y. The progression of the disease deregulates the levels of mitochondrial transport protein in vivo (3xTgAD and WT mice brains, C99 injected mice brains) and in SAD patients brains. The analyses of young and old mice brains and of SAD patients samples at different stages of the disease, allowed us to demonstrate an impact of aging in the regulation of mitochondrial transport protein levels. This phenomenon occurs also in addition with AD progression (3).These studies highlight new molecular mechanisms impacting mitochondrial homeostasis during AD progression. Our findings will bring new therapeutic research to slow down mitochondrial dysfunctions and/or to stimulate their renewal in AD context.(1). Vaillant-Beuchot L.*, Mary A.* et al. Acta Neuropathologica 2020.(2). Mary A.*, Vaillant-Beuchot L.* et al. Médecine/sciences 2021.(3). Vaillant-Beuchot et al. En cours de soumission
Eshleman, Jason Aaron. "Mitochondrial DNA and prehistoric population movements in western North America /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.
Murphy, Cheryl. "Influence of post-aerobic exercise nutrition on protein turnover and mitochondrial biogenesis." 2009. http://hdl.handle.net/2292/5429.
Granata, Cesare. "Effects of different exercise intensity and volume on markers of mitochondrial biogenesis in human skeletal muscle." Thesis, 2015. https://vuir.vu.edu.au/30176/.
Wang, Xiao Nan. "Skeletal muscle mitochondrial capacity and metabolism in lung transplant patients and resistance trained subjects." Thesis, 2000. https://vuir.vu.edu.au/15725/.
Hedges, Christopher. "The effects of physiological acidosis on skeletal muscle mitochondrial function, ROS balance, and intracellular signalling." Thesis, 2017. https://vuir.vu.edu.au/35976/.
Jamnick, Nicholas. "An examination of current methods to prescribe exercise intensity: validity of different approaches and effects on cell signalling events associated with mitochondrial biogenesis." Thesis, 2019. https://vuir.vu.edu.au/40459/.
Bartlett, Jonathan. "Exercise-induced cell signalling responses of human skeletal muscle: the effects of reduced carbohydrate availability." Thesis, 2012. https://vuir.vu.edu.au/29596/.
Woessner, Mary. "BEET-HF: The Effects of Dietary Inorganic Nitrate Supplementation on Aerobic Exercise Performance, Vascular Function, Cardiac Performance and Mitochondrial Respiration in Patients with Heart Failure with Reduced Ejection Fraction." Thesis, 2019. https://vuir.vu.edu.au/40041/.
Books on the topic "Mitochondrial movement":
Shaibani, Aziz. Ophthalmoplegia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0004.
Shaibani, Aziz. Ophthalmoplegia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0004.
Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Neurology and neurosurgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0014.
Forsyth, Rob, and Richard Newton. Specific conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0004.
Tick, Heather, and Eric B. Schoomaker. Transforming Pain Management Through the Integration of Complementary and Conventional Care. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190241254.003.0021.
McShane, Tony, Peter Clayton, Michael Donaghy, and Robert Surtees. Neurometabolic disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0213.
Book chapters on the topic "Mitochondrial movement":
Finsterer, Josef, and Salma Majid Wakil. "Genetics of Mitochondrial Disease with Focus on Movement Disorders." In Movement Disorder Genetics, 411–30. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17223-1_18.
Mehta, Arpan R., Siddharthan Chandran, and Bhuvaneish T. Selvaraj. "Assessment of Mitochondrial Trafficking as a Surrogate for Fast Axonal Transport in Human Induced Pluripotent Stem Cell–Derived Spinal Motor Neurons." In Methods in Molecular Biology, 311–22. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_16.
Lehninger, Albert L., Ernesto Carafoli, and Carlo S. Rossi. "Energy-Linked Ion Movements in Mitochondrial Systems." In Advances in Enzymology - and Related Areas of Molecular Biology, 259–320. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/9780470122747.ch6.
Kemble, R. J., S. Gabay-Laughnan, and J. R. Laughnan. "Movement of Genetic Information Between Plant Organelles: Mitochondria-Nuclei." In Genetic Flux in Plants, 79–87. Vienna: Springer Vienna, 1985. http://dx.doi.org/10.1007/978-3-7091-8765-4_5.
