Relevant bibliographies by topics / Cellular respiration

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Cellular respiration'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Cellular respiration"

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Rannels, D. Eugene. "Cellular neurobiology of respiration." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 1 (July 1, 1995): L1. http://dx.doi.org/10.1152/ajplung.1995.269.1.l1.

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Chandel, Navdeep S., G. R. Scott Budinger, Sang H. Choe, and Paul T. Schumacker. "Cellular Respiration during Hypoxia." Journal of Biological Chemistry 272, no. 30 (July 25, 1997): 18808–16. http://dx.doi.org/10.1074/jbc.272.30.18808.

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Brunori, M., A. Giuffr�, P. Sarti, G. Stubauer, and M. T. Wilson. "Nitric oxide and cellular respiration." Cellular and Molecular Life Sciences (CMLS) 56, no. 7-8 (November 1, 1999): 549–57. http://dx.doi.org/10.1007/s000180050452.

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Jones, Eyone, Harvey S. Penefsky, and Abdul-Kader Souid. "Caffeine Impairs HL-60 Cellular Respiration." Journal of Medical Sciences 2, no. 2 (May 29, 2009): 61–72. http://dx.doi.org/10.2174/1996327000902020061.

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Tao, Zhimin, Matthew P. Morrow, Tewodros Asefa, Krishna K. Sharma, Cole Duncan, Abhishek Anan, Harvey S. Penefsky, Jerry Goodisman, and Abdul-Kader Souid. "Mesoporous Silica Nanoparticles Inhibit Cellular Respiration." Nano Letters 8, no. 5 (May 2008): 1517–26. http://dx.doi.org/10.1021/nl080250u.

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Cascón, Alberto, Laura Remacha, Bruna Calsina, and Mercedes Robledo. "Pheochromocytomas and Paragangliomas: Bypassing Cellular Respiration." Cancers 11, no. 5 (May 16, 2019): 683. http://dx.doi.org/10.3390/cancers11050683.

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Pheochromocytomas and paragangliomas (PPGL) are rare neuroendocrine tumors that show the highest heritability of all human neoplasms and represent a paradoxical example of genetic heterogeneity. Amongst the elevated number of genes involved in the hereditary predisposition to the disease (at least nineteen) there are eleven tricarboxylic acid (TCA) cycle-related genes, some of which are also involved in the development of congenital recessive neurological disorders and other cancers such as cutaneous and uterine leiomyomas, gastrointestinal tumors and renal cancer. Somatic or germline mutation of genes encoding enzymes catalyzing pivotal steps of the TCA cycle not only disrupts cellular respiration, but also causes severe alterations in mitochondrial metabolite pools. These latter alterations lead to aberrant accumulation of “oncometabolites” that, in the end, may lead to deregulation of the metabolic adaptation of cells to hypoxia, inhibition of the DNA repair processes and overall pathological changes in gene expression. In this review, we will address the TCA cycle mutations leading to the development of PPGL, and we will discuss the relevance of these mutations for the transformation of neural crest-derived cells and potential therapeutic approaches based on the emerging knowledge of underlying molecular alterations.
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Tao, Zhimin, Henry G. Withers, Harvey S. Penefsky, Jerry Goodisman, and Abdul-Kader Souid. "Inhibition of Cellular Respiration by Doxorubicin." Chemical Research in Toxicology 19, no. 8 (August 2006): 1051–58. http://dx.doi.org/10.1021/tx050315y.

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Alsamri, Mohammed T., Suleiman Al-Hammadi, Barira Islam, and Abdul-Kader Souid. "Zoledronic acid and bone cellular respiration." Journal of Bone and Mineral Metabolism 36, no. 4 (August 1, 2017): 392–98. http://dx.doi.org/10.1007/s00774-017-0850-7.

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Bishop, T., and M. D. Brand. "Processes contributing to metabolic depression in hepatopancreas cells from the snail Helix aspersa." Journal of Experimental Biology 203, no. 23 (December 1, 2000): 3603–12. http://dx.doi.org/10.1242/jeb.203.23.3603.

