Relevant bibliographies by topics / Cell Metabolism

Academic literature on the topic 'Cell Metabolism'

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Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Cell Metabolism"

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CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.
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I. Bon, Lizaveta. "The Role of Hypoxia-Induced Factor in Cell Metabolism." Journal of Obesity and Fitness Management 1, no. 1 (January 25, 2023): 01–03. http://dx.doi.org/10.58489/2836-5070/003.

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Objective. Analysis and synthesis of literature data on morphological and functional properties and the diagnostic value of induced factor hypoxia. Methods. The basis of this study was a review of literature on this topic. Results. An important role in the adaptation of the organism to hypoxia belongs to a specific regulatory protein - hypoxia-induced factor (HIF), the activity of which increases with decreasing oxygen tension in the blood. HIF is a heterodimeric protein, the beta subunit of which is constantly expressed, and the synthesis of the alpha subunit is regulated by oxygen. Conclusion. Acute oxygen deficiency is the basis of a variety of pathological processes in many diseases and environmental factors. The hypoxia-induced factor is responsible for the formation of long-term adaptation to hypoxia, and therefore is a suitable target for pharmacological effects. The search for drugs that act as inducers or inhibitors of its synthesis is an important area in experimental pharmacology, since it allows not only to regulate the processes of adaptation to hypoxia, but more effectively treat cerebrovascular, cardiovascular, oncological and other diseases in whose genesis the leading role plays oxygen deficiency.
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Isogai, Tadamoto, Jin Suk Park, and Gaudenz Danuser. "Cell forces meet cell metabolism." Nature Cell Biology 19, no. 6 (May 31, 2017): 591–93. http://dx.doi.org/10.1038/ncb3542.

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Romero-Garcia, Susana, Jose Sullivan Lopez-Gonzalez, José Luis B´ez-Viveros, Dolores Aguilar-Cazares, and Heriberto Prado-Garcia. "Tumor cell metabolism." Cancer Biology & Therapy 12, no. 11 (December 2011): 939–48. http://dx.doi.org/10.4161/cbt.12.11.18140.

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Cairns, R. A., I. Harris, S. McCracken, and T. W. Mak. "Cancer Cell Metabolism." Cold Spring Harbor Symposia on Quantitative Biology 76 (January 1, 2011): 299–311. http://dx.doi.org/10.1101/sqb.2011.76.012856.

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Teuwen, Laure-Anne, Nihed Draoui, Charlotte Dubois, and Peter Carmeliet. "Endothelial cell metabolism." Current Opinion in Hematology 24, no. 3 (May 2017): 240–47. http://dx.doi.org/10.1097/moh.0000000000000335.

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Pearce, Edward J., and Bart Everts. "Dendritic cell metabolism." Nature Reviews Immunology 15, no. 1 (December 23, 2014): 18–29. http://dx.doi.org/10.1038/nri3771.

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Eelen, Guy, Pauline de Zeeuw, Lucas Treps, Ulrike Harjes, Brian W. Wong, and Peter Carmeliet. "Endothelial Cell Metabolism." Physiological Reviews 98, no. 1 (January 1, 2018): 3–58. http://dx.doi.org/10.1152/physrev.00001.2017.

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Endothelial cells (ECs) are more than inert blood vessel lining material. Instead, they are active players in the formation of new blood vessels (angiogenesis) both in health and (life-threatening) diseases. Recently, a new concept arose by which EC metabolism drives angiogenesis in parallel to well-established angiogenic growth factors (e.g., vascular endothelial growth factor). 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3-driven glycolysis generates energy to sustain competitive behavior of the ECs at the tip of a growing vessel sprout, whereas carnitine palmitoyltransferase 1a-controlled fatty acid oxidation regulates nucleotide synthesis and proliferation of ECs in the stalk of the sprout. To maintain vascular homeostasis, ECs rely on an intricate metabolic wiring characterized by intracellular compartmentalization, use metabolites for epigenetic regulation of EC subtype differentiation, crosstalk through metabolite release with other cell types, and exhibit EC subtype-specific metabolic traits. Importantly, maladaptation of EC metabolism contributes to vascular disorders, through EC dysfunction or excess angiogenesis, and presents new opportunities for anti-angiogenic strategies. Here we provide a comprehensive overview of established as well as newly uncovered aspects of EC metabolism.
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Gardiner, Clair M. "NK cell metabolism." Journal of Leukocyte Biology 105, no. 6 (January 24, 2019): 1235–42. http://dx.doi.org/10.1002/jlb.mr0718-260r.

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Verdegem, Dries, Stijn Moens, Peter Stapor, and Peter Carmeliet. "Endothelial cell metabolism: parallels and divergences with cancer cell metabolism." Cancer & Metabolism 2, no. 1 (2014): 19. http://dx.doi.org/10.1186/2049-3002-2-19.

