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Journal articles on the topic 'Metabolic activation'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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1

Pence, Brandt D., and Jeffrey A. Woods. "Metabolic Activation." Medicine & Science in Sports & Exercise 47 (May 2015): 716. http://dx.doi.org/10.1249/01.mss.0000478681.15510.ae.

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2

Oyarzún, Diego, Brian Ingalls, Richard Middleton, and Dimitrios Kalamatianos. "Optimal Metabolic Pathway Activation." IFAC Proceedings Volumes 41, no. 2 (2008): 12587–92. http://dx.doi.org/10.3182/20080706-5-kr-1001.02130.

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3

Wang, Ching Y., and Charles M. King. "Metabolic activation of benzidine." International Journal of Cancer 121, no. 7 (2007): 1640–41. http://dx.doi.org/10.1002/ijc.22905.

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4

Peter Guengerich, F. "Metabolic activation of carcinogens." Pharmacology & Therapeutics 54, no. 1 (January 1992): 17–61. http://dx.doi.org/10.1016/0163-7258(92)90050-a.

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5

White, Ian N. H., Melanie L. Green, Eric Bailey, and Peter B. Farmer. "Metabolic activation of olefins." Biochemical Pharmacology 35, no. 9 (May 1986): 1569–75. http://dx.doi.org/10.1016/0006-2952(86)90126-7.

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6

Holthaus, Lisa, Virag Sharma, Daniel Brandt, Anette-Gabriele Ziegler, Martin Jastroch, and Ezio Bonifacio. "Functional and metabolic fitness of human CD4+ T lymphocytes during metabolic stress." Life Science Alliance 4, no. 12 (September 27, 2021): e202101013. http://dx.doi.org/10.26508/lsa.202101013.

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Human CD4+ T cells are essential mediators of immune responses. By altering the mitochondrial and metabolic states, we defined metabolic requirements of human CD4+ T cells for in vitro activation, expansion, and effector function. T-cell activation and proliferation were reduced by inhibiting oxidative phosphorylation, whereas early cytokine production was maintained by either OXPHOS or glycolytic activity. Glucose deprivation in the presence of mild mitochondrial stress markedly reduced all three T-cell functions, contrasting the exposure to resveratrol, an antioxidant and sirtuin-1 activator, which specifically inhibited cytokine production and T-cell proliferation, but not T-cell activation. Conditions that inhibited T-cell activation were associated with the down-regulation of 2′,5′-oligoadenylate synthetase genes via interferon response pathways. Our findings indicate that T-cell function is grossly impaired by stressors combined with nutrient deprivation, suggesting that correcting nutrient availability, metabolic stress, and/or the function of T cells in these conditions will improve the efficacy of T-cell–based therapies.
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7

Park, B. K., D. J. Naisbitt, S. F. Gordon, N. R. Kitteringham, and M. Pirmohamed. "Metabolic activation in drug allergies." Toxicology 158, no. 1-2 (February 2001): 11–23. http://dx.doi.org/10.1016/s0300-483x(00)00397-8.

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8

Mekenyan, O., S. Dimitrov, N. Dimitrova, G. Dimitrova, T. Pavlov, G. Chankov, S. Kotov, K. Vasilev, and R. Vasilev. "Metabolic activation of chemicals:in-silicosimulation†." SAR and QSAR in Environmental Research 17, no. 1 (February 2006): 107–20. http://dx.doi.org/10.1080/10659360600562087.

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9

Skonberg, Christian, Jrgen Olsen, Kim Grimstrup Madsen, Steen Honor Hansen, and Mark P. Grillo. "Metabolic activation of carboxylic acids." Expert Opinion on Drug Metabolism & Toxicology 4, no. 4 (April 2008): 425–38. http://dx.doi.org/10.1517/17425255.4.4.425.

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10

Vrijsen, Raf, Yvette Michotte, and Albert Boeyé. "Metabolic activation of quercetin mutagenicity." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 232, no. 2 (October 1990): 243–48. http://dx.doi.org/10.1016/0027-5107(90)90130-v.