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Cells isolated from the hepatopancreas of the land snail Helix aspersa strongly depress respiration both immediately in response to lowered P(O2) (oxygen conformation) and, in the longer term, during aestivation. These phenomena were analysed by dividing cellular respiration into non-mitochondrial and mitochondrial respiration using the mitochondrial poisons myxothiazol, antimycin and azide. Non-mitochondrial respiration accounted for a surprisingly large proportion, 65+/−5 %, of cellular respiration in control cells at 70 % air saturation. Non-mitochondrial respiration decreased substantially as oxygen tension was lowered, but mitochondrial respiration did not, and the oxygen-conforming behaviour of the cells was due entirely to the oxygen-dependence of non-mitochondrial oxygen consumption. Non-mitochondrial respiration was still responsible for 45+/−2 % of cellular respiration at physiological oxygen tension. Mitochondrial respiration was further subdivided into respiration used to drive ATP turnover and respiration used to drive futile proton cycling across the mitochondrial inner membrane using the ATP synthase inhibitor oligomycin. At physiological oxygen tensions, 34+/−5 % of cellular respiration was used to drive ATP turnover and 22+/−4 % was used to drive proton cycling, echoing the metabolic inefficiency previously observed in liver cells from mammals, reptiles and amphibians. The respiration rate of hepatopancreas cells from aestivating snails was only 37 % of the control value. This was caused by proportional decreases in non-mitochondrial and mitochondrial respiration and in respiration to drive ATP turnover and to drive proton cycling. Thus, the fraction of cellular respiration devoted to different processes remained constant and the cellular energy balance was preserved in the hypometabolic state.
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Lobritz, Michael A., Peter Belenky, Caroline B. M. Porter, Arnaud Gutierrez, Jason H. Yang, Eric G. Schwarz, Daniel J. Dwyer, Ahmad S. Khalil, and James J. Collins. "Antibiotic efficacy is linked to bacterial cellular respiration." Proceedings of the National Academy of Sciences 112, no. 27 (June 22, 2015): 8173–80. http://dx.doi.org/10.1073/pnas.1509743112.

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Bacteriostatic and bactericidal antibiotic treatments result in two fundamentally different phenotypic outcomes—the inhibition of bacterial growth or, alternatively, cell death. Most antibiotics inhibit processes that are major consumers of cellular energy output, suggesting that antibiotic treatment may have important downstream consequences on bacterial metabolism. We hypothesized that the specific metabolic effects of bacteriostatic and bactericidal antibiotics contribute to their overall efficacy. We leveraged the opposing phenotypes of bacteriostatic and bactericidal drugs in combination to investigate their activity. Growth inhibition from bacteriostatic antibiotics was associated with suppressed cellular respiration whereas cell death from most bactericidal antibiotics was associated with accelerated respiration. In combination, suppression of cellular respiration by the bacteriostatic antibiotic was the dominant effect, blocking bactericidal killing. Global metabolic profiling of bacteriostatic antibiotic treatment revealed that accumulation of metabolites involved in specific drug target activity was linked to the buildup of energy metabolites that feed the electron transport chain. Inhibition of cellular respiration by knockout of the cytochrome oxidases was sufficient to attenuate bactericidal lethality whereas acceleration of basal respiration by genetically uncoupling ATP synthesis from electron transport resulted in potentiation of the killing effect of bactericidal antibiotics. This work identifies a link between antibiotic-induced cellular respiration and bactericidal lethality and demonstrates that bactericidal activity can be arrested by attenuated respiration and potentiated by accelerated respiration. Our data collectively show that antibiotics perturb the metabolic state of bacteria and that the metabolic state of bacteria impacts antibiotic efficacy.
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Dissertations / Theses on the topic "Cellular respiration"

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Liimatta, E. (Erkki). "Intracellular calcium, preconditioning and regulation of cellular respiration in heart." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514260865.