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Dissertations / Theses on the topic "Cell Metabolism"

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Pat, Sze Wa. "Cell metabolism in cell death and cell growth." HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/775.

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Iafelice, Bruno <1979&gt. "Miniaturized sensors for cell metabolism." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/397/1/Tesi_encripted.pdf.

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Iafelice, Bruno <1979&gt. "Miniaturized sensors for cell metabolism." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/397/.

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Chowdhury, Azazul Islam. "Role of Cell-cell Interactions and Palmitate on β-cells Function." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-230841.

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The islets of Langerhans secrets insulin in response to fluctuations of blood glucose level and efficient secretion requires extensive intra-islet communication. Secretory failure from islets is one of the hallmark in progression of type 2 diabetes.  Changes in islet structure and high levels of saturated free fatty acids may contribute to this failure. The aim of this thesis is to study the role of cell-cell interactions and palmitate on β-cells functions. To address the role of cell-cell interactions on β-cells functions MIN6 cells were cultured as monolayers and as pseudoislets. Glucose stimulated insulin secretion was higher in pseudoislets compared to monolayers. Transcript levels of mitochondrial metabolism as well glucose oxidation rate was higher in pseudoislets. Insulin receptor substrate-1 (IRS-1) phosphorylation was altered when cells were grown as pseudoislets. Proteins expression levels related to glycolysis, cellular connections and translational regulations were up-regulated in pseudoislets. We propose the superior capacity of pseudoislets compared to monolayers depend on metabolism, cell coupling, gene translation, protein turnover and differential IRS-1 phosphorylation. To address the role of palmitate on β-cells human islets were cultured in palmitate. Long term palmitate treatment decreased insulin secretion which is associated with up-regulation of suppressor of cytokine signaling-2 (SOCS2) and protein inhibitor of activated STAT-1 (PIAS1). Up-regulation of SOCS2 decreased phosphorylation of Akt at site T308, whereas PIAS1 decreased protein level of ATP- citrate lyase (ACLY) and ATP synthase subunit B (ATP5B). We propose long term palmitate treatment reduces phosphatidylinositol 3-kinase (PI3K) activity, attenuates formation of acetyl-CoA and decreases ATP synthesis which may aggravate β-cells dysfunction.
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Board, Mary. "A study of energy metabolism in neoplastic cells." Thesis, University of Oxford, 1990. http://ora.ox.ac.uk/objects/uuid:d3e13e31-3fe8-4cd8-ad71-50d4e7df4d27.

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Sidiq, Karzan Rafiq. "Cell wall metabolism in Bacillus subtilis." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3243.

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Cell wall is a unique and essential component of bacterial cell. It defines cell shape and protects cell from bursting through its own internal osmotic pressure. It also represents a significant drain on the cells resources, particularly in Gram positives, where the wall accounts for more than 20 % of the dry weight of the cell, and approximately 50 % of ‘‘old’’ cell wall is degraded and new material made to permit cell growth. After the discovery of penicillin, there has been active study of bacterial cell wall structure and metabolism, as it represents the major target for antibacterial compounds. The biosynthetic pathways for cell wall precursors has been well investigated in bacteria generally, but the coordination of cell wall metabolic processes and the fate of turnover cell wall materials have only been well characterised in Gram-negative bacteria (e.g Escherichia coli). In Gram-positive bacteria, it has generally been accepted that the old wall is released from the surface and lost to the environment during growth, with apparent recycling of this material during stationary phase for Bacillus subtilis. It is also known that the Gram-positive wall is subject to significant post-synthetic processing, involving the linkage of wall teichoic acids and the cleavage of molecules from the structure, e.g. D-alanine, although the function of these is unclear. Understanding the importance of these processes has relevance for both the pathogenicity and biotechnological use of bacteria, as well as for understanding bacterial cell biology. As it is known that the peptidoglycan fragments (e.g muropeptides) induce the innate immune response in higher organisms and so act as a signal for infection, particularly for Gram-positive bacteria. Thus, understanding how they are generated and recycled by the bacteria may offer potential insights into novel therapeutics, also the accumulation of cell wall muropeptides should be avoided in biotechnological products. In this thesis, the D-alanine metabolism was manipulated to understand the mechanistic details of cell wall metabolism and D-alanine recycling in B. subtilis, using genetic, biochemical, bioinformatics and fluorescent microscopy approaches. Through these analyses, a D-alanine transporter (DatA, formerly YtnA) was identified by genetic screening. The roles of DatA and the carboxypeptidases, LdcB and DacA, in recycling of cell wall derived D-alanine have experimentally been confirmed. We also found that D-alanine aminotransferase (Dat) can act to synthesis D-alanine under certain conditions. From the data obtained a model for peptidoglycan assembly (coordinated synthesis and turnover) during growth of B. subtilis has been developed to take into account the various aspects of cell wall metabolism.
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Tilney-Bassett, Amanda L. "Phospholipid metabolism in T-cell activation." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239331.

