97 results on '"Fazal L"'
Search Results
2. La fibrose dans l’hypertension artérielle : une histoire d’équilibre
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Azibani, F., Fazal, L., Chatziantoniou, C., Samuel, J.-L., and Delcayre, C.
- Published
- 2012
- Full Text
- View/download PDF
3. Tissue kallikrein is required for the cardioprotective effect of Cyclosporin A in myocardial ischemia in the mouse
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Youcef, G., Belaidi, E., Waeckel, L., Fazal, L., Clemessy, M., Vincent, M. P., Zadigue, G., Richer, C., Alhenc-Gelas, F., Ovize, M., and Pizard, A.
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- 2015
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4. P720Notch3 is an important mediator of cardiac adaptation to pressure overload
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Ragot, H, Merval, R, Baudet, M, Fazal, L, Polidano, E, Delcayre, C, Chatziantoniou, C, and Samuel, J-L
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- 2014
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5. P610Akt-mediated cardioprotective effects of aldosterone in type 2 diabetic mice
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Fazal, L, Azibani, F, Coutance, G, Birhy, N, Polidano, E, Merval, R, Vodovar, N, Launay, JM, Delcayre, C, and Samuel, JL
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- 2014
- Full Text
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6. P598Deleterious effects of cardiac aldosterone and exercise in type 2 diabetic mice
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Fazal, L, Polidano, E, Merval, R, Coutance, G, Delcayre, C, and Samuel, JL
- Published
- 2014
- Full Text
- View/download PDF
7. Notch3 is an important mediator of cardiac adaptation to pressure overload: 1055
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Samuel, J L, Ragot, H, Baudet, M, Fazal, L, Merval, R, Polidano, E, Delcayre, C, and Chatziantoniou, C
- Published
- 2014
8. Combined inhibition of SHP2 and ERK enhances anti-tumour effects in preclinical models
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Smyth, T., primary, Brothwood, J., additional, Fazal, L., additional, Hearn, K., additional, Hindley, C., additional, Johnson, C., additional, Jones, M., additional, Kandola, N., additional, Lyons, J., additional, Martins, V., additional, Miyadera, K., additional, Muench, S., additional, Munck, J., additional, Nakatsuru, Y., additional, Ochiiwa, H., additional, Saini, H., additional, Shah, A., additional, Wagner, S., additional, Wilsher, N., additional, and Wallis, N., additional
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- 2020
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9. SignalingP513Aldosterone inhibits Akt and Calcineurin pathways in hypertension-induced hypertrophy
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Azibani, F., Tournoux, F., Schlossarek, S., Polidano, E., Fazal, L., Merval, R., Carrier, L., Chatziantoniou, C., Samuel, J.L., and Delcayre, C.
- Published
- 2012
10. P306Aldosterone activates the insulin-activated AKT pathway in heart of diabetic type 2 mice
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Fazal, L., Azibani, F., Bihry, N., Merval, R., Polidano, E., Samuel, J-L., and Delcayre, C.
- Published
- 2012
11. P140Deficiency in Tissue Kallikrein abolishes the cardio protective effects of CsA during post-conditioning in mice
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Youcef, G., Belaidi, E., Fazal, L., Vinvent, M.P., De Paulis, D., Zadigue, G., Richer-Giudicelli, C., Alhenc-Gelas, F., Ovize, M., and Pizard, A.
- Published
- 2012
12. 232 (PB112) - Low SKP2 expression is predictive of sensitivity to an MDM2 antagonist in p53 wild-type AML
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Kucia-Tran, J., Bevan, L., Chessari, G., Fazal, L., Ferrari, N., Lyons, J., Saini, H., Wallis, N., Ward, G., and Ahn, M.
- Published
- 2022
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13. PS988 CHARACTERIZATION OF A NOVEL, POTENT SMALL MOLECULE MDM2 ANTAGONIST WHICH ACTIVATES WILD-TYPE P53 AND INDUCES APOPTOSIS IN AML
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Ferrari, N., primary, Bevan, L., additional, Castro, J., additional, Chessari, G., additional, Fazal, L., additional, Howard, S., additional, Kucia-Tran, J., additional, Sims, M., additional, Ward, G., additional, Wedge, S., additional, Willmore, E., additional, and Ahn, M., additional
- Published
- 2019
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14. Inhibition of mitochondrial MAO-A/4-HNE pathway mitigates post-Myocardial Infarction remodeling
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Santin, Y., primary, Fazal, L., additional, Sainte-Marie, Y., additional, Tortosa, F., additional, Teyssedre, L., additional, Rouquette, J., additional, Lezoualc'h, F., additional, and Mialet-Perez, J., additional
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- 2018
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15. Roles and Mechanisms of Action of Aldehydes Produced by Monoamine Oxidase-A in Cardiomyocyte Death and Heart Failure
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Santin, Y., primary, Sicard, P., additional, Yücel Yücel, Y., additional, Fazal, L., additional, Sainte-Marie, Y., additional, Dutaur, M., additional, Maggiorani, D., additional, Vindis, C., additional, Parini, A., additional, Lezoualc’h, F., additional, and Mialet-Perez, J., additional
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- 2017
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16. Rôle d’EPAC1 (Exchange Protein Directly Activated by cAMP Type 1) dans la régulation de l’homéostasie hydroélectrolytique
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Casemayou, A., primary, Buleon, M., additional, Lezoualch, F., additional, De Régibus, A., additional, Fazal, L., additional, Bascands, J.L., additional, Schanstra, J., additional, and Faguer, S., additional
- Published
- 2016