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11

Vrijsen, R., A. Broos, and A. Boeyé. "Metabolic activation of quercetin mutagenicity." Mutation Research/Environmental Mutagenesis and Related Subjects 234, no. 6 (December 1990): 408. http://dx.doi.org/10.1016/0165-1161(90)90137-d.

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12

Nemoto, Edwin M., Howard Yonas, Frank Pigula, and Simon Watkins. "Cerebral metabolic compartmentation: the effects of hypothermia and metabolic activation." International Congress Series 1235 (July 2002): 231–42. http://dx.doi.org/10.1016/s0531-5131(02)00192-9.

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13

Falezza, A., S. Cinelli, P. Ciliutti, and J. A. Vericat. "Metabolic activation in the inhibition of the metabolic cooperation assay." Mutation Research/Environmental Mutagenesis and Related Subjects 271, no. 2 (1992): 161. http://dx.doi.org/10.1016/0165-1161(92)91193-u.

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14

Nishikawa, Takuro, Kimiko Izumo, Emiko Miyahara, Masahisa Horiuchi, Yasuhiro Okamoto, Yoshifumi Kawano, and Toru Takeuchi. "Benzene Induces Cytotoxicity without Metabolic Activation." Journal of Occupational Health 53, no. 2 (March 2011): 84–92. http://dx.doi.org/10.1539/joh.10-002-oa.

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15

Nishikawa, Akiyoshi, Yukio Mori, In-Seon Lee, Takuji Tanaka, and Masao Hirose. "Cigarette Smoking, Metabolic Activation and Carcinogenesis." Current Drug Metabolism 5, no. 5 (October 1, 2004): 363–73. http://dx.doi.org/10.2174/1389200043335441.

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16

Baardman, Jeroen, Iris Licht, Menno PJ de Winther, and Jan Van den Bossche. "Metabolic–epigenetic crosstalk in macrophage activation." Epigenomics 7, no. 7 (October 2015): 1155–64. http://dx.doi.org/10.2217/epi.15.71.

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17

Liehr, Joachim G., Annie M. Ballatore, Beverly B. Dague, and Aysegul Ari Ulubelen. "Carcinogenicity and metabolic activation of hexestrol." Chemico-Biological Interactions 55 (1985): 157–76. http://dx.doi.org/10.1016/s0009-2797(85)80125-3.

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18

Stiborova, Marie. "Metabolic activation of nitroaromatics and arylamines." Toxicology Letters 189 (September 2009): S28. http://dx.doi.org/10.1016/j.toxlet.2009.06.047.

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19

Mizuno, Katsuhiko, Miki Katoh, Hirotoshi Okumura, Nao Nakagawa, Toru Negishi, Takanori Hashizume, Miki Nakajima, and Tsuyoshi Yokoi. "Metabolic Activation of Benzodiazepines by CYP3A4." Drug Metabolism and Disposition 37, no. 2 (November 12, 2008): 345–51. http://dx.doi.org/10.1124/dmd.108.024521.

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20

Xu, Daosong, and Martin E. Hemler. "Metabolic Activation-related CD147-CD98 Complex." Molecular & Cellular Proteomics 4, no. 8 (May 18, 2005): 1061–71. http://dx.doi.org/10.1074/mcp.m400207-mcp200.

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21

MOCHIZUKI, Masataka. "Metabolic Activation of Carcinogenic N-Nitrosodialkylamines." YAKUGAKU ZASSHI 110, no. 6 (1990): 359–73. http://dx.doi.org/10.1248/yakushi1947.110.6_359.

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22

BICKERS, DAVID R. "Metabolic Activation of Carcinogens by Keratinocytes." Annals of the New York Academy of Sciences 548, no. 1 Endocrine, Me (December 1988): 102–6. http://dx.doi.org/10.1111/j.1749-6632.1988.tb18796.x.

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23

Li, Hua-Bing, Chengcheng Jin, Yuanyuan Chen, and Richard A. Flavell. "Inflammasome activation and metabolic disease progression." Cytokine & Growth Factor Reviews 25, no. 6 (December 2014): 699–706. http://dx.doi.org/10.1016/j.cytogfr.2014.07.020.

