Academic literature on the topic 'Mitochondria'
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Journal articles on the topic "Mitochondria"
Amchenkova, A. A., L. E. Bakeeva, Y. S. Chentsov, V. P. Skulachev, and D. B. Zorov. "Coupling membranes as energy-transmitting cables. I. Filamentous mitochondria in fibroblasts and mitochondrial clusters in cardiomyocytes." Journal of Cell Biology 107, no. 2 (August 1, 1988): 481–95. http://dx.doi.org/10.1083/jcb.107.2.481.
Full textBanerjee, Partha S., Junfeng Ma, and Gerald W. Hart. "Diabetes-associated dysregulation ofO-GlcNAcylation in rat cardiac mitochondria." Proceedings of the National Academy of Sciences 112, no. 19 (April 27, 2015): 6050–55. http://dx.doi.org/10.1073/pnas.1424017112.
Full textSeo, Young Ah, Veronica Lopez, and Shannon L. Kelleher. "A histidine-rich motif mediates mitochondrial localization of ZnT2 to modulate mitochondrial function." American Journal of Physiology-Cell Physiology 300, no. 6 (June 2011): C1479—C1489. http://dx.doi.org/10.1152/ajpcell.00420.2010.
Full textScanlon, David P., and Michael W. Salter. "Strangers in strange lands: mitochondrial proteins found at extra-mitochondrial locations." Biochemical Journal 476, no. 1 (January 7, 2019): 25–37. http://dx.doi.org/10.1042/bcj20180473.
Full textDeng, Huichao, Xinhua Qiao, Ting Xie, Wenfeng Fu, Hang Li, Yanmei Zhao, Miaomiao Guo, et al. "SLC-30A9 is required for Zn2+ homeostasis, Zn2+ mobilization, and mitochondrial health." Proceedings of the National Academy of Sciences 118, no. 35 (August 25, 2021): e2023909118. http://dx.doi.org/10.1073/pnas.2023909118.
Full textZorov, Dmitry B., Magdalena Juhaszova, and Steven J. Sollott. "Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release." Physiological Reviews 94, no. 3 (July 2014): 909–50. http://dx.doi.org/10.1152/physrev.00026.2013.
Full textHenderson, V., and M. J. Song. "Morphology of mitochondria in a teleost, salmo gairdneri." Proceedings, annual meeting, Electron Microscopy Society of America 44 (August 1986): 194–95. http://dx.doi.org/10.1017/s0424820100142591.
Full textHaseeb, Abdul, Hong Chen, Yufei Huang, Ping Yang, Xuejing Sun, Adeela Iqbal, Nisar Ahmed, et al. "Remodelling of mitochondria during spermiogenesis of Chinese soft-shelled turtle (Pelodiscus sinensis)." Reproduction, Fertility and Development 30, no. 11 (2018): 1514. http://dx.doi.org/10.1071/rd18010.
Full textFu, Ailing. "Mitotherapy as a Novel Therapeutic Strategy for Mitochondrial Diseases." Current Molecular Pharmacology 13, no. 1 (January 15, 2020): 41–49. http://dx.doi.org/10.2174/1874467212666190920144115.
Full textQin, Lingyu, and Shuhua Xi. "The role of Mitochondrial Fission Proteins in Mitochondrial Dynamics in Kidney Disease." International Journal of Molecular Sciences 23, no. 23 (November 25, 2022): 14725. http://dx.doi.org/10.3390/ijms232314725.
Full textDissertations / Theses on the topic "Mitochondria"
Jugé, Romain. "Étude de la dynamique mitochondriale dans des cellules cutanées humaines : Mise en place de modèles pour des applications en cosmétologie." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSEN007.