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17. Alternative Ways to Die5Epac1 deletion prevents cardiomyocyte apoptosis during ischemia/reperfusion6Subcellular redistribution of mitogen and stress activated kinase 1 (MSK1) contributes to protection against oxidative stress- induced apoptosis in cardiac myocytes7Excessive ROS production in mitochondria switches off protective mitochondrial kinase signaling
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Laudette, M, primary, Apostolopoulos, A, primary, Tanno, M, primary, Fazal, L, additional, Pons, S, additional, Tortosa, F, additional, Sicard, P, additional, Mialet-Perez, J, additional, Ghaleh, B, additional, Lezoualc'h, F, additional, Mellidis, K, additional, Barlaka, E, additional, Moraiti, A, additional, Lazou, A, additional, Ohwada, W, additional, Yano, T, additional, Miki, T, additional, Kuno, A, additional, Ishikawa, S, additional, Tatekoshi, Y, additional, Nishizawa, K, additional, Mizuno, M, additional, and Miura, T, additional
- Published
- 2016
- Full Text
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18. Le renouveau attendu des antagonistes du récepteur de l’aldostérone
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Fazal, L., primary, Azibani, F., additional, Samuel, J.-L., additional, and Delcayre, C., additional
- Published
- 2013
- Full Text
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19. 878 PRE-CLINICAL CHARACTERISATION OF A NOVEL DIRECT ACTING ANTIVIRAL AGENT WITH A NEW MODE OF ACTION
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Wilsher, N., primary, Saalau-Bethell, S., additional, Woodhead, A., additional, Millemaggi, A., additional, Graham, B., additional, Hamlett, C., additional, Murray, C., additional, Norton, D., additional, Rees, D., additional, Chiarparin, E., additional, Willems, H., additional, Lewis, J., additional, Fazal, L., additional, Carr, M., additional, Hodder, M., additional, Reader, M., additional, Thompson, N., additional, Pathuri, P., additional, Rich, S., additional, Hiscock, S., additional, Martins, V., additional, and Sanders, M., additional
- Published
- 2012
- Full Text
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20. Poster session 3
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Nanka, O., primary, Krejci, E., additional, Pesevski, Z., additional, Sedmera, D., additional, Smart, N., additional, Rossdeutsch, A., additional, Dube, K. N., additional, Riegler, J., additional, Price, A. N., additional, Taylor, A., additional, Muthurangu, V., additional, Turner, M., additional, Lythgoe, M. F., additional, Riley, P. R., additional, Kryvorot, S., additional, Vladimirskaya, T., additional, Shved, I., additional, Schwarzl, M., additional, Seiler, S., additional, Huber, S., additional, Steendijk, P., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Caprio, C., additional, Baldini, A., additional, Chiavacci, E., additional, Dolfi, L., additional, Verduci, L., additional, Meghini, F., additional, Cremisi, F., additional, Pitto, L., additional, Kuan, T.-C., additional, Chen, M.-C., additional, Yang, T.-H., additional, Wu, W.-T., additional, Lin, C. S., additional, Rai, H., additional, Kumar, S., additional, Sharma, A. K., additional, Mastana, S., additional, Kapoor, A., additional, Pandey, C. M., additional, Agrawal, S., additional, Sinha, N., additional, Orlowska-Baranowska, E. H., additional, Placha, G., additional, Gora, J., additional, Baranowski, R., additional, Abramczuk, E., additional, Hryniewiecki, T., additional, Gaciong, Z., additional, Verschuren, J. J. W., additional, Wessels, J. A. M., additional, Trompet, S., additional, Stott, D. J., additional, Sattar, N., additional, Buckley, B., additional, Guchelaar, H. J., additional, Jukema, J. W., additional, Gharanei, M., additional, Hussain, A., additional, Mee, C. J., additional, Maddock, H. L., additional, Wijnen, W. J., additional, Van Den Oever, S., additional, Van Der Made, I., additional, Hiller, M., additional, Tijsen, A. J., additional, Pinto, Y. M., additional, Creemers, E. E., additional, Nikulina, S. U. Y., additional, Chernova, A., additional, Petry, A., additional, Rzymski, T., additional, Kracun, D., additional, Riess, F., additional, Pike, L., additional, Harris, A. L., additional, Gorlach, A., additional, Katare, R., additional, Oikawa, A., additional, Riu, F., additional, Beltrami, A. P., additional, Cesseli, D., additional, Emanueli, C., additional, Madeddu, P., additional, Zaglia, T., additional, Milan, G., additional, Franzoso, M., additional, Pesce, P., additional, Sarais, C., additional, Sandri, M., additional, Mongillo, M., additional, Butler, T. J., additional, Seymour, A.-M. L., additional, Ashford, D., additional, Jaffre, F., additional, Bussen, M., additional, Flohrschutz, I., additional, Martin, G. R., additional, Engelhardt, S., additional, Kararigas, G., additional, Nguyen, B. T., additional, Jarry, H., additional, Regitz-Zagrosek, V., additional, Van Bilsen, M., additional, Daniels, A., additional, Munts, C., additional, Janssen, B. J. A., additional, Van Der Vusse, G. J., additional, Van Nieuwenhoven, F. A., additional, Montalvo, C., additional, Villar, A. V., additional, Merino, D., additional, Garcia, R., additional, Llano, M., additional, Ares, M., additional, Hurle, M. A., additional, Nistal, J. F., additional, Dembinska-Kiec, A., additional, Beata Kiec-Wilk, B. K. W., additional, Anna Polus, A. P., additional, Urszula Czech, U. C., additional, Tatiana Konovaleva, T. K., additional, Gerd Schmitz, G. S., additional, Bertrand, L., additional, Balteau, M., additional, Timmermans, A., additional, Viollet, B., additional, Sakamoto, K., additional, Feron, O., additional, Horman, S., additional, Vanoverschelde, J. L., additional, Beauloye, C., additional, De Meester, C., additional, Martinez, E., additional, Martin, R., additional, Miana, M., additional, Jurado, R., additional, Gomez-Hurtado, N., additional, Bartolome, M. V., additional, San