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Tueller, Josephine Anna. "Investigation of Therapeutic Immune Cell Metabolism." BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8704.

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This thesis addresses multiple approaches to investigating mechanisms of immune linked disease. There are four projects outlined below which describe the work of these investigations. First, educating students about techniques to study disease and therapies is an important area of research. Flow cytometry is a common technique in immunology and its versatility and high throughput abilities can be applied to many fields. While it is very useful, flow cytometry is a complex technique that requires training to operate and understand, and there are very few reports about administering effective training. This thesis outlines the first report of a full semester university course about flow cytometry. Students who completed the course reported increased confidence in their skill levels in conceptual, technical and analytical areas. Second, in the fight against cancer, immunotherapies may provide the necessary adaptability to successfully combat many cancer types. By strengthening and educating the immune system, clinicians can help patients fight cancer without resorting to harmful chemotherapeutics, or immunotherapies can be used in tandem with current treatments. Chimeric antigen receptor (CAR) T cells and checkpoint blockade are two of the most successful immunotherapies. CAR T cells combine the extraordinary binding ability of an antibody with T cell signaling molecules via genetic engineering, for a faster and more efficient cancer killing version of the patient's own T cells. These have been remarkably successful, but results depend on the specific signaling co-receptors that are included in the design. Increased understanding of co-receptor function could help in making CAR T cell design more specific, and enable CAR T cells to be effective against more types of cancers. Metabolic function is crucial in understanding T cell therapeutics because T cells need to use energy efficiently enough to compete with ravenous cancer cells. This thesis outlines an ongoing investigation into a co-receptor's effect on CAR T cell metabolism, suggesting that co-receptors can alter CAR T cell metabolism by increasing maximal respiration. Third, CD5 is a negative regulatory co-receptor on T cells that can modulate T cell activation. Related inhibitory co-receptors (PD-1 and CTLA-4) are currently being effectively blocked as checkpoint therapies to reactivate T cells towards cancerous cells. This thesis outlines ongoing work investigating CD5's impact on cellular metabolism. We have found that T cells without CD5 are hypermetabolic as compared to normal naïve T cells. CD5 deficient T cells also have higher maximal respiration, higher basal respiration and higher glycolytic capacity. These differences are also present transiently after non-specific activation. Thus, CD5 significantly regulates the ability of a T cell to use energy, suggesting that CD5 may be a good target for creating more efficient T cell immunotherapies. Fourth, in a separate project, this thesis examines environmental causes of disease. Asthma and allergies are common and growing problems in children and adults. Evaporative cooling can be a less expensive alternative to central cooling, but its effects on allergens and other bioaerosols in the home remains unclear. This project examines the relationship between evaporative cooling and bioaerosols (dust mites, bacterial endotoxin, and fungal β-(1→3)-D-glucans) in low income homes in Utah. We report significantly higher levels of these bioaerosols, particularly fungi in homes with evaporative cooling after adjusting for home-specific factors.
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Thomas, Geraint Mark Howard. "Lithium and phosphoinositide metabolism." Thesis, University of Wolverhampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238120.

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Hooper, Nigel Mark. "Metabolism of neuropeptides by cell-surface peptidases." Thesis, University of Leeds, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235486.

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Books on the topic "Cell Metabolism"

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Mazurek, Sybille, and Maria Shoshan, eds. Tumor Cell Metabolism. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5.

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Fiskum, Gary, ed. Cell Calcium Metabolism. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4.

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Shrestha, Bindesh, ed. Single Cell Metabolism. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4939-9831-9.

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1928-, Beutler Ernest, ed. Red cell metabolism. Edinburgh: Churchill Livingstone, 1986.

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J, Morgan Michael, ed. Carbohydrate metabolism in cultured cells. New York: Plenum Press, 1986.

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Cartledge, T. G. Biosynthesis and the integration of cell metabolism. Oxford: Butterworth-Heinemann, 1992.

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1951-, Merrill Alfred H., and Hannun Yusuf A. 1955-, eds. Sphingolipid metabolism and cell signaling. San Diego: Academic Press, 2000.

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Lands, William E. M., 1930-, ed. Biochemistry of arachidonic acid metabolism. Boston: Nijhoff, 1985.

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NATO, Advanced Research Workshop on the Organization of Cell Metabolism (1985 Hanstholm Denmark). The organization of cell metabolism. New York: Plenum Press, 1986.

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Welch, G. Rickey, and James S. Clegg, eds. The Organization of Cell Metabolism. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5311-9.

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Book chapters on the topic "Cell Metabolism"

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Günther, Ulrich L., Mei G. Chong, Tatiana Volpari, Katarzyna M. Koczula, Karen Atkins, Christopher M. Bunce, and Farhat L. Khanim. "Metabolic Fluxes in Cancer Metabolism." In Tumor Cell Metabolism, 315–48. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5_14.