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24

Letteron, Philippe, Veronique Descatoire, Marina Tinel, Patrick Maurel, Gilles Labbe, Jacqueline Loeper, Dominique Larrey, Eric Freneaux, and Dominique Pessayre. "Metabolic activation of the antidepressant tianeptine." Biochemical Pharmacology 38, no. 19 (October 1989): 3241–46. http://dx.doi.org/10.1016/0006-2952(89)90620-5.

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25

Letteron, Philippe, Gilles Labbe, Veronique Descatoire, Claude Degott, Jacqueline Loeper, Marina Tinel, Dominique Larrey, and Dominique Pessayre. "Metabolic activation of the antidepressant tianeptine." Biochemical Pharmacology 38, no. 19 (October 1989): 3247–51. http://dx.doi.org/10.1016/0006-2952(89)90621-7.

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26

Hanna, Patrick E. "Metabolic Activation and Detoxification of Arylamines." Current Medicinal Chemistry 3, no. 3 (June 1996): 195–210. http://dx.doi.org/10.2174/092986730303220225103338.

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Abstract: A number of important therapeutic agents, such as the sulfonamide antibacterials, dapsone, and procainamide are primary arylamines. Human exposure to arylamines also occurs through smoking tobacco and consuming cooked meat, and in various occupational settings. The principal detoxification pathway for most primary arylamines involves metabolic conversion to an arylamide in an acetyl coenzyme A-dependent, N-acetyltransferase-catalyzed reaction. Although arylamines produce a wide range of toxicological responses, including hypersensitivity reactions and carcinogenesis, metabolic transformation to an N-hydroxyarylamine is required for most such compounds to manifest their untoward effects. Further conjugative metabolism of the N-hydroxylated arylamines is often involved in the production of reactive, electrophilic metabolites which form covalent adducts with biological macromolecules. This review describes the roles of specific enzyme systems in the biotransformation of arylamines and the chemical characteristics of arylamine metabolites that influence their toxicity, fate and disposition. The influence of interindividual genetic variability on the toxification and detoxification of arylamines is also addressed. In particular, genetic regulation of acetyltransferase activity is an important determinant of susceptibility to the toxicity and carcinogenicity of arylamines.
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27

Ott, Hagen, Moa Andresen Bergström, Ruth Heise, Claudia Skazik, Gabriele Zwadlo-Klarwasser, Hans F. Merk, Jens M. Baron, and Ann-Therese Karlberg. "Cutaneous Metabolic Activation of Carvoxime, a Self-Activating, Skin-Sensitizing Prohapten." Chemical Research in Toxicology 22, no. 2 (February 16, 2009): 399–405. http://dx.doi.org/10.1021/tx8003642.

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28

Leiter, Sarah M., Victoria E. R. Parker, Alena Welters, Rachel Knox, Nuno Rocha, Graeme Clark, Felicity Payne, et al. "Hypoinsulinaemic, hypoketotic hypoglycaemia due to mosaic genetic activation of PI3-kinase." European Journal of Endocrinology 177, no. 2 (August 2017): 175–86. http://dx.doi.org/10.1530/eje-17-0132.