Roman, J. A., additional, Lahera, V., additional, Nieto, M. L., additional, Cachofeiro, V., additional, Rochais, F., additional, Sturny, R., additional, Mesbah, K., additional, Miquerol, L., additional, Kelly, R. G., additional, Messaoudi, S., additional, Gravez, B., additional, Tarjus, A., additional, Pelloux, V., additional, Samuel, J. L., additional, Delcayre, C., additional, Launay, J. M., additional, Clement, K., additional, Farman, N., additional, Jaisser, F., additional, Hadyanto, L., additional, Castellani, C., additional, Vescovo, G., additional, Ravara, B., additional, Tavano, R., additional, Pozzobon, M., additional, De Coppi, P., additional, Papini, E., additional, Vettor, R., additional, Thiene, G., additional, Angelini, A., additional, Meloni, M., additional, Caporali, A., additional, Cesselli, D., additional, Fortunato, O., additional, Avolio, E., additional, Schindler, R., additional, Simrick, S., additional, Brand, T., additional, Smart, N. S., additional, Herman, A., additional, Roura Ferrer, S., additional, Rodriguez Bago, J., additional, Soler-Botija, C., additional, Pujal, J. M., additional, Galvez-Monton, C., additional, Prat-Vidal, C., additional, Llucia-Valldeperas, A., additional, Blanco, J., additional, Bayes-Genis, A., additional, Foldes, G., additional, Maxime, M., additional, Ali, N. N., additional, Schneider, M. D., additional, Harding, S. E., additional, Reni, C., additional, Mangialardi, G., additional, De Pauw, A., additional, Sekkali, B., additional, Friart, A., additional, Ding, H., additional, Graffeuil, A., additional, Catalucci, D., additional, Balligand, J. L., additional, Azibani, F., additional, Tournoux, F., additional, Schlossarek, S., additional, Polidano, E., additional, Fazal, L., additional, Merval, R., additional, Carrier, L., additional, Chatziantoniou, C., additional, Buyandelger, B., additional, Linke, W., additional, Zou, P., additional, Kostin, S., additional, Ku, C., additional, Felkin, L., additional, Birks, E., additional, Barton, P., additional, Sattler, M., additional, Knoell, R., additional, Schroder, K., additional, Benkhoff, S., additional, Shimokawa, H., additional, Grisk, O., additional, Brandes, R. P., additional, Parepa, I. R., additional, Mazilu, L., additional, Suceveanu, A. I., additional, Suceveanu, A., additional, Rusali, L., additional, Cojocaru, L., additional, Matei, L., additional, Toringhibel, M., additional, Craiu, E., additional, Pires, A. L., additional, Pinho, M., additional, Pinho, S., additional, Sena, C., additional, Seica, R., additional, Leite-Moreira, A., additional, Dabroi, F., additional, Schiaffino, S., additional, Kiseleva, E., additional, Krukov, N., additional, Nikitin, O., additional, Ardatova, L., additional, Mourouzis, I., additional, Pantos, C., additional, Kokkinos, A. D., additional, Cokkinos, D. V., additional, Scoditti, E., additional, Massaro, M., additional, Carluccio, M. A., additional, Pellegrino, M., additional, Calabriso, N., additional, Gastaldelli, A., additional, Storelli, C., additional, De Caterina, R., additional, Lindner, D., additional, Zietsch, C., additional, Schultheiss, H.-P., additional, Tschope, C., additional, Westermann, D., additional, Everaert, B. R., additional, Nijenhuis, V. J., additional, Reith, F. C. M., additional, Hoymans, V. Y., additional, Timmermans, J. P., additional, Vrints, C. J., additional, Simova, I., additional, Mateev, H., additional, Katova, T., additional, Haralanov, L., additional, Dimitrov, N., additional, Mironov, N., additional, Golitsyn, S. P., additional, Sokolov, S. F., additional, Yuricheva, Y. U. A., additional, Maikov, E. B., additional, Shlevkov, N. B., additional, Rosenstraukh, L. V., additional, Chazov, E. I., additional, Radosinska, J., additional, Knezl, V., additional, Benova, T., additional, Slezak, J., additional, Urban, L., additional, Tribulova, N., additional, Virag, L., additional, Kristof, A., additional, Kohajda, Z. S., additional, Szel, T., additional, Husti, Z., additional, Baczko, I., additional, Jost, N., additional, Varro, A., additional, Sarusi, A., additional, Farkas, A. S., additional, Orosz, S. Z., additional, Forster, T., additional, Farkas, A., additional, Zakhrabova-Zwiauer, O. M., additional, Hardziyenka, M., additional, Nieuwland, R., additional, Tan, H. L., additional, Raaijmakers, A. J. A., additional, Bourgonje, V. J. A., additional, Kok, G. J. M., additional, Van Veen, A. A. B., additional, Anderson, M. E., additional, Vos, M. A., additional, Bierhuizen, M. F. A., additional, Benes, J., additional, Sebestova, B., additional, Ghouri, I. A., additional, Kemi, O. J., additional, Kelly, A., additional, Burton, F. L., additional, Smith, G. L., additional, Ozdemir, S., additional, Acsai, K., additional, Doisne, N., additional, Van Der Nagel, R., additional, Beekman, H. D. M., additional, Van Veen, T. A. B., additional, Sipido, K. R., additional, Antoons, G., additional, Harmer, S. C., additional, Mohal, J. S., additional, Kemp, D., additional, Tinker, A., additional, Beech, D., additional, Burley, D. S., additional, Cox, C. D., additional, Wann, K. T., additional, Baxter, G. F., additional, Wilders, R., additional, Verkerk, A., additional, Fragkiadaki, P., additional, Germanakis, G., additional, Tsarouchas, K., additional, Tsitsimpikou, C., additional, Tsardi, M., additional, George, D., additional, Tsatsakis, A., additional, Rodrigues, P., additional, Barros, C., additional, Najmi, A. K., additional, Khan, V., additional, Akhtar, M., additional, Pillai, K. K., additional, Mujeeb, M., additional, Aqil, M., additional, Bayliss, C. R., additional, Messer, A. E., additional, Leung, M.-C., additional, Ward, D., additional, Van Der Velden, J., additional, Poggesi, C., additional, Redwood, C. S., additional, Marston, S., additional, Vite, A., additional, Gandjbakhch, E., additional, Gary, F., additional, Fressart, V., additional, Leprince, P., additional, Fontaine, G., additional, Komajda, M., additional, Charron, P., additional, Villard, E., additional, Falcao-Pires, I., additional, Gavina, C., additional, Hamdani, N., additional, Stienen, G. J. M., additional, Niessens, H. W. M., additional, Leite-Moreira, A. F., additional, Paulus, W. J., additional, Memo, M., additional, Marston, S. B., additional, Vafiadaki, E., additional, Qian, J., additional, Arvanitis, D. A., additional, Sanoudou, D., additional, Kranias, E. G., additional, Elmstedt, N., additional, Lind, B., additional, Ferm-Widlund, K., additional, Westgren, M., additional, Brodin, L.