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Yoon, Jeong-Yeol. "Cell Metabolism." In Tissue Engineering, 33–54. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-83696-2_3.

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Maclouf, Jacques. "Cell-Cell Signalling." In Biochemistry of Arachidonic Acid Metabolism, 297–309. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2597-0_18.

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Patnaik, Akash, Jason W. Locasale, and Lewis C. Cantley. "Cancer Cell Metabolism." In Insulin-like Growth Factors and Cancer, 245–61. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0598-6_13.

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Li, Ting, Christopher Copeland, and Anne Le. "Glutamine Metabolism in Cancer." In The Heterogeneity of Cancer Metabolism, 17–38. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_2.

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AbstractMetabolism is a fundamental process for all cellular functions. For decades, there has been growing evidence of a relationship between metabolism and malignant cell proliferation. Unlike normal differentiated cells, cancer cells have reprogrammed metabolism in order to fulfill their energy requirements. These cells display crucial modifications in many metabolic pathways, such as glycolysis and glutaminolysis, which include the tricarboxylic acid (TCA) cycle, the electron transport chain (ETC), and the pentose phosphate pathway (PPP) [1]. Since the discovery of the Warburg effect, it has been shown that the metabolism of cancer cells plays a critical role in cancer survival and growth. More recent research suggests that the involvement of glutamine in cancer metabolism is more significant than previously thought. Glutamine, a nonessential amino acid with both amine and amide functional groups, is the most abundant amino acid circulating in the bloodstream [2]. This chapter discusses the characteristic features of glutamine metabolism in cancers and the therapeutic options to target glutamine metabolism for cancer treatment.
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Obre, Emilie, and Rodrigue Rossignol. "Metabolic Remodeling in Bioenergetic Disorders and Cancer." In Tumor Cell Metabolism, 3–22. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5_1.

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Kurelac, Ivana, Michele Vidone, Giulia Girolimetti, Claudia Calabrese, and Giuseppe Gasparre. "Mitochondrial Mutations in Cancer Progression: Causative, Bystanders, or Modifiers of Tumorigenesis?" In Tumor Cell Metabolism, 199–231. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5_10.

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Martínez-Reyes, Inmaculada, and José M. Cuezva. "The Relevance of the Mitochondrial H+-ATP Synthase in Cancer Biology." In Tumor Cell Metabolism, 233–56. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5_11.

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Márquez, Javier, José M. Matés, Francisco J. Alonso, Mercedes Martín-Rufián, Carolina Lobo, and José A. Campos-Sandoval. "Canceromics Studies Unravel Tumor’s Glutamine Addiction After Metabolic Reprogramming." In Tumor Cell Metabolism, 257–86. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5_12.

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Löffler, Monika, Elizabeth A. Carrey, and Elke Zameitat. "Essential Role of Mitochondria in Pyrimidine Metabolism." In Tumor Cell Metabolism, 287–311. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5_13.

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Conference papers on the topic "Cell Metabolism"

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Mointire, V. L., A. J. Frangos, G. B. Rhee, G. S. Eskin, and R. E. Hall. "RHEOLOGY AND CELL ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643988.