Full textThe skin is a specialized type of epithelium, both vital and fragile, which evolves with age and is continuously exposed to environmental stresses, such as solar radiations. While data is available about the response of the mitochondrial network and the fate of damaged mitochondria after chemical or environmental stresses in numerous experimental systems, little is known about these processes in skin cells. The aim of the present thesis was to study the impact (i) of UVB irradiation on mitochondrial dynamics (especially mitochondrial fragmentation) in normal human epidermal keratinocytes, which represent the first line of defence against environmental insults; (ii) of poisoning mitochondria of keratinocytes and normal human fibroblasts with chemical drugs. In a first axis, we developed an original method (called Mitoshape) based on confocal microscopy, to estimate qualitatively and quantitatively the morphology of the mitochondrial network within live cells following UVB irradiation. Using this technology, we demonstrated that UVB irradiation induces mitochondrial fragmentation in normal human keratinocytes, and studied the biochemical actors involved in this response. In a second axis, we showed that the use of mitochondrial poisons could damage mitochondria of keratinocytes and normal human fibroblasts and induce bulk autophagy, although it is not possible to formally rule out the involvement of a PINK1/PARKIN-dependent pathway of mitophagy. In addition to its fundamental interest, this work (performed in collaboration with the cosmetic company SILAB in the context of a CIFRE PhD fellowship from ANRT) paves the way for the screening of novel bioactive agents able to protect and restore mitochondria following stresses
Mortz, Mathieu. "Flexibilités bioénergétique et génomique mitochondriales chez l’oiseau." Thesis, Lyon, 2019. https://n2t.net/ark:/47881/m6v40tjz.
Full textBirds are endotherms that exhibit a remarkable metabolic flexibility in response to energetic constraints related to their lifestyles. This flexibility is notably involved during nutritional transitions in order to adjust metabolic intensity to the available energy resources, a prerequisite for survival. Mitochondria, that produce most of cellular ATP production, are involved in the modulations observed during a fast and during refeeding. The aim of this thesis was to investigate the flexibility of mitochondrial functions in response to fasting and refeeding in Muscovy ducks (Cairina moschata). Several aspects, ranging from bioenergetics and anatomical organization to genomics and evolution of species, were analysed to better understand the modulations involved to adjust mitochondrial functioning to energy constraints. A first study described the kinetics of the installation of fasting-induced muscle hypometabolism and the associated improved mitochondrial bioenergetics efficiency and showed that maximum acclimation was reached after 3 days. Mitochondrial networks remodelling, investigated by antibodies (Western blot) and confocal microscopy, showed a bidirectional flexibility with an increased fusion at the beginning of the fast preceding an increased fragmentation observable after 4 days of fasting. A second study suggested the potential involvement of a nitric oxide synthase (NOS) activity detected in mitochondrial fractions in the modulations of mitochondrial bioenergetics induced by fasting. The activity of mitochondrial NOS was found to be increased by fasting and its in vitro modulation mimicked the effects induced by fasting in nourished birds, in a rapid and reversible manner. A third study explored the flexibility of the mitochondrial genome in order to detect the presence of open reading frames (ORF) potentially encoding bioactive peptides similar to those described in mammals and that are encoded by small regions included in the 12S and 16S genes. Our genetic analyses demonstrated the presence of ORFs incorporated into the 16S rRNA coding gene of most avian species. The molecular evolution of these ORFs among bird species was found to be similar to that calculated for all mitochondrial genes coding for subunits of the respiratory chain. Among the detected ORFs, some corresponded to those described in mammals (humanin and SHLP6) but others had never been described. A fourth study showed that the very strong nucleotide conservation of ORFs located in the 16S gene, and observed in mammals, birds and terrestrial ectotherms, was not an artifact linked to a constraint imposed by the structure of the encoded rRNA. Indeed, the strong nucleotide conservation was not found on alignments of sequences generated by simulations of evolution that took into account the secondary and tertiary structures of 16S rRNA. In the 3 groups of vertebrates, the ORF coding humanin, a peptide identified in humans, underwent a specific negative selection pressure in order to maintain its amino-acid composition during evolution. In conclusion, this thesis highlighted the remarkable bioenergetics and genomic flexibilities of mitochondrial function in birds, which could contribute to the metabolic adjustments required during nutritional transitions. Our results have also opened up a new field of investigation concerning the putative peptides encoded by the mitochondrial genome and their biological roles remain to be explored
Al, Amir Dache Zahra. "Étude de la structure de l'ADN circulant d'origine mitochondriale." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT059.