-A., additional, Mansfield, C., additional, West, T., additional, Ferenczi, M., additional, Wijnker, P. J. M., additional, Foster, D. B., additional, Coulter, A., additional, Frazier, A., additional, Murphy, A. M., additional, Shah, M., additional, Sikkel, M. B., additional, Desplantez, T., additional, Collins, T. P., additional, O' Gara, P., additional, Lyon, A. R., additional, Macleod, K. T., additional, Ottesen, A. H., additional, Louch, W. E., additional, Carlson, C., additional, Landsverk, O. J. B., additional, Stridsberg, M., additional, Sjaastad, I., additional, Oie, E., additional, Omland, T., additional, Christensen, G., additional, Rosjo, H., additional, Cartledge, J., additional, Clark, L. A., additional, Ibrahim, M., additional, Siedlecka, U., additional, Navaratnarajah, M., additional, Yacoub, M. H., additional, Camelliti, P., additional, Terracciano, C. M., additional, Chester, A., additional, Gonzalez-Tendero, A., additional, Torre, I., additional, Garcia-Garcia, F., additional, Dopazo, J., additional, Gratacos, E., additional, Taylor, D., additional, Bhandari, S., additional, Seymour, A.-M., additional, Fliegner, D., additional, Jost, J., additional, Bugger, H., additional, Ventura-Clapier, R., additional, Carpi, A., additional, Campesan, M., additional, Canton, M., additional, Menabo, R., additional, Pelicci, P. G., additional, Giorgio, M., additional, Di Lisa, F., additional, Hancock, M., additional, Venturini, A., additional, Al-Shanti, N., additional, Stewart, C., additional, Ascione, R., additional, Angelini, G., additional, Suleiman, M.-S., additional, Kravchuk, E., additional, Grineva, E., additional, Galagudza, M., additional, Kostareva, A., additional, Bairamov, A., additional, Krychtiuk, K. A., additional, Watzke, L., additional, Kaun, C., additional, Demyanets, S., additional, Pisoni, J., additional, Kastl, S. P., additional, Huber, K., additional, Maurer, G., additional, Wojta, J., additional, Speidl, W. S., additional, Varga, Z. V., additional, Farago, N., additional, Zvara, A., additional, Kocsis, G. F., additional, Pipicz, M., additional, Csonka, C., additional, Csont, T., additional, Puskas, G. L., additional, Ferdinandy, P., additional, Klevstigova, M., additional, Silhavy, J., additional, Manakov, D., additional, Papousek, F., additional, Novotny, J., additional, Pravenec, M., additional, Kolar, F., additional, Novakova, O., additional, Novak, F., additional, Neckar, J., additional, Barallobre-Barreiro, J., additional, Didangelos, A., additional, Yin, X., additional, Fernandez-Caggiano, M., additional, Drozdov, I., additional, Willeit, P., additional, Domenech, N., additional, Mayr, M., additional, Lemoine, S., additional, Allouche, S., additional, Coulbault, L., additional, Galera, P., additional, Gerard, J. L., additional, Hanouz, J. L., additional, Suveren, E., additional, Whiteman, M., additional, Studneva, I. M., additional, Pisarenko, O., additional, Shulzhenko, V., additional, Serebryakova, L., additional, Tskitishvili, O., additional, Timoshin, A., additional, Fauconnier, J., additional, Meli, A. C., additional, Thireau, J., additional, Roberge, S., additional, Lompre, A. M., additional, Jacotot, E., additional, Marks, A. M., additional, Lacampagne, A., additional, Dietel, B., additional, Altendorf, R., additional, Daniel, W. G., additional, Kollmar, R., additional, Garlichs, C. D., additional, Parente, V., additional, Balasso, S., additional, Pompilio, G., additional, Colombo, G., additional, Milano, G., additional, Squadroni, L., additional, Cotelli, F., additional, Pozzoli, O., additional, Capogrossi, M. C., additional, Ajiro, Y., additional, Saegusa, N., additional, Iwade, K., additional, Giles, W. R., additional, Stafforini, D. M., additional, Spitzer, K. W., additional, Sirohi, R., additional, Candilio, L., additional, Babu, G., additional, Roberts, N., additional, Lawrence, D., additional, Sheikh, A., additional, Kolvekar, S., additional, Yap, J., additional, Hausenloy, D. J., additional, Yellon, D. M., additional, Aslam, M., additional, Rohrbach, S., additional, Schlueter, K.-D., additional, Piper, H. M., additional, Noll, T., additional, Guenduez, D., additional, Malinova, L., additional, Ryabukho, V. P., additional, Lyakin, D. V., additional, Denisova, T. P., additional, Montoro-Garcia, S., additional, Shantsila, E., additional, Lip, G. Y. H., additional, Kalaska, B., additional, Sokolowska, E., additional, Kaminski, K., additional, Szczubialka, K., additional, Kramkowski, K., additional, Mogielnicki, A., additional, Nowakowska, M., additional, Buczko, W., additional, Stancheva, N., additional, Mekenyan, E., additional, Gospodinov, K., additional, Tisheva, S., additional, Darago, A., additional, Rutkai, I., additional, Kalasz, J., additional, Czikora, A., additional, Orosz, P., additional, Bjornson, H. D., additional, Edes, I., additional, Papp, Z., additional, Toth, A., additional, Riches, K., additional, Warburton, P., additional, O'regan, D. J., additional, Ball, S. G., additional, Turner, N. A., additional, Wood, I. C., additional, Porter, K. E., additional, Kogaki, S., additional, Ishida, H., additional, Nawa, N., additional, Takahashi, K., additional, Baden, H., additional, Ichimori, H., additional, Uchikawa, T., additional, Mihara, S., additional, Miura, K., additional, Ozono, K., additional, Lugano, R., additional, Padro, T., additional, Garcia-Arguinzonis, M., additional, Badimon, L., additional, Ferraro, F., additional, Viner, R., additional, Ho, J., additional, Cutler, D., additional, Matchkov, V., additional, Aalkjaer, C., additional, Krijnen, P. A. J., additional, Hahn, N. E., additional, Kholova, I., additional, Sipkens, J. A., additional, Van Alphen, F. P., additional, Simsek, S., additional, Schalkwijk, C. G., additional, Van