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The subject of this work is to examine the hypothesis that some sublytic levels of mechanical perturbation of cells can stimulate cell metabolism. As a marker metabolite, we have chosen arachidonic acid. Principal metabolites for platelets include the cyclooxygenase product thromboxane A2(TXA2) and the lipoxygenase product 12-hydroperoxy-eicosatetraenoic acid (12-HPETE). Polymorphonuclear leukocytes (PMNLs) initally produce principally 5-HPETE, somtimes leading to the formation leukotrienes, though many other metabolites of arachidonic acid have been isolated from activated neutrophils. Human umbilical vein endothelial cells utilize arachidonic acid to produce mainly prostaglandin I2(PGI2). All of these metabolites are biologically active and modulate cell function - sometimes in quite contrasting ways. We will show that levels of sublytic mechanical stress exposure can stimulate arachidonic acid metabolism in all three of the cell types mentioned above. The biological implications of this stress/metabolism coupling may be quite far reaching.Human platelets, leukocytes and endothelial cells all appear to be sensitive to mechanical stress induced activation of arachidonic acid metabolism. Sheared PRP exhibited greatly increased synthesis of 12-HETE and surprisingly little thromboxane B2 production. This indicates that shear stress stimulation of platelets may produce quite different arachidonic acid metabolism than that seen with many direct chemical stimuli, such as thrombin or collagen.Our data demonstrate that a substance derived from shear induced platelet activation may activate the C-5 lipoxygenase of human PMNL under stress, leading to the production of LTB4. We hypothesize that this substance maybe 12-HPETE. LTB4 is known to be a very potent chemotactic factor and to induce PMNL aggregation and degranulation. Our studies provide further evidence that lipoxygenase products of one cell type can modulate production of lipoxygenase products in a second cell type, and that shear stress can initiate cell activation. This kind of coupling could have far reaching implications in terms of our understanding of cell/cell interaction in flowing systems, such as acute inflammation, artificial organ implantation and tumor metastasis.The data on PGI2 production by endothelial cells demonstrate that physiological levels of shear stress can dramatically increase arachidonic acid metabolism. Step increases in shear stress lead to a burst in production of PGI2 which decayed to a steady state value in several minutes. This longer term stimulation of prostacyclin production rate increased linearly with shear stress over the range of 0-24 dynes/cm2. In addition, pulsatile flow of physiological frequency and amplitude caused approximately 2.4 times the PGI2 production rate as steady flow with the same mean stress. Although only PGI2 was measured, it is likely that other arachidonic acid metabolites of endothelial cells are also affected by shear stress.The ability of cells to respond to external stimuli involves the transduction of a signal across the plasma membrane. One such external stimulus appears to be fluid shear stress. Steady shear flow induces cell rotation in suspended cells, leading to a periodic membrane loading, with the peak stress proportional to the bulk shear stress. On anchorage-dependent cells, such as endothelial cells, steady shear stress may act by amplifying the natural thermal or Brownian fluttering or rippling of the membrane. There are several possible mechanisms by which shear stress induced membrane perturbation could mimic a hormone/receptor interaction, leading to increased intracellular metabolism. Shear stress may induce increased phospholipase C activity, caused by translocation of the enzyme, increased substrate (arachidonic acid) pool availability to phospholipase C (particularly from that stored in phosphoinositols) due to shear-induced membrane movements or changes in membrane fluidity, direct activation of calcium - activated phospholipase A2 by increased membrane calcium ion permeability, or most probably by a combination of these mechanisms.
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Orsi, Gianni, Carmelo De Maria, Federico Vozzi, Mariangela Guzzardi, Arti Ahluwalia, and Giovanni Vozzi. "ENMET: Endothelial Cell Metabolism Mathematical Model." In 2009 Ninth International Conference on Intelligent Systems Design and Applications. IEEE, 2009. http://dx.doi.org/10.1109/isda.2009.200.

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Okhalnikov, A. D., A. O. Motorina, M. S. Gavrish, and A. A. Babaev. "EVALUATION OF CHANGES IN THE MITOCHONDRIAL ARCHITECTURE IN ASTROCYTES IN AN IN VITRO MODEL OF ALZHEIMER’S DISEASE." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-354.

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Alzheimer’s disease is a neurodegenerative disease whose pathogenesis is inextricably linked with a long-term disruption of metabolic processes in neuronal and glial cells. According to the literature data, mitochondrial dysfunction contributes to the activation of various signaling mechanisms leading to reprogramming of cell metabolism, which contributes to the development of the disease.
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Shirakashi, Ryo, Tomomi Yoshida, Christophe Provin, Kiyoshi Takano, Yasuyuki Sakai, and Teruo Fujii. "Steady Measurement of Glucose Metabolism of Hepatocyte." In ASME/JSME 2007 Thermal Engineering Heat Transfer Summer Conference collocated with the ASME 2007 InterPACK Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/ht2007-32750.

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Production of hybrid artificial organs for implantation is one of the main topics of tissue engineering. A large organ consisting of soft tissues requires a high cell density, c.a. 108 cells/mL, to satisfy the same physiological metabolic rate per organ-volume as an organ in vivo. Therefore, the supply of oxygen and nutrition to all the cells composing the soft tissue is always critical problem for the in vitro artificial organ production. Energy metabolic rates, such as oxygen and glucose metabolism rate, of single cell at various temperatures are the basic data for designing the oxygen and nutrition transport in an artificial organ. It is reported that several conditions including pH, temperature, oxygen or glucose concentration have effects on energy metabolism, although these interactions are not clearly quantitatively measured mainly because of the problems of measuring systems. In this study, convenient method to measure glucose consumption rate of hepatocyte (HepG2 cell line) at different temperature and glucose concentration is proposed. A device for the measurement was developed which consists of a small closed chamber with an inlet and an outlet of culture medium at the both ends of the chamber. On the one side of the walls in the chamber, confluent HepG2 on a coverslip was installed. Culture medium supplemented with various concentration of glucose was supplied to the open flow chamber in a constant flow rate. The whole chamber was in a thermostatic bath to keep the temperature in the chamber constant. Glucose consumption rate can be calculated by measuring the difference between glucose concentration of inlet culture medium and outlet culture medium, the flow rate and the number of cells in the chamber. Enzymatic analysis using D-Glucose-HK allows quantification of the sample glucose concentration. The advantages of the proposed method include; 1) small number of cells is required for the measurement, c. a. 105cells, 2) the flow pattern and the glucose supply are in steady state. Especially the latter advantage made it possible to evaluate the effects of different conditions on the glucose consumption rate. Since the most of the metabolic rate were measured under unsteady state, conditions, such as pH, oxygen concentration and glucose concentration, were changed sometime drastically during the measurement. The results provided the several parameters of Michaelis-Menten kinetics at various temperatures.
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Rück, A., J. Breymayer, and S. Kalinina. "Correlated FLIM and PLIM for cell metabolism." In SPIE BiOS, edited by Ammasi Periasamy, Peter T. C. So, and Karsten König. SPIE, 2016. http://dx.doi.org/10.1117/12.2213390.