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Objective Genetic activation of the insulin signal-transducing kinase AKT2 causes syndromic hypoketotic hypoglycaemia without elevated insulin. Mosaic activating mutations in class 1A phospatidylinositol-3-kinase (PI3K), upstream from AKT2 in insulin signalling, are known to cause segmental overgrowth, but the metabolic consequences have not been systematically reported. We assess the metabolic phenotype of 22 patients with mosaic activating mutations affecting PI3K, thereby providing new insight into the metabolic function of this complex node in insulin signal transduction. Methods Three patients with megalencephaly, diffuse asymmetric overgrowth, hypoketotic, hypoinsulinaemic hypoglycaemia and no AKT2 mutation underwent further genetic, clinical and metabolic investigation. Signalling in dermal fibroblasts from one patient and efficacy of the mTOR inhibitor Sirolimus on pathway activation were examined. Finally, the metabolic profile of a cohort of 19 further patients with mosaic activating mutations in PI3K was assessed. Results In the first three patients, mosaic mutations in PIK3CA (p.Gly118Asp or p.Glu726Lys) or PIK3R2 (p.Gly373Arg) were found. In different tissue samples available from one patient, the PIK3CA p.Glu726Lys mutation was present at burdens from 24% to 42%, with the highest level in the liver. Dermal fibroblasts showed increased basal AKT phosphorylation which was potently suppressed by Sirolimus. Nineteen further patients with mosaic mutations in PIK3CA had neither clinical nor biochemical evidence of hypoglycaemia. Conclusions Mosaic mutations activating class 1A PI3K cause severe non-ketotic hypoglycaemia in a subset of patients, with the metabolic phenotype presumably related to the extent of mosaicism within the liver. mTOR or PI3K inhibitors offer the prospect for future therapy.
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29

Kedderis, Gregory L., and Gerald T. Miwa. "The metabolic activation of nitroheterocyclic therapeutic agents." Drug Metabolism Reviews 19, no. 1 (January 1988): 33–62. http://dx.doi.org/10.3109/03602538809049618.

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30

Leung, Louis, Amit S. Kalgutkar, and R. Scott Obach. "Metabolic activation in drug-induced liver injury." Drug Metabolism Reviews 44, no. 1 (January 30, 2012): 18–33. http://dx.doi.org/10.3109/03602532.2011.605791.

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31

McCoy, Francis, Rashid Darbandi, Hoi Chang Lee, Kavitha Bharatham, Tudor Moldoveanu, Christy R. Grace, Keela Dodd, et al. "Metabolic Activation of CaMKII by Coenzyme A." Molecular Cell 52, no. 3 (November 2013): 325–39. http://dx.doi.org/10.1016/j.molcel.2013.08.043.

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32

McCoy, Francis, Rashid Darbandi, Hoi Chang Lee, Kavitha Bharatham, Tudor Moldoveanu, Christy R. Grace, Keela Dodd, et al. "Metabolic Activation of CaMKII by Coenzyme A." Molecular Cell 52, no. 3 (November 2013): 468. http://dx.doi.org/10.1016/j.molcel.2013.10.027.

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33

Paulson, Olaf B., and Ian Law. "Hemodynamic and metabolic features of cerebral activation." International Congress Series 1235 (July 2002): 205–12. http://dx.doi.org/10.1016/s0531-5131(02)00188-7.

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34

OKUDA, HARUHIRO, and TADASHI WATABE. "Metabolic activation of carcinogens by conjugation reactions." Eisei kagaku 34, no. 2 (1988): 75–91. http://dx.doi.org/10.1248/jhs1956.34.75.

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35

NOMURA, Wataru, and Yoshiharu INOUE. "Activation of TOR Signaling by Metabolic Stress." KAGAKU TO SEIBUTSU 54, no. 4 (2016): 273–80. http://dx.doi.org/10.1271/kagakutoseibutsu.54.273.

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36

Yoshii, Fumihito, and Ranjan Duara. "Cerebro-cerebellar metabolic relationship during behavioral activation." Nosotchu 12, no. 3 (1990): 265–70. http://dx.doi.org/10.3995/jstroke.12.265.

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37

Kam, Yoonseok, Pam Swain, Natalia Romero, and Brian Dranka. "Bi-phasic Metabolic Responses During Macrophage Activation." Free Radical Biology and Medicine 112 (November 2017): 205–6. http://dx.doi.org/10.1016/j.freeradbiomed.2017.10.325.

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38

Parke, D. V., C. Ioannides, and D. F. V. Lewis. "Metabolic Activation of Carcinogens and Toxic Chemicals." Human Toxicology 7, no. 5 (September 1988): 397–404. http://dx.doi.org/10.1177/096032718800700503.