Buul, J. D., additional, Van Hinsbergh, V. W. M., additional, Niessen, H. W. M., additional, Caro, C. G., additional, Seneviratne, A., additional, Monaco, C., additional, Hou, D., additional, Singh, J., additional, Gilson, P., additional, Burke, M. G., additional, Heraty, K. B., additional, Krams, R., additional, Coppola, G., additional, Albrecht, K., additional, Schgoer, W., additional, Wiedemann, D., additional, Bonaros, N., additional, Steger, C., additional, Theurl, M., additional, Stanzl, U., additional, Kirchmair, R., additional, Amadesi, S., additional, Spinetti, G., additional, Cangiano, E., additional, Valgimigli, M., additional, Miller, A. M., additional, Cardinali, A., additional, Vierlinger, K., additional, Pagano, G., additional, Liccardo, D., additional, Zincarelli, C., additional, Femminella, G. D., additional, Lymperopoulos, A., additional, De Lucia, C., additional, Koch, W. J., additional, Leosco, D., additional, Rengo, G., additional, Hinkel, R., additional, Husada, W., additional, Trenkwalder, T., additional, Di, Q., additional, Lee, S., additional, Petersen, B., additional, Bock-Marquette, I., additional, Niemann, H., additional, Di Maio, M., additional, Kupatt, C., additional, Nourian, M., additional, Yassin, Z., additional, Kelishadi, R., additional, Memarian, S. H., additional, Heidari, A., additional, Leuner, A., additional, Poitz, D. M., additional, Brunssen, C., additional, Ravens, U., additional, Strasser, R. H., additional, Morawietz, H., additional, Vogt, F., additional, Grahl, A., additional, Flege, C., additional, Marx, N., additional, Borinski, M., additional, De Geest, B., additional, Jacobs, F., additional, Muthuramu, I., additional, Gordts, S. C., additional, Van Craeyveld, E., additional, Herijgers, P., additional, Weinert, S., additional, Medunjanin, S., additional, Herold, J., additional, Schmeisser, A., additional, Braun-Dullaeus, R. C., additional, Wagner, A. H., additional, Moeller, K., additional, Adolph, O., additional, Schwarz, M., additional, Schwale, C., additional, Bruehl, C., additional, Nobiling, R., additional, Wieland, T., additional, Schneider, S. W., additional, Hecker, M., additional, Cross, A., additional, Strom, A., additional, Cole, J., additional, Goddard, M., additional, Hultgardh-Nilsson, A., additional, Nilsson, J., additional, Mauri, C., additional, Mitkovskaya, N. P., additional, Kurak, T. A., additional, Oganova, E. G., additional, Shkrebneva, E. I., additional, Kot, Z. H. N., additional, Statkevich, T. V., additional, Molica, F., additional, Burger, F., additional, Matter, C. 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P., additional, Roncon-Albuquerque, R., additional, Oyeyipo, I. P., additional, Olatunji, L. A., additional, Usman, T. O., additional, Olatunji, V. A., additional, Bacova, B., additional, Viczenczova, C., additional, Dosenko, V., additional, Goncalvesova, E., additional, Vanrooyen, J., additional, Maulik, S. K., additional, Seth, S., additional, Dinda, A. K., additional, Jaiswal, A., additional, Mearini, G., additional, Khajetoorians, D., additional, Kraemer, E., additional, Gedicke-Hornung, C., additional, Precigout, G., additional, Eschenhagen, T., additional, Voit, T., additional, Garcia, L., additional, Lorain, S., additional, Mendes-Ferreira, P., additional, Maia-Rocha, C., additional, Adao, R., additional, Cerqueira, R. J., additional, Mendes, M. J., additional, Castro-Chaves, P., additional, De Keulenaer, G. W., additional, Bras-Silva, C., additional, Ruiter, G., additional, Wong, Y. 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J., additional, Llacer, A., additional, Galasso, G., additional, Ferrara, N., additional, Akhmedov, A., additional, Klingenberg, R., additional, Brokopp, C., additional, Hof, D., additional, Zoller, S., additional, Corti, R., additional, Gay, S., additional, Von Eckardstein, A., additional, Hoerstrup, S. P., additional, Luescher, T. F., additional, Heijman, J., additional, Zaza, A., additional, Johnson, D. M., additional, Rudy, Y., additional, Peeters, R. L. M., additional, Volders, P. G. A., additional, Westra, R. L., additional, Fujita, S., additional, Okamoto, R., additional, Taniguchi, M., additional, Konishi, K., additional, Goto, I., additional, Sugimoto, K., additional, Nakamura, M., additional, Shiraki, K., additional, Buechler, C., additional, and Ito, M., additional
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21. Poster session 2
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Perez-Pomares, J. M., primary, Ruiz-Villalba, A., additional, Ziogas, A., additional, Segovia, J. C., additional, Ehrbar, M., additional, Munoz-Chapuli, R., additional, De La Rosa, A., additional, Dominguez, J. N., additional, Hove-Madsen, L., additional, Sankova, B., additional, Sedmera, D., additional, Franco, D., additional, Aranega Jimenez, A., additional, Babaeva, G., additional, Chizh, N., additional, Galchenko, S., additional, Sandomirsky, B., additional, Schwarzl, M., additional, Seiler, S., additional, Steendijk, P., additional, Huber, S., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Simrick, S., additional, Kreutzer, R., additional, Rao, C., additional, Terracciano, C. M., additional, Kirchhof, P., additional, Fabritz, L., additional, Brand, T., additional, Theveniau-Ruissy, M., additional, Parisot, P., additional, Francou, A., additional, Saint-Michel, E., additional, Mesbah, K., additional, Kelly, R. G., additional, Wu, H.-T., additional, Sie, S.-S., additional, Chen, C.-Y., additional, Kuan, T.-C., additional, Lin, C. S., additional, Ismailoglu, Z., additional, Guven, M., additional, Yakici, A., additional, Ata, Y., additional, Ozcan, S., additional, Yildirim, E., additional, Ongen, Z., additional, Miroshnikova, V., additional, Demina, E., additional, Rodygina, T., additional, Kurjanov, P., additional, Denisenko, A., additional, Schwarzman, A., additional, Rubanenko, A., additional, Shchukin, Y., additional, Germanov, A., additional, Goldbergova, M., additional, Parenica, J., additional, Lipkova, J., additional, Pavek, N., additional, Kala, P., additional, Poloczek, M., additional, Vasku, A., additional, Parenicova, I., additional, Spinar, J., additional, Gambacciani, C., additional, Chiavacci, E., additional, Evangelista, M., additional, Vesentini, N., additional, Kusmic, C., additional, Pitto, L., additional, Chernova, A., additional, Nikulina, S. U. 