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Your search keyword '"Ostrakhovitch, Elena A."' showing total 7 results
Start Over Author "Ostrakhovitch, Elena A." Publisher elsevier
7 results on '"Ostrakhovitch, Elena A."'

1. Contributors

Author

Aaseth, Jan, primary, Aggett, Peter, additional, Aitio, Antero, additional, Åkesson, Agneta, additional, Albin, Maria, additional, Alexander, Jan, additional, Andersen, Christian B.I., additional, Andersen, Ole, additional, Apostoli, Pietro, additional, Aschner, Michael, additional, Bakadlag, Rowa, additional, Barregard, Lars, additional, Bellinger, David C., additional, Bergdahl, Ingvar A., additional, Berlinger, Balazs, additional, Bernard, Alfred, additional, Bigert, Carolina, additional, Bjerregaard, Poul, additional, Blain, Robyn, additional, Blomqvist, Lennart K., additional, Bocca, Beatrice, additional, Bose-O'Reilly, Stephan, additional, Broberg, Karin, additional, Brown, Ronald P., additional, Budtz-Jørgensen, Esben, additional, Caito, Samuel W., additional, Carle, Tiffany, additional, Chen, Chien-Jen, additional, Chen, Xiao, additional, Chen, Lung-Chi, additional, Chou, C.-H. Selene J., additional, Cohen, Mitchell D., additional, Costa, Max, additional, De Palma, Giuseppe, additional, Elder, Alison, additional, Elinder, Carl-Gustaf, additional, Fadeel, Bengt, additional, Faroon, Obaid M., additional, Fowler, Bruce A., additional, Fujishiro, Hitomi, additional, Fustinoni, Silvia, additional, Gerhardsson, Lars, additional, Grandjean, Philippe, additional, Gustavsson, Per, additional, Hedberg, Yolanda, additional, Himeno, Seiichiro, additional, Huang, Xi, additional, Hultman, Per A., additional, Iavicoli, Ivo, additional, Jin, Taiyi, additional, Jones, Robert L., additional, Karlsson, Hanna L., additional, Keith, Larry S., additional, Kim, Yangho, additional, Klein, Catherine B., additional, Kleinman, Michael, additional, Kotelchuck, David, additional, Kusaka, Yukinori, additional, Landrigan, Philip J., additional, Leffler, Per E., additional, Leso, Veruscka, additional, Li, Alex Heng, additional, Lison, Dominique, additional, Liu, Shan, additional, Lucchini, Roberto G., additional, Maciejczyk, Polina, additional, Mann, Koren K., additional, Maples-Reynolds, Nikki, additional, Maroney, Michael J., additional, Martins, Airton C., additional, Matsui, Mary S., additional, Moffett, Daphne B., additional, Møller, Lisbeth Birk, additional, Mumtaz, M. Moiz, additional, Nakano, Makiko, additional, Nemery, Benoit, additional, Nogawa, Koji, additional, Nordberg, Gunnar F., additional, Nordberg, Monica, additional, Ortiz, Angelica, additional, Oskarsson, Agneta, additional, Ostrakhovitch, Elena A., additional, Pałczyński, Cezary M., additional, Pawlas, Natalia, additional, Pelclova, Daniela, additional, Pesonen, Maria, additional, Pollard, K. Michael, additional, Rink, Lothar, additional, Ruggieri, Flavia, additional, Ruiz, Patricia, additional, Sandstead, Harold H., additional, Santonen, Tiina, additional, Sato, Kazuhiro, additional, Satoh, Hiroshi, additional, Saxena, Deepak, additional, Schoeters, Greet, additional, Sjögren, Bengt, additional, Skerfving, Staffan, additional, Smith, Donald R., additional, Sullivan, Dexter W., additional, Sumi, Daigo, additional, Sun, Hong, additional, Suojalehto, Hille, additional, Tanaka, Akiyo, additional, Tenenbein, Milton, additional, Thurston, George D., additional, Tomei Torres, Francisco A., additional, Toprak, Muhammet S., additional, Tylenda, Carolyn A., additional, Tyson, Julian F., additional, Umemura, Tomohiro, additional, Whittaker, Margaret H., additional, Wolf, Jana, additional, Yan, Wenbo, additional, Yokel, Robert A., additional, and Zalups, Rudolfs K., additional