Full textPlasma transports blood cells with a mixture of compounds, including nutrients, waste, antibodies, and chemical messengers...throughout the body. Non-soluble factors such as circulating DNA and extracellular vesicles have recently been added to the list of these components and have been the subject of extensive research due to their role in intercellular communication. Circulating DNA (cirDNA) is composed of cell-free and particle-associated DNA fragments, which can be released by all cell types. cirDNA is derived not only from genomic DNA but also from extrachromosomal mitochondrial DNA. Numerous studies carried out lately indicate that the quantitative and qualitative analysis of cirDNA represents a breakthrough in clinical applications as a non-invasive biomarker for diagnosis, prognosis and therapeutic follow-up. However, despite the promising future of cirDNA in clinical applications, particularly in oncology, knowledge regarding its origins, composition and functions, that could considerably optimize its diagnostic value, is still lacking.The main goal of my thesis was to identify and characterize the structural properties of extracellular DNA of mitochondrial origin. By examining the integrity of this DNA, as well as the size and density of associated structures, this work revealed the presence of dense particles larger than 0.2 µm containing whole mitochondrial genomes. We characterized these structures by electron microscopy and flow cytometry and identified intact mitochondria in the extracellular medium in vitro and ex vivo (in plasma samples from healthy individuals). Oxygen consumption by these mitochondria was detected by the Seahorse technology, suggesting that at least some of these intact extracellular mitochondria may be functional.In addition, I contributed to other studies carried out in the team, such as studies aiming at evaluating (1) the influence of pre-analytical and demographic parameters on the quantification of nuclear and mitochondrial cirDNA on a cohort of 104 healthy individuals and 118 patients with metastatic colorectal cancer, (2) the influence of hypoxia on the release of cirDNA in vitro and in vivo, and (3) the potential of cirDNA analysis in the early detection and screening of cancer.This manuscript present a recent review on cirDNA and its different mechanisms of release, which go hand in hand with the structural characterization of this DNA, its functional aspects and its clinical applications. In addition, this thesis provides new knowledge on the structure of extracellular mitochondrial DNA and opens up new avenues for reflection, particularly on the potential impact that could have those circulating mitochondria on cell-cell communication, inflammation and clinical applications
Beinat, Marine. "Caractérisation génétique des atteintes hépatiques mitochondriales." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T007/document.
Full textGenetic characterization of mitochondrial liver damage
Reinhardt, Camille. "Impact de la voie d’import mitochondrial contrôlée par le complexe AIF/CHCHD4 sur la survie des cellules cancéreuses et la réponse aux traitements anticancéreux." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS542.
Full textIn the vast majority of cases, mitochondria are required for tumorigenesis and also for the tumoral response to signals generated by the microenvironmental factors (e.g. nutrient deprivation, hypoxia) or to the effects of anti-cancer treatments (e.g. chemotherapy, radiotherapy). As almost all mitochondrial proteins are nuclear-encoded and imported into the organelle, specialized import machineries have evolved in order to meet the need for protein import. Among these machineries, the one that operates in the intermembrane space and is controlled by CHCHD4/Mia40, regulates the import of a group of proteins (substrates) that play important roles in survival and stress response. Substrates of CHCHD4/Mia40 are involved in a broad panel of mitochondrial activities that includes the biogenesis of respiratory chain complexes, lipid homeostasis, calcium storage, as well as ultrastructure and mitochondrial dynamics. This thesis program was dedicated to the study of the CHCHD4/Mia40 import pathway in cancer cells, with a particular interest for one of the CHCHD4/Mia40 substrates that shapes mitochondrial ultrastructure. Using RNA interference approach and recombinant protein overexpression technique, in a colon cancer model, we showed that the expression of this substrate had a crucial effect on proliferation and tumor growth. Our data also involved this protein in the response to anti-cancer treatments. All together, this work opens a new field of investigations that will not only shed new lights on the metabolic plasticity of cancer cells but also help to identify new metabolic biomarkers
Renken, Christian Wolfgang. "The structure of mitochondria /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3141929.
Full textCraig, Elaine. "Protein import into cardiac mitochondria." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ39261.pdf.
Full textEsteves, Pauline. "Etude de l’action anti-tumorale de la protéine mitochondriale UCP2." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T024.