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J., additional, Mangold, A., additional, Puthenkalam, S., additional, Distelmaier, K., additional, Adlbrecht, C., additional, Lang, I. M., additional, Koizumi, T., additional, Inoue, I., additional, Komiyama, N., additional, Nishimura, S., additional, Korneeva, O. N., additional, Drapkina, O. M., additional, Fornai, L., additional, Angelini, A., additional, Kiss, A., additional, Giskes, F., additional, Eijkel, G., additional, Fedrigo, M., additional, Valente, M. L., additional, Thiene, G., additional, Heeren, R. M. A., additional, Padro, T., additional, Casani, L., additional, Suades, R., additional, Bertoni, B., additional, Carminati, R., additional, Carlini, V., additional, Pettinari, L., additional, Martinelli, C., additional, Gagliano, N., additional, Noppe, G., additional, Buchlin, P., additional, Marquet, N., additional, Baeyens, N., additional, Morel, N., additional, Baysa, A., additional, Sagave, J., additional, Dahl, C. 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M., additional, Abonnenc, M., additional, Da Costa Martins, P., additional, Srivastava, S., additional, Gautel, M., additional, De Windt, L., additional, Comelli, L., additional, Lande, C., additional, Ucciferri, N., additional, Ikonen, L., additional, Vuorenpaa, H., additional, Kujala, K., additional, Sarkanen, J.-R., additional, Heinonen, T., additional, Ylikomi, T., additional, Aalto-Setala, K., additional, Capros, H., additional, Sprincean, N., additional, Usurelu, N., additional, Egorov, V., additional, Stratu, N., additional, Matchkov, V., additional, Bouzinova, E., additional, Moeller-Nielsen, N., additional, Wiborg, O., additional, Gutierrez, P. S., additional, Aparecida-Silva, R., additional, Borges, L. F., additional, Moreira, L. F. P., additional, Dias, R. R., additional, Kalil, J., additional, Stolf, N. A. G., additional, Zhou, W., additional, Suntharalingam, K., additional, Brand, N., additional, Vilar Compte, R., additional, Ying, L., additional, Bicknell, K., additional, Dannoura, A., additional, Dash, P., additional, Brooks, G., additional, Tsimafeyeu, I., additional, Tishova, Y., additional, Wynn, N., additional, Oyeyipo, I. P., additional, Olatunji, L. A., additional, Maegdefessel, L., additional, Azuma, J., additional, Toh, R., additional, Raaz, U., additional, Merk, D. R., additional, Deng, A., additional, Spin, J. M., additional, Tsao, P. S., additional, Tedeschi, L., additional, Taranta, M., additional, Naldi, I., additional, Grimaldi, S., additional, Cinti, C., additional, Bousquenaud, M., additional, Maskali, F., additional, Poussier, S., additional, Marie, P. Y., additional, Boutley, H., additional, Karcher, G., additional, Wagner, D. 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F., additional, Villar, A. V., additional, Perez-Moreno, A., additional, Gilabert, R., additional, and Ros, E., additional
- Published
- 2012
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22. P36 Aldosterone protects the insulin-activated AKT pathway in heart of diabetic type 2 mice
- Author
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Fazal, L., primary, Azibani, F., additional, Bihry, N., additional, Merval, R., additional, Polidano, E., additional, Lise Samuel, J., additional, and Delcayre, C., additional
- Published
- 2012
- Full Text
- View/download PDF
23. Sunday, 18 July 2010
- Author
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Schuchardt, M., primary, Toelle, M., additional, Huang, T., additional, Wiedon, A., additional, Van Der Giet, M., additional, Mill, C., additional, George, S., additional, Jeremy, J., additional, Santulli, G., additional, Illario, M., additional, Cipolletta, E., additional, Sorriento, D., additional, Del Giudice, C., additional, Anastasio, A., additional, Trimarco, B., additional, Iaccarino, G., additional, Jobs, A., additional, Wagner, C., additional, Kurtz, A., additional, De Wit, C., additional, Koller, A., additional, Suvorava, T., additional, Weber, M., additional, Dao, V., additional, Kojda, G., additional, Tsaousi, A., additional, Lyon, C., additional, Williams, H., additional, Barth, N., additional, Loot, A., additional, Fleming, I., additional, Keul, P., additional, Lucke, S., additional, Graeler, M., additional, Heusch, G., additional, Levkau, B., additional, Biessen, E., additional, De Jager, S., additional, Bermudez-Pulgarin, B., additional, Bot, I., additional, Abia, R., additional, Van Berkel, T., additional, Renger, A., additional, Noack, C., additional, Zafiriou, M., additional, Dietz, R., additional, Bergmann, M., additional, Zelarayan, L., additional, Hammond, J., additional, Hamelet, J., additional, Van Assche, T., additional, Belge, C., additional, Vanderper, A., additional, Langin, D., additional, Herijgers, P., additional, Balligand, J., additional, Perrot, A., additional, Neubert, M., additional, Posch, M., additional, Oezcelik, C., additional, Waldmuller, S., additional, Berger, F., additional, Scheffold, T., additional, Bouvagnet, P., additional, Ozcelik, C., additional, Lebreiro, A., additional, Martins, E., additional, Lourenco, P., additional, Cruz, C., additional, Martins, M., additional, Bettencourt, P., additional, Maciel, M., additional, Abreu-Lima, C., additional, Pilichou, K., additional, Bauce, B., additional, Rampazzo, A., additional, Carturan, E., additional, Corrado, D., additional, Thiene, G., additional, Basso, C., additional, Piccini, I., additional, Fortmueller, L., additional, Kuhlmann, M., additional, Schaefers, M., additional, Carmeliet, P., additional, Kirchhof, P., additional, Fabritz, L., additional, Sanchez, J., additional, Rodriguez-Sinovas, A., additional, Agullo, E., additional, Garcia-Dorado, D., additional, Lymperopoulos, A., additional, Rengo, G., additional, Gao, E., additional, Zincarelli, C., additional, Koch, W., additional, Morgan, P., additional, Diez, A., additional, Perez, N., additional, Cingolani, H., additional, Zahradnikova, A., additional, Polakova, E., additional, Zahradnik, I., additional, Fluschnik, N., additional, Sossalla, S., additional, Ort, K., additional, Neef, S., additional, Hasenfuss, G., additional, Maier, L., additional, Weinert, S., additional, Poitz, D., additional, Herold, J., additional, Schmeisser, A., additional, Strasser, J., additional, Braun-Dullaeus, R., additional, Nazari-Jahantigh, M., additional, Weber, C., additional, Schober, A., 