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Abstract Heart muscle has to work constantly throughout the life and its energy metabolism is heavily dependent on a continuous supply of oxygen. Energy metabolism must be effectively regulated to meet the demands of changing workloads in different circumstances. If the oxygen supply is interrupted, the function of the heart is easily disturbed and cells injured. Calcium metabolism is of great importance in these pathological conditions. In this thesis respiratory regulation was studied by non-destructive optical methods in mouse heart. The myoglobin-deficient mouse was used as an experimental model to avoid the artefact caused by intracellular myoglobin. Results show that increased consumption of energy and oxygen lead to concomitant reduction of cytochrome aa3 and oxidation of flavoproteins. This finding supports the view that cell respiration in intact myocardium is dominantly regulated at the level of the respiratory chain. The intracellular Ca2+ accumulation during ischemia is one of the major causes of irreversible ischemia-reperfusion injury. Ischemic preconditioning (IPC) has been shown to protect the heart muscle significantly from ischemic damage. In this thesis Ca2+ accumulation during ischemia and reperfusion was studied in perfused rat heart using Fura-2 as a fluorescent Ca2+ indicator. As there is a significant decrease in intracellular pH during prolonged ischemia, the pH-dependency of Fura-2 signal was taken into account. It was found that IPC attenuates Ca2+accumulation during ischemia and this was connected to a decrease in mitochondrial membrane potential. Both IPC and the pharmacologically induced preconditioning with the mitoKATP opener diaxozide were shown to be associated with increased production of superoxide monitored by means of lucigenin chemiluminescence. The superoxide production correlated with the oxidation-reduction state of flavoproteins. We also describe here a method for measuring of intracellular free Ca2+ in mouse heart during ischemia by simultaneous monitoring of Fura-2 and the pH probe BCECF fluorescence by means of dual wavelength excitation of both probes. The paradoxical decrease of Fura-2 fluorescence during ischemia indicating decreasing intracellular Ca2+ concentration was due to the pH effect on the dissociation constant of the Fura-2-Ca2+ complex. When the pH-dependency of Fura-2 was compensated, an extensive Ca2+ accumulation during ischemia was detected. Much of the previous literature on this subject must be re-evaluated because the pH-dependency of intracellular Ca2+ probes has been largely overlooked.
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Robertson, Laura, LaShay Jennings, Scott Honeycutt, Karin Keith, and Chih-Che Tai. "Photosynthesis and Cellular Respiration (LS1): A Hands-On Approach for Grades 6–12." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/770.

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Robertson, Laura, LaShay Jennings, Kari Eubanks, and Scott Honeycutt. "Photosynthesis and Cellular Respiration (LS1): A Hands-On Approach Supporting the NGSS and ELA CCSS." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/1313.

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Presley, Tennille D. "Electron paramagnetic resonance (EPR) oximetry as a quantitative tool to measure cellular respiration in pathophysiological conditions." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1187014988.

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Cui, Xiaoyu. "Regulation of Cellular Bioenergetics by Na/K-ATPase." University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1481294995657855.

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Vo, Thi Thanh Phuong. "An investigation of the use of concept mapping in teaching and learning cellular respiration in a Vietnamese university." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0007/MQ37656.pdf.

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Pape, Jenny Adele. "Characterizing the Function of PAS kinase in Cellular Metabolism and Neurodegenerative Disease." BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8552.

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The second identified substrate of PAS kinase discussed is Pbp1. The human homolog of Pbp1 is ataxin-2, mutations in which are a known risk factor for amyotrophic lateral sclerosis (ALS). As diet and sex have been shown to be important factors regarding PAS kinase function, they also are strong contributing factors to ALS and are extensively reviewed herein. Pbp1 is known to be sequestered by PAS kinase under glucose depravation, and it can sequester additional proteins along with it to regulate different cellular pathways. To shed light on the pathways affected by Pbp1, we performed a yeast two-hybrid assay and mass spectrometry, identifying 32 novel interacting partners of Pbp1 (ataxin-2). We provide further analysis of the direct binding partner Ptc6, measuring mitophagy, mitochondrial content, colocalization, and respiration. This work elucidates novel molecular mechanisms behind the function of PAS kinase and yields valuable insights into the role of PAS kinase in disease.
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Winger, Alison Marie. "Impact of 4-hydroxy-2-nonenal in Arabidopsis mitochondria." University of Western Australia. Biochemistry and Molecular Biology Discipline Group, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0121.