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Rück, A., C. Hauser, S. Lorenz, S. Mosch, S. Rotte, M. Kessler, and S. Kalinina. "Cell metabolism, tumour diagnosis and multispectral FLIM." In SPIE BiOS, edited by Ammasi Periasamy, Karsten König, and Peter T. C. So. SPIE, 2013. http://dx.doi.org/10.1117/12.2003729.

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Spiridonova, E. V., I. S. Nesterkina, V. V. Gurina, and N. V. Ozolina. "INFLUENCE OF CADMIUM ON PLANT CELL METABOLISM." In The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-1143-1145.

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Kalinina, S., D. Bisinger, J. Breymayer, and A. Ruck. "Cell metabolism, FLIM and PLIM and applications." In SPIE BiOS, edited by Ammasi Periasamy, Peter T. C. So, and Karsten König. SPIE, 2015. http://dx.doi.org/10.1117/12.2079166.

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Skala, Melissa C. "Autofluorescence lifetime imaging of single cell metabolism." In Label-free Biomedical Imaging and Sensing (LBIS) 2024, edited by Natan T. Shaked and Oliver Hayden. SPIE, 2024. http://dx.doi.org/10.1117/12.2685585.

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Occhipinti, Annalisa, and Claudio Angione. "A Computational Model of Cancer Metabolism for Personalised Medicine." In Building Bridges in Medical Science 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.03.001.3.

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Cancer cells must rewrite their ‘‘internal code’’ to satisfy the demand for growth and proliferation. Such changes are driven by a combination of genetic (e.g., genes’ mutations) and non-genetic factors (e.g., tumour microenvironment) that result in an alteration of cellular metabolism. For this reason, understanding the metabolic and genomic changes of a cancer cell can provide useful insight on cancer progression and survival outcomes. In our work, we present a computational framework that uses patient-specific data to investigate cancer metabolism and provide personalised survival predictions and cancer development outcomes. The proposed model integrates patient-specific multi-omics data (i.e., genomic, metabolomic and clinical data) into a metabolic model of cancer to produce a list of metabolic reactions affecting cancer progression. Quantitative and predictive analysis, through survival analysis and machine learning techniques, is then performed on the list of selected reactions. Since our model performs an analysis of patient-specific data, the outcome of our pipeline provides a personalised prediction of survival outcome and cancer development based on a subset of identified multi-omics features (genomic, metabolomic and clinical data). In particular, our work aims to develop a computational pipeline for clinicians that relates the omic profile of each patient to their survival probability, based on a combination of machine learning and metabolic modelling techniques. The model provides patient-specific predictions on cancer development and survival outcomes towards the development of personalised medicine.
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Reports on the topic "Cell Metabolism"

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Boss, W. Cell signalling and phospholipid metabolism. Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/5943691.

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Boss, W. F. Cell signalling and phospholipid metabolism. Office of Scientific and Technical Information (OSTI), January 1990. http://dx.doi.org/10.2172/7045128.

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Boss, W. F. Cell signalling and phospholipid metabolism. Final report. Office of Scientific and Technical Information (OSTI), December 1990. http://dx.doi.org/10.2172/10168282.

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Granot, David, and Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, January 2003. http://dx.doi.org/10.32747/2003.7585189.bard.

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Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .
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Ben-Arie, Ruth, John M. Labavitch, and Amos Blumenfeld. Hormonal Regulation of Cell Wall Metabolism During Fruit Ripening. United States Department of Agriculture, August 1987. http://dx.doi.org/10.32747/1987.7568074.bard.

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Blumwald, Eduardo, and Avi Sadka. Citric acid metabolism and mobilization in citrus fruit. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7587732.bard.