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J., additional, Dizayee, S., additional, Kaestner, S., additional, Kuck, F., additional, Piekorz, R., additional, Hein, P., additional, Matthes, J., additional, Nurnberg, B., additional, Herzig, S., additional, Hertel, F., additional, Switalski, A., additional, Bender, K., additional, Kienitz, M.-C., additional, Pott, L., additional, Fornai, L., additional, Angelini, A., additional, Erika Amstalden Van Hove, E., additional, Fedrigo, M., additional, Heeren, R., additional, Kruse, M., additional, Pongs, O., additional, Lehmann, H., additional, Martens-Lobenhoffer, J., additional, Roehl, F., additional, Radicke, S., additional, Cotella, C., additional, Sblattero, D., additional, Schaefer, M., additional, Wettwer, E., additional, Santoro, C., additional, Seyler, C., additional, Kulzer, M., additional, Zitron, E., additional, Scholz, E., additional, Welke, F., additional, Thomas, D., additional, Karle, C., additional, Schmidt, K., additional, Dobrev, D., additional, Houshmand, N., 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D., additional, Khodjaeva, E., additional, Ibadov, R., additional, Khalikulov, K., additional, Mansurov, A., additional, Astvatsatryan, A., additional, Senan, M., additional, Nemeth, A., additional, Lenkey, Z., additional, Ajtay, Z., additional, Cziraki, A., additional, Sulyok, E., additional, Horvath, I., additional, Lobenhoffer, J., additional, Bode-Boger, S., additional, Li, J., additional, He, Y., additional, Yang, X., additional, Wang, F., additional, Xu, H., additional, Li, X., additional, Zhao, X., additional, Lin, Y., additional, Juszynski, M., additional, Ciszek, B., additional, Jablonska, A., additional, Stachurska, E., additional, Ratajska, A., additional, Atkinson, A., additional, Inada, S., additional, Sleiman, R., additional, Zhang, H., additional, Boyett, M., additional, Dobrzynski, H., additional, Fedorenko, O., additional, Hao, G., additional, Yanni, J., additional, Buckley, D., additional, Anderson, R., additional, Ma, Y., additional, Ma, X., additional, Hu, Y., additional, Yang, Y., additional, Huang, D., additional, Liu, F., additional, Huang, Y., additional, Liu, C., additional, Jedrzejczyk, T., additional, Balwicki, L., additional, Wierucki, L., additional, Zdrojewski, T., additional, Agarkova, I., additional, Vogel, J., additional, Korybalska, K., additional, Pyda, M., additional, Witowski, J., additional, Ibatov, A., additional, Sozmen, N., additional, Seymen, A., additional, Tuncay, E., additional, Turan, B., additional, Chen, B., additional, Houston-Feenstra, L., additional, Chiong, J. R., additional, Jutzy, K., additional, Furundzija, V., additional, Kaufmann, J., additional, Meyborg, H., additional, Fleck, E., additional, Stawowy, P., additional, Ksiezycka-Majczynska, E., additional, Lubiszewska, B., additional, Kruk, M., additional, Kurjata, P., additional, Ruzyllo, W., additional, Driesen, R., additional, Coenen, T., additional, Fagard, R., additional, Sipido, K., additional, Petrov, V., additional, Aksentijevic, D., additional, Lygate, C., additional, Makinen, K., additional, Sebag-Montefiore, L., additional, Medway, D., additional, Schneider, J., additional, Neubauer, S., additional, Gasser, R., additional, Holzwart, E., additional, Rainer, P., additional, Von Lewinski, D., additional, Maechler, H., additional, Gasser, S., additional, Roessl, U., additional, Pieske, B., additional, Krueger, J., additional, Kintscher, U., additional, Podramagi, T., additional, Paju, K., additional, Piirsoo, A., additional, Roosimaa, M., additional, Kadaja, L., additional, Orlova, E., additional, Ruusalepp, A., additional, Seppet, E., additional, Auquier, J., additional, Ginion, A., additional, Hue, L., additional, Horman, S., additional, Beauloye, C., additional, Vanoverschelde, J., additional, Bertrand, L., additional, Fekete, V., additional, Zvara, A., additional, Pipis, J., additional, Konya, C., additional, Csonka, C., additional, Kraigher-Krainer, E., additional, Von Lewinksi, D., additional, Gonzalez-Loyola, A., additional, Barba, I., additional, Fernandez-Sanz, C., additional, Ruiz-Meana, M., additional, Forteza, M., additional, Bodi Peris, V., additional, Monleon, D., additional, Mainar, L., additional, Morales, J., additional, Moratal, D., additional, Trapero, I., additional, Chorro, F., additional, Leszek, P., additional, Sochanowicz, B., additional, Szperl, M., additional, Kolsut, P., additional, Piotrowski, W., additional, Rywik, T., additional, Danko, B., additional, Kruszewski, M., additional, Stanley, W., additional, Khairallah, R., additional, Khanna, N., additional, O'shea, K., additional, Kristian, T., additional, Hecker, P., additional, Des Rosiers, R., additional, Fiskum, G., additional, Fernandez-Alfonso, M., additional, Guzman-Ruiz, R., additional, Somoza, B., additional, Gil-Ortega, M., additional, Attane, C., additional, Castan-Laurell, I., additional, Valet, P., additional, Ruiz-Gayo, M., additional, Denissevich, T., additional, Schrepper, A., additional, Schwarzer, M., additional, Amorim, P., additional, Schoepe, M., additional, Mohr, F., additional, Doenst, T., additional, Chiellini, G., additional, Ghelardoni, S., additional, Saba, A., additional, Marchini, M., additional, Frascarelli, S., additional, Raffaelli, A., additional, Scanlan, T., additional, Zucchi, R., additional, Van