Full textDysregulation of cellular metabolism has been associated with malignant transformation. Switching from oxidative phosphorylation (OXPHOS) to glycolysis for ATP production allows cancer cells to be less oxygen dependent, thus favoring invasion processes. Effects on metabolism, and more particularly mitochondria metabolism, thus represent a potential therapeutic target for cancer therapy. Uncoupling protein 2 (UCP2) is a member of UCPs, a subfamily of the mitochondrial carriers. The function of UCP2 is still controversial but we recently showed its role in the modulation of cell metabolism. Therefore, UCP2 is a good candidate to address the crosstalk between metabolic alteration and promotion of cancer progression and invasion. We show that cancer cells overexpressing UCP2 shift their metabolism from glycolysis toward oxidative phosphorylation and become poorly tumorigenic. Altered expression of glycolytic and oxidative enzymes underlies the cell metabolic shift. Moreover, UCP2 overexpression is associated with an increased adenosine monophosphate-activated protein kinase (AMPK) signaling together with a downregulation of hypoxia-induced factor (HIF) expression. In line with our previous observations, UCP2 does not function as an uncoupling protein but rather controls mitochondrial substrate routing. To address UCP2 role in cancer in vivo, we investigate the impact of Ucp2 deletion in two colorectal cancer mice models: a transgenic mice model APCmin/+ and a chemical cancer mice model (azoxymethane + dextran disulfate (AOM-DSS)). These two models are complementary because they allow us to determine if the role of UCP2 in cancer differs in only one genetic background (APC) compared with an inflammatory model (AOM + DSS). We found in those two colorectal cancer models that UCP2 is more expressed in tumors instead of the adjacent healthy mucosa. Deletion of Ucp2 in APCmin/+ mice leads to decrease in animal survival and Ucp2 deletion is associated in both mice models with an increased number of tumors. Altogether the results suggest that tumor initiation could be increased with Ucp2 deletion. UCP2 thus appears as a critical regulator of cellular metabolism with a relevant action against tumor maintenance and malignancy
Ruby, Vincent. "Étude des évènements mitochondriaux impliqués dans le contrôle de l'apoptose par rbf1, l'homologue de drosophile du gène suppresseur de tumeur rb." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLV039/document.
Full textThe gene rb is the first tumor suppressor discovered in humans. Its prevents the appearance of tumors by regulating negatively the cell cycle. The role of pRb in apoptosis is more complex and the molecular mechanisms triggered by this transcription factor are not completely elucidated. There is a rb homologue in drosophila: rbf1. I participated in the characterization of mitochondrial events induced during activation of apoptosis by Rbf1 in a proliferating tissue of this model organism, the wing disc. In this apoptosis pathway, the Debcl protein, the only drosophila pro-apoptotic member of the Bcl-2 family, is activated and induces recruitment and oligomerization of Drp1, the main effector of mitochondrial fission. This triggers the mitochondrial fragmentation and the accumulation of mitochondrial reactive oxygen species (ROS). Both events participate to the transmission of the apoptotic signal. I have also been able to highlight the implication of factors involved in maintaining mitochondrial quality control which ensures the integrity of the mitochondria and, if necessary, triggers the degradation of damaged elements by mitophagy. Finally, I have contributed to the study of the links between translation and apoptosis induced by Rbf1. In this study, we show that the Poly-A Binding Protein (PABP) can suppress the Rbf1-induced notch phenotype in adults while cell death induced during larval stage was not inhibited but increased. These results prompted us to study the compensation mechanisms induced by the translational apparatus, which allowed us to show that a mRNA translation-related mechanism could counteract the loss of tissue resulting from Rbf1-induced apoptosis independently of apoptosis inhibition
Heller, Anne Sabine [Verfasser], and Achim [Akademischer Betreuer] Göpferich. "Targeting mitochondria by mitochondrial fusion, mitochondria-specific peptides and nanotechnology / Anne Sabine Heller. Betreuer: Achim Göpferich." Regensburg : Universitätsbibliothek Regensburg, 2013. http://d-nb.info/103321664X/34.
Full textBooks on the topic "Mitochondria"
St. John, Justin C., ed. Mitochondrial DNA, Mitochondria, Disease and Stem Cells. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-101-1.
Full textJohn, Justin C. St. Mitochondrial DNA, mitochondria, disease, and stem cells. New York: Humana Press, 2013.