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Accumulation of citric acid is a major determinant of maturity and fruit quality in citrus. Many citrus varieties accumulate citric acid in concentrations that exceed market desires, reducing grower income and consumer satisfaction. Citrate is accumulated in the vacuole of the juice sac cell, a process that requires both metabolic changes and transport across cellular membranes, in particular, the mitochondrial and the vacuolar (tonoplast) membranes. Although the accumulation of citrate in the vacuoles of juice cells has been clearly demonstrated, the mechanisms for vacuolar citrate homeostasis and the components controlling citrate metabolism and transport are still unknown. Previous results in the PIs’ laboratories have indicated that the expression of a large number of a large number of proteins is enhanced during fruit development, and that the regulation of sugar and acid content in fruits is correlated with the differential expression of a large number of proteins that could play significant roles in fruit acid accumulation and/or regulation of acid content. The objectives of this proposal are: i) the characterization of transporters that mediate the transport of citrate and determine their role in uptake/retrieval in juice sac cells; ii) the study of citric acid metabolism, in particular the effect of arsenical compounds affecting citric acid levels and mobilization; and iii) the development of a citrus fruit proteomics platform to identify and characterize key processes associated with fruit development in general and sugar and acid accumulation in particular. The understanding of the cellular processes that determine the citrate content in citrus fruits will contribute to the development of tools aimed at the enhancement of citrus fruit quality. Our efforts resulted in the identification, cloning and characterization of CsCit1 (Citrus sinensis citrate transporter 1) from Navel oranges (Citrus sinesins cv Washington). Higher levels of CsCit1 transcripts were detected at later stages of fruit development that coincided with the decrease in the juice cell citrate concentrations (Shimada et al., 2006). Our functional analysis revealed that CsCit1 mediates the vacuolar efflux of citrate and that the CsCit1 operates as an electroneutral 1CitrateH2-/2H+ symporter. Our results supported the notion that it is the low permeable citrateH2 - the anion that establishes the buffer capacity of the fruit and determines its overall acidity. On the other hand, it is the more permeable form, CitrateH2-, which is being exported into the cytosol during maturation and controls the citrate catabolism in the juice cells. Our Mass-Spectrometry-based proteomics efforts (using MALDI-TOF-TOF and LC2- MS-MS) identified a large number of fruit juice sac cell proteins and established comparisons of protein synthesis patterns during fruit development. So far, we have identified over 1,500 fruit specific proteins that play roles in sugar metabolism, citric acid cycle, signaling, transport, processing, etc., and organized these proteins into 84 known biosynthetic pathways (Katz et al. 2007). This data is now being integrated in a public database and will serve as a valuable tool for the scientific community in general and fruit scientists in particular. Using molecular, biochemical and physiological approaches we have identified factors affecting the activity of aconitase, which catalyze the first step of citrate catabolism (Shlizerman et al., 2007). Iron limitation specifically reduced the activity of the cytosolic, but not the mitochondrial, aconitase, increasing the acid level in the fruit. Citramalate (a natural compound in the juice) also inhibits the activity of aconitase, and it plays a major role in acid accumulation during the first half of fruit development. On the other hand, arsenite induced increased levels of aconitase, decreasing fruit acidity. We have initiated studies aimed at the identification of the citramalate biosynthetic pathway and the role(s) of isopropylmalate synthase in this pathway. These studies, especially those involved aconitase inhibition by citramalate, are aimed at the development of tools to control fruit acidity, particularly in those cases where acid level declines below the desired threshold. Our work has significant implications both scientifically and practically and is directly aimed at the improvement of fruit quality through the improvement of existing pre- and post-harvest fruit treatments.
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Otegui, Marisa, Kevin Eliceiri, Jenu Chacko, and Han Nim Lee. Multiparametric optical label-free imaging to analyze plant cell wall assembly and metabolism. Office of Scientific and Technical Information (OSTI), April 2023. http://dx.doi.org/10.2172/1969880.

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Pell, Eva J., Sarah M. Assmann, Amnon Schwartz, and Hava Steinberger. Ozone Altered Stomatal/Guard Cell Function: Whole Plant and Single Cell Analysis. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7573082.bard.