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[Truncated abstract] A range of biotic and abiotic stresses increase levels of reactive oxygen species (ROS) in plants due to perturbations of chloroplast and mitochondrial metabolism and the generation of ROS in defence responses. The polyunsaturated fatty acids of membrane lipids are susceptible to ROS induced peroxidation yielding various aldehydes, alkenals and hydroxyalkenals including the cytotoxic compound 4-hydroxy- 2-nonenal (HNE). HNE has the potential to cause substantial oxidative damage in cells via its reactivity with sulfhydryl groups of cysteine (Cys) and lipoic acid, the imidazole group of histidine (His) and the ?-amino group of lysine (Lys) protein residues. Analysis of the components of the plant respiratory electron transport chain to HNE revealed a particular susceptibility to inhibition of activity of the alternative oxidase (Aox). Incubation with HNE prevented dimerisation of Aox protein, suggesting that one site of modification was the conserved cysteine residue involved in dimerisation and activation of this enzyme (Cys1). However, a naturally occurring isoform of Aox lacking Cys1 and unable to dimerise, LeAox1b from tomato, was equally sensitive to HNE inhibition, showing that other amino acid residues in Aox also interact with HNE and are likely responsible for inactivation of the enzyme. ... The broader impact of HNE on the whole Arabidopsis mitochondrial proteome was examined by use of various 2-dimensional gel separation techniques coupled with use of HNE-adduct antibodies. 32 proteins involved in a number of mitochondrial functions were found to be susceptible to modification by HNE, including components of the electron transport chain, the TCA cycle, as well as proteins involved amino acid metabolism and stress-responses. Implications of modification of these proteins by HNE are discussed. As HNE is produced in vivo during oxidative stress, the profile of mitochondrial targets of HNE was examined from Arabidopsis cell cultures exposed to various oxidative stress inducers. Menadione and hydrogen peroxide induced oxidative stress throughout the cell, while antimycin A initiated a mitochondrial targeted stress. A differential profile of mitochondrial proteins was observed to be modified by HNE in the various treatments. These results also showed that induction of stress within a whole cell can impact lipid peroxidation within the mitochondria. Overall, this work showed the presence and production of HNE in plant cells, and that HNE, both exogenous and endogenous, has the ability to modify a specific subset of mitochondrial proteins. In several cases this HNE modification was shown to have functional or structural consequences.
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Aebig, Trudy J. "Cell cycle-dependent association of plectin 1b regulates mitochondrial morphology and function." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307440587.

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Moda, Bruno Spinetti. "Estudos do gene nuclear MSC6 envolvido na tradução mitocondrial em Saccharomyces cerevisiae." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-23012017-141051/.

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A mitocôndria é um componente essencial para a célula eucariótica, sendo que mutações que comprometam seu funcionamento podem causar as doenças mitocondriais. Estudos a respeito da biogênese mitocondrial para compreender seu funcionamento são importantes para que seja possível elaborar novas formas de tratamento. Saccharomyces cerevisiae é considerada o melhor modelo de estudo de biogênese mitocondrial. Neste trabalho, estudamos o gene nuclear MSC6, de S. cerevisiae, que foi capaz de suprimir a mutação dominante produzida no gene HER2/QRS1, um gene essencial no processo de tradução mitocondrial. A proteína codificada por MSC6 não tinha função conhecida. Verificamos sua presença na matriz mitocondrial, e que a sua ausência prejudica o processo respiratório. Também verificamos uma possível interação de Msc6p com Fmt1p, uma enzima envolvida no início do processo de tradução mitocondrial. Ficou clara a participação de Msc6p no processo traducional mitocondrial, mas novos estudos serão necessários para determinar sua função específica.
Mitochondria is necessary in many cellular processes, therefore, compromised mutations of its operation can cause severe damage to the cell, known as mitochondrial disorders. Thus is necessary the realization of mitochondrial biogenesis studies in order to fully understand its functioning in health and disease. Mitochondria biogenesis studies are favored in Saccharomyces cerevisiae. In this work, we have studied the MSC6 nuclear gene of S. cerevisiae that was able to suppress the HER2/QRS1 dominant mutant, another essential gene for the mitochondrial translation process. Msc6p has a PPR protein motif likely associated to RNA binding but with unknown function. We discovered that Msc6p is localized in the mitochondrial matrix, also that disruption of MSC6 implies in respiratory. We also find a possible interaction between Msc6p and Fmt1p, an enzyme required for mitochondrial translation initiation. In conclusion, is clear the role of MSC6 in the mitochondrial translational process, but further studies are required to indicate the specific function of Msc6p.
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Books on the topic "Cellular respiration"