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1 The spatial parameters and electronic structures of 100 exogenous and endogenous chemicals have been determined by computer graphics, from which their oxidative metabolism by the cytochromes P-448 (activation) or the other families of cytochromes P-450 (generally detoxication) have been predicted. 2 The spatial parameters of these chemicals primarily determine the family of cytochrome P-450 by which the chemicals are metabolized and the electronic structures primarily determine their ease of oxidative metabolism. 3 The role of oxidative metabolism of xenobiotics by the cytochromes P-448, and their binding to the cytosolic Ah receptor, are considered in relationship to the mechanisms of chemical toxicity, mutagenicity, carcinogenicity, and co-carcinogenicity. 4 The mechanisms of chemical toxicity and carcinogenesis are considered in respect of activation through cytochrome P-448-mediated, conformationally-hindered oxygenation to reactive intermediates which, unlike most cytochrome P-450-oxygenated metabolites, are not acceptable substrates for conjugation and detoxication and therefore react with essential intracellular macromolecules. 5 The computer graphic method of determining the molecular conformations and electronic structures of molecules is a rapid, scientifically-based procedure for evaluation of the potential toxicity, mutagenicity and carcinogenicity of chemicals.
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39

Santilli, F., N. Vazzana, R. Liani, M. T. Guagnano, and G. Davì. "Platelet activation in obesity and metabolic syndrome." Obesity Reviews 13, no. 1 (September 15, 2011): 27–42. http://dx.doi.org/10.1111/j.1467-789x.2011.00930.x.

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40

Rueff, J., A. Laires, M. Kranendonk, A. Rodrigues, J. Gaspar, H. Borba, and M. Monteiro. "Metabolic activation of mutagens by human haemoglobin." Mutation Research/Environmental Mutagenesis and Related Subjects 234, no. 6 (December 1990): 402. http://dx.doi.org/10.1016/0165-1161(90)90125-8.

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41

Schlosser, Michael J., and George F. Kalf. "Metabolic activation of hydroquinone by macrophage peroxidase." Chemico-Biological Interactions 72, no. 1-2 (1989): 191–207. http://dx.doi.org/10.1016/0009-2797(89)90027-6.

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42

Morimoto, Akio, Kyoko Imai-Matsumura, and Naotoshi Murakami. "Metabolic activation of the fetal rat brain." Neuroscience Letters 111, no. 1-2 (March 1990): 34–38. http://dx.doi.org/10.1016/0304-3940(90)90340-f.

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43

Sun, Ying, Xin Xin, Kehan Zhang, Tiantian Cui, Ying Peng, and Jiang Zheng. "Cytochrome P450 mediated metabolic activation of chrysophanol." Chemico-Biological Interactions 289 (June 2018): 57–67. http://dx.doi.org/10.1016/j.cbi.2018.04.015.

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44

Cibrián, Danay, and Francisco Sánchez-Madrid. "CD69: from activation marker to metabolic gatekeeper." European Journal of Immunology 47, no. 6 (June 2017): 946–53. http://dx.doi.org/10.1002/eji.201646837.

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45

Ding, Zifang, Xu Wang, Ning Zhang, Chen Sun, Guode Zhao, Ying Peng, and Jiang Zheng. "Metabolic Activation of Perampanel Mediated by CYP1A2." Chemical Research in Toxicology 35, no. 3 (February 24, 2022): 490–98. http://dx.doi.org/10.1021/acs.chemrestox.1c00396.

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46

Daniela, Ventro, Adam T. Utley, and Kelvin P. Lee. "CD28 Activation Induces Metabolic Adaptation in Multiple Myeloma Cells." Blood 124, no. 21 (December 6, 2014): 4708. http://dx.doi.org/10.1182/blood.v124.21.4708.4708.