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Original objectives (revisions from original proposal are highlighted) 1. Elucidate the direct effects O3 and H2O2 on guard cell function, utilizing assays of stomatal response in isolated epidermal peels and whole cell gas exchange. 2. Determine the mechanistic basis of O3 and H2O2 effects on the plasma membrane through application of the electrophysiological technique of patch clamping to isolated guard cells. 3. Determine the relative sensitivity of Israeli cultivars of economically important crops to O3 and determine whether differential leaf conductance responses to O3 can explain relative sensitivity to the air pollutant: transfer of technological expertise to Israel. Background to the topic For a long time O3 has been known to reduce gas exchange in plants; it has however been unclear if O3 can affect the stomatal complex directly. Ion channels are essential in stomatal regulation, but O3 has never before been shown to affect these directly. Major conclusions, solution, achievements 1. Ozone inhibits light-induced stomatal opening in epidermal peels isolated from Vicia faba, Arabidopsis thaliana and Nicotiana tabacum in V. faba plants this leads to reduced assimilation without a direct effect on the photosynthetic apparatus. Stomatal opening is more sensitive to O3 than stomatal closure. 2. Ozone causes inhibition of inward K+ channels (involved in stomatal opening) while no detectable effect is observed o the outward K+ channels (stomatal closure). 3. Hydrogen peroxide inhibits stomatal opening and induces stomatal closure in epidermal peels isolated from Vicia faba. 4. Hydrogen peroxide enhances stomatal closure by increasing K+ efflux from guard cells via outward rectifying K+ channels. 5. Based on epidermal peel experiments we have indirectly shown that Ca2+ may play a role in the guard cell response to O3. However, direct measurement of the guard cell [Ca2+]cyt did not show a response to O3. 6. Three Israeli cultivars of zucchini, Clarita, Yarden and Bareqet, were shown to be relatively sensitive to O3 (0.12 ml1-1 ). 7. Two environmentally important Israeli pine species are adversely affected by O3, even at 0.050 ml1-1 , a level frequently exceeded under local tropospheric conditions. P. brutia may be better equipped than P. halepensis to tolerate O3 stress. 8. Ozone directly affects pigment biosynthesis in pine seedlings, as well as the metabolism of O5 precursors, thus affecting the allocation of resources among various metabolic pathways. 9. Ozone induces activity of antioxidant enzymes, and of ascorbate content i the mesophyll and epidermis cells of Commelina communis L. Implications, both scientific and agricultural We have improved the understanding of how O3 and H2O2 do affect guard cell and stomatal function. We have shown that economical important Israeli species like zucchini and pine are relatively sensitive to O3.
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Pines, Mark, Mitsuo Yamauchi, Isaac Plavnik, and Shmuel Hurwitz. Collagen Metabolism in Vivo and in Cell Culture as Related to Skin Quality in Broilers. United States Department of Agriculture, December 1993. http://dx.doi.org/10.32747/1993.7603836.bard.

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Wolf, Shmuel, and William J. Lucas. Involvement of the TMV-MP in the Control of Carbon Metabolism and Partitioning in Transgenic Plants. United States Department of Agriculture, October 1999. http://dx.doi.org/10.32747/1999.7570560.bard.

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The function of the 30-kilodalton movement protein (MP) of tobacco mosaic virus (TMV) is to facilitate cell-to-cell movement of viral progeny in infected plants. Our earlier findings have indicated that this protein has a direct effect on plasmodesmal function. In addition, these studies demonstrated that constitutive expression of the TMV MP gene (under the control of the CaMV 35S promoter) in transgenic tobacco plants significantly affects carbon metabolism in source leaves and alters the biomass distribution between the various plant organs. The long-term goal of the proposed research was to better understand the factors controlling carbon translocation in plants. The specific objectives were: A) To introduce into tobacco and potato plants a virally-encoded (TMV-MP) gene that affects plasmodesmal functioning and photosynthate partitioning under tissue-specific promoters. B) To introduce into tobacco and potato plants the TMV-MP gene under the control of promoters which are tightly repressed by the Tn10-encoded Tet repressor, to enable the expression of the protein by external application of tetracycline. C) To explore the mechanism by which the TMV-MP interacts with the endogenous control o~ carbon allocation. Data obtained in our previous project together with the results of this current study established that the TMV-MP has pleiotropic effects when expressed in transgenic tobacco plants. In addition to its ability to increase the plasmodesmal size exclusion limit, it alters carbohydrate metabolism in source leaves and dry matter partitioning between the various plant organs, Expression of the TMV-MP in various tissues of transgenic potato plants indicated that sugars and starch levels in source leaves are reduced below those of control plants when the TMV-MP is expressed in green tissue only. However, when the TMV-MP was expressed predominantly in PP and CC, sugar and starch levels were raised above those of control plants. Perhaps the most significant result obtained from experiments performed on transgenic potato plants was the discovery that the influence of the TMV-MP on carbohydrate allocation within source leaves was under developmental control and was exerted only during tuber development. The complexity of the mode by which the TMV-MP exerts its effect on the process of carbohydrate allocation was further demonstrated when transgenic tobacco plants were subjected to environmental stresses such as drought stress and nutrients deficiencies, Collectively, these studies indicated that the influence of the TMV-MP on carbon allocation L the result of protein-protein interaction within the source tissue. Based on these results, together with the findings that plasmodesmata potentiate the cell-to-cell trafficking of viral and endogenous proteins and nucleoproteins complexes, we developed the theme that at the whole plant level, the phloem serves as an information superhighway. Such a long-distance communication system may utilize a new class of signaling molecules (proteins and/or RNA) to co-ordinate photosynthesis and carbon/nitrogen metabolism in source leaves with the complex growth requirements of the plant under the prevailing environmental conditions. The discovery that expression of viral MP in plants can induce precise changes in carbon metabolism and photoassimilate allocation, now provide a conceptual foundation for future studies aimed at elucidating the communication network responsible for integrating photosynthetic productivity with resource allocation at the whole-plant level. Such information will surely provide an understanding of how plants coordinate the essential physiological functions performed by distantly-separated organs. Identification of the proteins involved in mediating and controlling cell-to-cell transport, especially at the companion cell-sieve element boundary, will provide an important first step towards achieving this goal.
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