Find full textTomar, Namrata, ed. Mitochondria. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2309-1.
Full textMokranjac, Dejana, and Fabiana Perocchi, eds. Mitochondria. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6824-4.
Full textSchaffer, Stephen W., and M.-Saadeh Suleiman, eds. Mitochondria. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-69945-5.
Full textScheffler, Immo E. Mitochondria. New York, USA: John Wiley & Sons, Inc., 1999. http://dx.doi.org/10.1002/0471223891.
Full textLeister, Dario, and Johannes M. Herrmann, eds. Mitochondria. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-365-3.
Full textA, Pon Liza, and Schon Eric A, eds. Mitochondria. San Diego, Calif: Academic, 2001.
Find full textW, Schaffer S., and Suleiman M. -Saadeh, eds. Mitochondria: The dynamic organelle. New York: Springer, 2007.
Find full textVan Aken, Olivier, and Allan G. Rasmusson, eds. Plant Mitochondria. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1653-6.
Full textBook chapters on the topic "Mitochondria"
Hangay, George, Susan V. Gruner, F. W. Howard, John L. Capinera, Eugene J. Gerberg, Susan E. Halbert, John B. Heppner, et al. "Mitochondrion, (pl., Mitochondria)." In Encyclopedia of Entomology, 2441–42. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_4638.
Full textValk, Jacob, and Marjo S. van der Knaap. "Mitochondria and Mitochondrial Dysfunction." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 128–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-02568-0_23.
Full textMorava, E., and J. A. M. Smeitink. "Mitochondria and Mitochondrial Disorders." In Magnetic Resonance of Myelination and Myelin Disorders, 195–203. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27660-2_23.
Full textvan der Knaap, Marjo S., and Jacob Valk. "Mitochondria and Mitochondrial Disorders." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 140–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03078-3_20.
Full textMattedi, Francesca, George Chennell, and Alessio Vagnoni. "Detailed Imaging of Mitochondrial Transport and Precise Manipulation of Mitochondrial Function with Genetically Encoded Photosensitizers in Adult Drosophila Neurons." In Methods in Molecular Biology, 385–407. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_20.
Full textHassinen, Ilmo. "Regulation of Mitochondrial Respiration in Heart Muscle." In Mitochondria, 3–25. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-69945-5_1.
Full textO’Rourke, Brian. "Mitochondrial Ion Channels." In Mitochondria, 221–38. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-69945-5_10.
Full textHalestrap, Andrew P., Samatha J. Clarke, and Igor Khalilin. "The Mitochondrial Permeability Transition Pore – from Molecular Mechanism to Reperfusion Injury and Cardioprotection." In Mitochondria, 241–69. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-69945-5_11.
Full textSuleiman, M.-Saadeh, and Stephen W. Schaffer. "The Apoptotic Mitochondrial Pathway – Modulators, Interventions and Clinical Implications." In Mitochondria, 271–90. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-69945-5_12.
Full textMurphy, Elizabeth, and Charles Steenbergen. "The Role of Mitochondria in Necrosis Following Myocardial Ischemia-Reperfusion." In Mitochondria, 291–301. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-69945-5_13.
Full textConference papers on the topic "Mitochondria"
Li, Ching-Wen, Pao-Hsin Yen, and Gou-Jen Wang. "A Cascade Microfluidic Device for High Quality Mitochondria Extraction." In ASME 2015 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/detc2015-46117.
Full textVitkovac, Aleksandra, Tanja Pajić, Marta Bukumira, Marina Stanić, Mihailo Rabasović, and Nataša Todorović. "Slight cooling during growth induced changes in filamentous fungi hypha mitochondrial morphology." In 2nd International Conference on Chemo and Bioinformatics. Institute for Information Technologies, University of Kragujevac, 2023. http://dx.doi.org/10.46793/iccbi23.334v.
Full textGetmanskaya, Alexandra, Nikolai Sokolov, and Vadim Turlapov. "Multiclass U-Net Segmentation of Brain Electron Microscopy Data." In 31th International Conference on Computer Graphics and Vision. Keldysh Institute of Applied Mathematics, 2021. http://dx.doi.org/10.20948/graphicon-2021-3027-508-518.