Published
2022
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3. Contributors

Author

Aaseth, Jan, primary, Aggett, Peter, additional, Aitio, Antero, additional, Åkesson, Agneta, additional, Albin, Maria, additional, Alexander, Jan, additional, Andersen, Christian B.I., additional, Andersen, Ole, additional, Apostoli, Pietro, additional, Aschner, Michael, additional, Bakadlag, Rowa, additional, Barregard, Lars, additional, Bellinger, David C., additional, Bergdahl, Ingvar A., additional, Berlinger, Balazs, additional, Bernard, Alfred, additional, Bigert, Carolina, additional, Bjerregaard, Poul, additional, Blain, Robyn, additional, Blomqvist, Lennart K., additional, Bocca, Beatrice, additional, Bose-O'Reilly, Stephan, additional, Broberg, Karin, additional, Brown, Ronald P., additional, Budtz-Jørgensen, Esben, additional, Caito, Samuel W., additional, Carle, Tiffany, additional, Chen, Chien-Jen, additional, Chen, Xiao, additional, Chen, Lung-Chi, additional, Chou, C.-H. Selene J., additional, Cohen, Mitchell D., additional, Costa, Max, additional, De Palma, Giuseppe, additional, Elder, Alison, additional, Elinder, Carl-Gustaf, additional, Fadeel, Bengt, additional, Faroon, Obaid M., additional, Fowler, Bruce A., additional, Fujishiro, Hitomi, additional, Fustinoni, Silvia, additional, Gerhardsson, Lars, additional, Grandjean, Philippe, additional, Gustavsson, Per, additional, Hedberg, Yolanda, additional, Himeno, Seiichiro, additional, Huang, Xi, additional, Hultman, Per A., additional, Iavicoli, Ivo, additional, Jin, Taiyi, additional, Jones, Robert L., additional, Karlsson, Hanna L., additional, Keith, Larry S., additional, Kim, Yangho, additional, Klein, Catherine B., additional, Kleinman, Michael, additional, Kotelchuck, David, additional, Kusaka, Yukinori, additional, Landrigan, Philip J., additional, Leffler, Per E., additional, Leso, Veruscka, additional, Li, Alex Heng, additional, Lison, Dominique, additional, Liu, Shan, additional, Lucchini, Roberto G., additional, Maciejczyk, Polina, additional, Mann, Koren K., additional, Maples-Reynolds, Nikki, additional, Maroney, Michael J., additional, Martins, Airton C., additional, Matsui, Mary S., additional, Moffett, Daphne B., additional, Møller, Lisbeth Birk, additional, Mumtaz, M. Moiz, additional, Nakano, Makiko, additional, Nemery, Benoit, additional, Nogawa, Koji, additional, Nordberg, Gunnar F., additional, Nordberg, Monica, additional, Ortiz, Angelica, additional, Oskarsson, Agneta, additional, Ostrakhovitch, Elena A., additional, Pałczyński, Cezary M., additional, Pawlas, Natalia, additional, Pelclova, Daniela, additional, Pesonen, Maria, additional, Pollard, K. Michael, additional, Rink, Lothar, additional, Ruggieri, Flavia, additional, Ruiz, Patricia, additional, Sandstead, Harold H., additional, Santonen, Tiina, additional, Sato, Kazuhiro, additional, Satoh, Hiroshi, additional, Saxena, Deepak, additional, Schoeters, Greet, additional, Sjögren, Bengt, additional, Skerfving, Staffan, additional, Smith, Donald R., additional, Sullivan, Dexter W., additional, Sumi, Daigo, additional, Sun, Hong, additional, Suojalehto, Hille, additional, Tanaka, Akiyo, additional, Tenenbein, Milton, additional, Thurston, George D., additional, Tomei Torres, Francisco A., additional, Toprak, Muhammet S., additional, Tylenda, Carolyn A., additional, Tyson, Julian F., additional, Umemura, Tomohiro, additional, Whittaker, Margaret H., additional, Wolf, Jana, additional, Yan, Wenbo, additional, Yokel, Robert A., additional, and Zalups, Rudolfs K., additional

Published
2021
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6. Stimulation of phosphoinositide 3-kinase/Akt signaling by copper and zinc ions: mechanisms and consequences.