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Abstract Alterations in cancer cell metabolism is a century old concept recently recognized as one of the hallmarks of cancer. Cancer cells, including multiple myeloma (MM), largely shift how they utilize the glucose they consume to glycolysis from that of oxidative phosphorylation (OXPHOS). This phenomenon supports the cancer cell’s large anabolic demands for continuous growth and proliferation and is reinforced by key signaling pathways. However, as a cancer of the previously non-dividing plasma cell, these metabolic adaptations are only beginning to be documented in MM. CD28 is classically known as the T-cell co-stimulatory receptor, but is also expressed on normal plasma cells and their malignant counterparts. Previous data suggests that CD28 is required for MM cell survival, protective during stress induced conditions, and correlates with poor prognosis in the clinic. Furthermore, studies using the anti-CD28 activating monoclonal antibody (mAb) have identified phosphatidyl-inositol 3-kinase (PI3K)/Akt activation to be a key driver of its pro-survival function. Akt is also an important integrator of cellular metabolism and cell growth and proliferation signaling pathways. Therefore, its CD28 mediated activation may uncover the mechanism by which MM cells are able to metabolically sustain stress induced conditions and thrive thereafter. Herein, we show that when CD28 is activated by anti-CD28 mAb (10µg/ml) under stressful conditions (media serum reduction), Akt (T308) phosphorylation increases, resulting in an increase of total protein and cell surface expression of the glucose transporter, GLUT1. To assess if cells take in more glucose in the presence of anti-CD28 mAb they were cultured in glucose free media and glucose was then added back at concentrations of 0.5, 1 and 5mM with or without activating anti-CD28 mAb. Significant increases in glucose uptake were seen in the 5mM anti-CD28 mAb treatment group when compared to the untreated control, correlating positively with the increase in GLUT1 protein expression. To evaluate whether or not CD28 activation induces a preferential for glycolytic breakdown of glucose, the same treatment conditions were repeated and lactate production/oxygen consumption, as a measure of glycolysis and OXPHOS respectively, were measured in a fluorometric kinetic assay. Lactate production significantly increased in MM cells treated with anti-CD28 mAb compared to untreated controls, confirming its role in enhancing glycolysis for cell growth and survival. This data is further supported by increased cell death observed in murine MM cells treated with the glycolysis inhibitor, 2-Deoxyglucose (2-DG). Interestingly, the level of oxygen consumption was comparable in all groups suggesting not only minimal effect in response to CD28 activation, but also relatively unimpaired OXPHOS in MM cells. Furthermore, analysis of mitochondrial biogenesis using the mitotracker green stain and production of reactive oxygen species by 2’,7’-difchlorofluorescin diacetate (DCFDA) oxidation in murine MM cells also revealed both processes to be intact and increased in the presence of CD28 activation. Taken together, these results suggest that CD28 signaling plays a strategic role in shifting the metabolic axis to that of increased glucose uptake and consumption via glycolysis through phosphorylation of PI3K/Akt and upregulation of GLUT1 expression. Pharmacological inhibition of CD28 is therefore an attractive avenue for therapeutic intervention in MM and we have previously shown that interfering with CD28 and its interacting ligands, CD80/CD86, using the CTLA4-Ig fusion protein, is effective in this regard. Disclosures No relevant conflicts of interest to declare.
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47

Kaidashev, Igor P. "Activation of NF-kB under the Metabolic Syndrome." International Journal of Physiology and Pathophysiology 3, no. 3 (2012): 287–97. http://dx.doi.org/10.1615/intjphyspathophys.v3.i3.90.

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48

Hinson, Jack A., Neil R. Pumford, and Sidney D. Nelson. "The Role of Metabolic Activation in Drug Toxicity." Drug Metabolism Reviews 26, no. 1-2 (January 1994): 395–412. http://dx.doi.org/10.3109/03602539409029805.

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49

Kim, Dong-Hak, and Young-Jin Chun. "Human Cytochrome P450 Metabolic Activation in Chemical Toxicity." Toxicological Research 23, no. 3 (September 30, 2007): 189–96. http://dx.doi.org/10.5487/tr.2007.23.3.189.

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50

Ye, Leping, Zhi-Jian Su, and Ren-Shan Ge. "Inhibitors of Testosterone Biosynthetic and Metabolic Activation Enzymes." Molecules 16, no. 12 (December 2, 2011): 9983–10001. http://dx.doi.org/10.3390/molecules16129983.

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