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Sarangarajan, Rangaprasad, and Shireesh Apte, eds. Cellular Respiration and Carcinogenesis. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-435-3.

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NATO Advanced Research Workshop on Thiol Metabolism and Redox Regulation of Cellular Functions (2002 Pisa, Italy). Thiol metabolism and redox regulation of cellular functions. Amsterdam: IOS Press, 2002.

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Harris, S., J. Harris, and P. Narini. Cellular Respiration. Permacharts Inc., 1999.

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P, Apte Shireesh, and Sarangarajan Rangaprasad, eds. Cellular respiration and carcinogenesis. New York: Springer, 2008.

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Apte, Shireesh, and Rangaprasad Sarangarajan. Cellular Respiration and Carcinogenesis. Humana, 2014.

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P, Apte Shireesh, and Sarangarajan Rangaprasad, eds. Cellular respiration and carcinogenesis. New York: Springer, 2008.

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Apte, Shireesh, and Rangaprasad Sarangarajan. Cellular Respiration and Carcinogenesis. Springer, 2009.

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P, Apte Shireesh, and Sarangarajan Rangaprasad, eds. Cellular respiration and carcinogenesis. New York: Springer, 2008.

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Gijsbert, Osterhoudt, and Barhydt Jos, eds. Cell respiration and cell survival: Processes, types and effects. Hauppauge, N.Y: Nova Science Publishers, 2009.

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Thomson, Robert G., and Peter Abramoff. Cellular Respiration: Separate from Laboratory Outlines in Biology VI. W. H. Freeman, 1995.

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Book chapters on the topic "Cellular respiration"

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Stauffer, Sarah, Aaron Gardner, Dewi Ayu Kencana Ungu, Ainara López-Córdoba, and Matthias Heim. "Cellular Respiration." In Labster Virtual Lab Experiments: Basic Biology, 43–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-57996-1_4.

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Scatena, Roberto, Patrizia Bottoni, and Bruno Giardina. "Cellular Respiration and Dedifferentiation." In Cellular Respiration and Carcinogenesis, 45–54. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_4.

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Ristow, Michael, and José M. Cuezva. "Oxidative Phosphorylation and Cancer: The Ongoing Warburg Hypothesis." In Cellular Respiration and Carcinogenesis, 1–18. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_1.

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Gonzalez-Cuyar, Luis F., Fabio Tavora, Iusta Caminha, George Perry, Mark A. Smith, and Rudy J. Castellani. "Cellular Respiration and Tumor Suppressor Genes." In Cellular Respiration and Carcinogenesis, 131–44. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_10.

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Newell, M. Karen, Elizabeth M. Villalobos-Menuey, Marilyn Burnett, and Robert E. Camley. "Uncoupling Cellular Respiration: A Link to Cancer Cell Metabolism and Immune Privilege." In Cellular Respiration and Carcinogenesis, 145–60. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_11.

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Werner, Erica. "How Cancer Cells Escape Death." In Cellular Respiration and Carcinogenesis, 161–78. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_12.

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Brière, Jean-Jacques, Paule Bénit, and Pierre Rustin. "The Electron Transport Chain and Carcinogenesis." In Cellular Respiration and Carcinogenesis, 19–32. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_2.

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Carrico, Pauline M., Nadine Hempel, and J. Andrés Melendez. "Respiratory Control of Redox Signaling and Cancer." In Cellular Respiration and Carcinogenesis, 33–44. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_3.