Full textAltaee, Muddather, Samaraa Youns, Abdullah Al-Nuaymia, Sara Dabdob, and Muhammad Alkataan. "The Protective Effects of a Phenolic Clove Extract on Mitochondria: An Animal Study." In 5th International Conference on Biomedical and Health Sciences, 439–43. Cihan University-Erbil, 2024. http://dx.doi.org/10.24086/biohs2024/paper.1201.
Full textJoseph Mathuram, T. L., Y. Su, M. Hatzoglou, Y. Perry, Y. Wu, and A. Blumental-Perry. "Mitochondria-to-Nucleus Retrograde Signaling Via Mitochondrial DNA Encoded Non-coding RNA Regulates Mitochondrial Bioenergetics." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4400.
Full textBelury, Martha. "Targeting inflammation and mitochondria with dietary linoleic acid for cardiometabolic health when research comes full circle." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/ivnn3784.
Full textChen, Chang-Lin, Jia-Chen Tsai, Wei-Ling Huang, Ying-Hsuan Meng, Ju-Chun Huang, Ying-Chieh Chen, and Chuang-Rung Chang. "Mitochondria dynamics and pathogenesis." In PROCEEDINGS OF THE 3RD INTERNATIONAL SEMINAR ON METALLURGY AND MATERIALS (ISMM2019): Exploring New Innovation in Metallurgy and Materials. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0002464.
Full textBrandenberger, Christina, and Jahar Bhattacharya. "Alveolar Mitochondria Are Motile." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2536.
Full textNovaković, Ivana, Milena Janković, Ana Marjanović, Marija Branković, Marina Svetel, and Jasna Jančić. "Challenges in rare diseases: The example of mitochondrial diseases." In Proceedings of the International Congress Public Health - Achievements and Challenges, 161. Institute of Public Health of Serbia "Dr Milan Jovanović Batut", 2024. http://dx.doi.org/10.5937/batutphco24114n.
Full textZhao, Tinghan, Sweety Singh, Yuanwei Zhang, and Kevin D. Belfield. "Novel mitochondria penetrating peptide for live-cell long-term tracking of mitochondria." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2019. http://dx.doi.org/10.1364/omp.2019.om3d.5.
Full textReports on the topic "Mitochondria"
Ostersetzer-Biran, Oren, and Alice Barkan. Nuclear Encoded RNA Splicing Factors in Plant Mitochondria. United States Department of Agriculture, February 2009. http://dx.doi.org/10.32747/2009.7592111.bard.
Full textAachi, Venkat. Preliminary Characterization of Mitochondrial ATP-sensitive Potassium Channel (MitoKATP) Activity in Mouse Heart Mitochondria. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1666.
Full textKumar, Om. do you know about mitochondria ? ResearchHub Technologies, Inc., December 2023. http://dx.doi.org/10.55277/researchhub.11eubx1d.
Full textKurtz, Andreas. Mitochondria Polymorphism in Neurofibromatosis Type 1. Fort Belvoir, VA: Defense Technical Information Center, November 2001. http://dx.doi.org/10.21236/ada400622.
Full textKurtz, Andreas. Mitochondria Polymorphism in Neurofibromatosis Type 1. Fort Belvoir, VA: Defense Technical Information Center, November 2002. http://dx.doi.org/10.21236/ada411354.
Full textKurtz, Andreas C. Mitochondria Polymorphism in Neurofibromatosis Type 1. Fort Belvoir, VA: Defense Technical Information Center, November 2003. http://dx.doi.org/10.21236/ada420949.
Full textSiedow, J. N. Molecular studies of functional aspects of plant mitochondria. Office of Scientific and Technical Information (OSTI), March 1992. http://dx.doi.org/10.2172/7194216.
Full textDr. Carol Lynn George, Dr Carol Lynn George. Can our cell's mitochondria power a cell phone? Experiment, December 2013. http://dx.doi.org/10.18258/1755.
Full textOstersetzer-Biran, Oren, and Jeffrey Mower. Novel strategies to induce male sterility and restore fertility in Brassicaceae crops. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604267.bard.
Full textSick, Thomas J. Pro-Apoptotic Changes in Brain Mitochondria After Toxic Exposure. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada397717.
Full text