Wolkowicz, Paul. "Evidence for Hexagonal II Phase Lipid Involvement in Mitochondrial Ca2+ Movements." In Advances in Experimental Medicine and Biology, 131–38. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-0007-7_15.
Somlyo, A. V., M. Bond, R. Broderick, and A. P. Somlyo. "Calcium and Magnesium Movements Through Sarcoplasmic Reticulum, Endoplasmic Reticulum, and Mitochondria." In Advances in Experimental Medicine and Biology, 221–29. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-0007-7_24.
Lonsdale, David M. "Movement of Genetic Material Between the Chloroplast and Mitochondrion in Higher Plants." In Genetic Flux in Plants, 51–60. Vienna: Springer Vienna, 1985. http://dx.doi.org/10.1007/978-3-7091-8765-4_3.
Wong, Agnes. "Disorders Affecting the Extraocular Muscles." In Eye Movement Disorders. Oxford University Press, 2008. http://dx.doi.org/10.1093/oso/9780195324266.003.0023.
Schapira, A. H. V., and S. Przedborski. "Mitochondrial Dysfunction." In Encyclopedia of Movement Disorders, 181–84. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374105-9.00265-3.
Simon, D. K. "Mitochondrial Encephalopathies." In Encyclopedia of Movement Disorders, 185–87. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374105-9.00351-8.
Conference papers on the topic "Mitochondrial movement":
Pajic, Tanja, Miroslav Zivic, Mihailo Rabasovic, Aleksandar Krmpot, and Natasa Todorovic. "THE DAMPENING OF LIPID DROPLET OSCILLATORY MOVEMENT IN NITROGEN STARVED FILAMENTOUS FUNGI BY A LOW DOSE OF MITOCHONDRIAL RESPIRATION INHIBITOR." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.226p.
Perner, Petra. "The Study of the Internal Mitochondrial Movement of the Cells by Data Mining with Prototype-Based Classification." In 2014 International Conference on Intelligent Networking and Collaborative Systems (INCoS). IEEE, 2014. http://dx.doi.org/10.1109/incos.2014.30.
Yang, Liu, Chao Ma, and Wen li Chen. "The observation of mitochondrial movement and ATG5 position in Arabidopsis during the process of infection with virulent and avirulent P. syringae strains." In SPIE BiOS, edited by Samuel Achilefu and Ramesh Raghavachari. SPIE, 2012. http://dx.doi.org/10.1117/12.907215.
Ferreira, Marcos Venâncio Araújo, Rafael Henrique Neves Gomes, Fabiana Carla dos Santos Correia, Mariana Beber Chamon, Sérgio Roberto Pereira da Silva Júnior, Isadora Chain Lima, Marcus Vinicius de Sousa, Murilo Justino de Almeida, Daniel Sabino de Oliveira, and Thiago Cardoso Vale. "Idiopathic basal ganglia calcification and Hoarding disorder." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.499.
Reznikov, Konstantin M., and Pavel D. Kolesnichenko. "THE EFFECT OF DRUGS ON THE THREE-DIMENSIONAL STRUCTURE OF CARDIOMYOCYTES." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.24.
Pelloux, S., C. Ojeda, and Y. Tourneur. "An original method to quantify mitochondria movement in cultured cardiomyocytes." In Computers in Cardiology, 2005. IEEE, 2005. http://dx.doi.org/10.1109/cic.2005.1588229.
Sardet, C., C. Rouvière, B. Flannery, and J. Davoust. "Time lapse confocal microscopy of mitochondrial movements in ascidian embryos." In The living cell in four dimensions. AIP, 1991. http://dx.doi.org/10.1063/1.40578.
Reports on the topic "Mitochondrial movement":
Sadot, Einat, Christopher Staiger, and Mohamad Abu-Abied. Studies of Novel Cytoskeletal Regulatory Proteins that are Involved in Abiotic Stress Signaling. United States Department of Agriculture, September 2011. http://dx.doi.org/10.32747/2011.7592652.bard.