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Srivastava, Sarika, and Carlos T. Moraes. "Cellular Adaptations to Oxidative Phosphorylation Defects in Cancer." In Cellular Respiration and Carcinogenesis, 55–72. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_5.

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Ferreira, Túlio César, and Élida Geralda Campos. "Regulation of Glucose and Energy Metabolism in Cancer Cells by Hypoxia Inducible Factor 1." In Cellular Respiration and Carcinogenesis, 73–90. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-435-3_6.

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Conference papers on the topic "Cellular respiration"

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Jungil Park, Sunyoung Ahn, Youngmi Kim Pak, and James Jungho Pak. "2 × 3 array oxygen sensor for measuring cellular respiration level." In 2009 4th IEEE International Conference on Nano/Micro Engineered and Molecular Systems. IEEE, 2009. http://dx.doi.org/10.1109/nems.2009.5068754.

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Harvenda, Valendry, Yanuar Hamzah, Arfianti, Tetty Marta Linda, and Lazuardi Umar. "Influence of artificial light color on cellular respiration of green algae photosynthesis activity." In THE 8TH NATIONAL PHYSICS SEMINAR 2019. AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5132655.

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Sreedhar, Annapoorna, and Yunfeng Zhao. "Abstract 216: The effect of UCP2 upregulation on cellular redox status and mitochondrial respiration." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-216.

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Urayama, Paul, Taylor Phillips, Thomas A. Finn, Bibek Dhakal, and Karthik Vishwanath. "Distinguishing cellular respiration vs. oxidative stress in turbid media using UV-excited autofluorescence spectroscopy." In Label-free Biomedical Imaging and Sensing (LBIS) 2021, edited by Natan T. Shaked and Oliver Hayden. SPIE, 2021. http://dx.doi.org/10.1117/12.2578724.

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Park, J., J. H. Chang, S. Ahn, Y. K. Pak, S. Han, and J. J. Pak. "Array type dissolved oxygen sensor and measurement system for simultaneous measurement of cellular respiration level." In TRANSDUCERS 2009 - 2009 International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2009. http://dx.doi.org/10.1109/sensor.2009.5285960.

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Retone, Lourence E., and Maricar S. Prudente. "Effects of Technology-Integrated Brain-Friendly Teaching on Retention and Understanding in Photosynthesis and Cellular Respiration." In IC4E 2020: 2020 the 11th International Conference on E-Education, E-Business, E-Management, and E-Learning. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3377571.3377590.

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Wegiel, Barbara, David Gallo, Eva Czismadia, Kellie Cunningham, Pankaj Seth, Jenny Persson, Leszek Helczynski, and Leo Otterbein. "Abstract LB-358: Heme oxygenase-1 and carbon monoxide arrest tumor growth via modulation of cellular respiration." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-358.

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Masood, Mona, Wan Fauzy, and Irfan Umar. "EFFECTIVENESS OF AN ONLINE INTERACTIVE MULTIMEDIA SYSTEM: APPLYING MASTERY AND COOPERATIVE LEARNING ON THE TOPIC OF CELLULAR RESPIRATION." In International Technology, Education and Development Conference. IATED, 2016. http://dx.doi.org/10.21125/inted.2016.1633.

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Alves, Glenda Quaresma, Juliardnas Rigamont dos Reis, Abel Fernando Barros Rodrigues, Giordanna De Gregoriis, Felipe de Melo Rodrigues e. Oliveira, Isabela Lopes Matias Batista, and Dionne Cavalcante Monteiro. "Simulator of the Glycolytic Pathway in a Virtual Reality Environment as a Learning Resource for Teaching Cellular Respiration." In IHC 2018: 17th Brazilian Symposium on Human Factors in Computing Systems. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3274192.3274242.

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Kliment, Corrine, Jennifer Nguyen, Yawen Lu, Steven Claypool, Sumana Raychaudhuri, Shigeki Watanabe, Pablo Iglesias, Venkataramana Sidhaye, and Douglas Robinson. "From Dictyostelium to human airway epithelium: adenine nucleotide translocase enhances cellular respiration and ciliary function disrupted by cigarette smoke." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa506.

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