Author

Barthel A, Ostrakhovitch EA, Walter PL, Kampkötter A, and Klotz LO

Subjects
Animals, Cations, Divalent, Copper chemistry, Humans, Zinc chemistry, Copper pharmacology, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt metabolism, Signal Transduction drug effects, Zinc pharmacology
Abstract

The phosphoinositide 3'-kinase (PI3K)/Akt signaling cascade controls cellular processes such as apoptosis and proliferation. Moreover, it is a mediator of insulin effects on target cells and as such is a major regulator of fuel metabolism. The PI3K/Akt cascade was demonstrated to be activated by stressful stimuli, including heat shock and reactive oxygen species (ROS). This minireview focuses on activation of the pathway by exposure of cells to heavy metal ions, Cu2+ and Zn2+. It is hypothesized that stimulation of PI3K/Akt is the molecular mechanism underlying the known insulin-mimetic effects of copper and zinc ions. Following a brief summary of PI3K/Akt signaling and of activation of the cascade by Cu2+ and Zn2+, mechanisms of metal-induced PI3K/Akt activation are discussed with a focus on the role of ROS and of cellular thiols (glutathione, thioredoxin) and protein tyrosine phosphatases in Cu2+ and Zn2+ signaling. Finally, consequences of metal-induced PI3K/Akt activation are discussed, focusing on the modulation of FoxO-family transcription factors by Cu2+ and Zn2+.

Published
2007
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7. Copper ions strongly activate the phosphoinositide-3-kinase/Akt pathway independent of the generation of reactive oxygen species.

Author

Ostrakhovitch EA, Lordnejad MR, Schliess F, Sies H, and Klotz LO

Subjects
Calcium-Calmodulin-Dependent Protein Kinases metabolism, Cations, Divalent pharmacology, Enzyme Activation drug effects, Fibroblasts cytology, Glycogen Synthase Kinase 3, Glycogen Synthase Kinases, HeLa Cells, Humans, Hydrogen Peroxide pharmacology, Models, Biological, Phosphorylation, Proto-Oncogene Proteins c-akt, Reactive Oxygen Species metabolism, Receptors, Growth Factor metabolism, Signal Transduction, Skin cytology, Copper pharmacology, Phosphatidylinositol 3-Kinases metabolism, Protein Serine-Threonine Kinases metabolism, Proto-Oncogene Proteins metabolism
Abstract

Copper is implicated in metabolic disorders, such as Wilson's disease or Alzheimer's disease. Analysis of signaling pathways regulating cellular survival and function in response to a copper stress is crucial for understanding the pathogenesis of such diseases. Exposure of human skin fibroblasts or HeLa cells to Cu(2+) resulted in a dose- and time-dependent activation of the antiapoptotic kinase Akt/protein kinase B, starting at concentrations as low as 3 microM. Only Cu(II), but not Cu(I), had this effect. Activation of Akt was accompanied by phosphorylation of a downstream target of Akt, glycogen synthase kinase-3. Inhibitors of phosphoinositide-3-kinase (PI3K) completely blocked activation of Akt by Cu(2+), indicating a requirement of PI3K for Cu(2+)-induced activation of Akt. Indeed, cellular PI3K activity was strongly enhanced after exposure to Cu(2+). Copper ions may lead to the formation of reactive oxygen species, such as hydrogen peroxide. Activation of Akt by hydrogen peroxide or growth factors is known to proceed via the activation growth factor receptors. In line with this, pretreatment with inhibitors of growth factor receptor tyrosine kinases blocked activation of Akt by hydrogen peroxide and growth factors, as did a src-family tyrosine kinase inhibitor or the broad-spectrum tyrosine kinase inhibitor genistein. Activation of Akt by Cu(2+), however, remained unimpaired, implying (i) that tyrosine kinase activation is not involved in Cu(2+) activation of Akt and (ii) that activation of the PI3K/Akt pathway by Cu(2+) is initiated independently of that induced by reactive oxygen species. Comparison of the time course of the oxidation of 2',7'-dichlorodihydrofluorescein in copper-treated cells with that of Akt activation led to the conclusion that production of hydroperoxides cannot be an upstream event in copper-induced Akt activation. Rather, both activation of Akt and generation of ROS are proposed to occur in parallel, regulating cell survival after a copper stress., ((c)2001 Elsevier Science.)

Published
2002
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