Den Akker, N., additional, Molin, D., additional, Kolk, F., additional, Jeukens, F., additional, Olde Engberink, R., additional, Post, M., additional, Verbruggen, S., additional, Schulten, H., additional, Rochais, F., additional, Kelly, R., additional, Aberg, M., additional, Johnell, M., additional, Wickstrom, M., additional, Siegbahn, A., additional, Dimitrakis, P., additional, Groppalli, V., additional, Ott, D., additional, Seifriz, F., additional, Suter, T., additional, Zuppinger, C., additional, Kashcheyeu, Y., additional, Mueller, R., additional, Wiesen, M., additional, Gruendemann, D., additional, Falcao-Pires, I., additional, Fontes-Sousa, A., additional, Lopes-Conceicao, L., additional, Bras-Silva, C., additional, Leite-Moreira, A., additional, Bukauskas, F., additional, Palacios-Prado, N., additional, Norheim, F., additional, Raastad, T., additional, Thiede, B., additional, Drevon, C., additional, Haugen, F., additional, Lindner, D., additional, Westermann, D., additional, Zietsch, C., additional, Schultheiss, H.-P., additional, Tschoepe, C., additional, Horn, M., additional, Graham, H., additional, Hall, M., additional, Richards, M., additional, Clarke, J., additional, Dibb, K., additional, Trafford, A., additional, Cheng, C.-F., additional, Lin, H., additional, Eigeldiger-Berthou, S., additional, Buntschu, P., additional, Frobert, A., additional, Flueck, M., additional, Tevaearai, H., additional, Kadner, A., additional, Mikhailov, A., additional, Torrado, M., additional, Centeno, A., additional, Lopez, E., additional, Lourido, L., additional, Castro Beiras, A., additional, Popov, T., additional, Srdanovic, I., additional, Petrovic, M., additional, Canji, T., additional, Kovacevic, M., additional, Jovelic, A., additional, Sladojevic, M., additional, Panic, G., additional, Kararigas, G., additional, Fliegner, D., additional, Regitz-Zagrosek, V., additional, De La Rosa Sanchez, A., additional, Dominguez, J., additional, Sedmera, D., additional, Franco, D., additional, Medunjanin, S., additional, Burgbacher, F., additional, Han, W., additional, Zhang, J., additional, Gao, X., additional, Bayliss, C., additional, Song, W., additional, Stuckey, D., additional, Dyer, E., additional, Leung, M.-C., additional, Monserrat, L., additional, Marston, S., additional, Fusco, A., additional, Paillard, M., additional, Liang, J., additional, Strub, G., additional, Gomez, L., additional, Hait, N., additional, Allegood, J., additional, Lesnefsky, E., additional, Spiegel, S., additional, Zuchi, C., additional, Coiro, S., additional, Bettini, M., additional, Ciliberti, G., additional, Mancini, I., additional, Tritto, I., additional, Becker, L., additional, Ambrosio, G., additional, Adam, T., additional, Sharp, S., additional, Opie, L., additional, Lecour, S., additional, Khaliulin, I., additional, Parker, J., additional, Halestrap, A., additional, Kandasamy, A., additional, Osterholt, M., additional, Miro-Casas, E., additional, Boengler, K., additional, Menazza, S., additional, Canton, M., additional, Sheeran, F., additional, Di Lisa, F., additional, Pepe, S., additional, Borchi, E., additional, Manni, M., additional, Bargelli, V., additional, Giordano, C., additional, D'amati, G., additional, Nediani, C., additional, Raimondi, L., additional, Micova, P., additional, Balkova, P., additional, Kolar, F., additional, Neckar, J., additional, Novak, F., additional, Novakova, O., additional, Schuchardt, M., additional, Pruefer, N., additional, Pruefer, J., additional, Jankowski, V., additional, Jankowski, J., additional, Su, Y., additional, Zervou, S., additional, Seidel, B., additional, Radovits, T., additional, Barnucz, E., additional, Aggeli, I., additional, Kefaloyianni, E., additional, Beis, I., additional, Gaitanaki, C., additional, Lacerda, L., additional, Somers, S., additional, Paur, H., additional, Nikolaev, V., additional, Lyon, A., additional, Silva, S., additional, Gomes, M., additional, Ferreira, P., additional, Capuano, V., additional, Ferron, L., additional, Ruchon, Y., additional, Ben Mohamed, F., additional, Renaud, J.-F., additional, Goncalves, N., additional, Gavina, C., additional, Pinho, S., additional, Moura, C., additional, Amorim, M., additional, Pinho, P., additional, Christ, T., additional, Molenaar, P., additional, Kaumann, A., additional, Kletsiou, E., additional, Giannakopoulou, M., additional, Bozas, E., additional, Iliodromitis, E., additional, Anastasiou-Nana, M., additional, Papathanassoglou, E., additional, Chottova Dvorakova, M., additional, Mistrova, E., additional, Slavikova, J., additional, Hynie, S., additional, Sida, P., additional, Klenerova, V., additional, Zakrzewicz, A., additional, Hoffmann, C., additional, Hohberg, M., additional, Chlench, S., additional, Maroski, J., additional, Drab, M., additional, Siegel, G., additional, Pries, A., additional, Schrot, G., additional, Wilck, N., additional, Fechner, M., additional, Arias, A., additional, Meiners, S., additional, Baumann, G., additional, Stangl, V., additional, Stangl, K., additional, Ludwig, A., additional, Christ, A., additional, Eijgelaar, W., additional, Daemen, M., additional, Penfold, M., additional, Schall, T., additional, Hintenberger, R., additional, Kaun, C., additional, Pfaffenberger, S., additional, Maurer, G., additional, Huber, K., additional, Wojta, J., additional, Demyanets, S., additional, Titov, V., additional, Chin-Dusting, J., additional, Vaisman, B., additional, Khong, S., additional, Remaley, A., additional, Andrews, K., additional, Hoeper, A., additional, Khalid, A., additional, Fuglested, B., additional, Aasum, E., additional, Larsen, T., additional, Diebold, I., additional, Petry, A., additional, Djordjevic, T., additional, Belaiba, R., additional, Fratz, S., additional, Hess, J., additional, Kietzmann, T., additional, Goerlach, A., additional, Chess, D., additional, Walsh, K., additional, Van Der Velden, J., additional, Moreira-Goncalves, D., additional, Paulus, W., additional, Niessen, H., additional, Perlini, S., additional, Azibani, F., additional, Tournoux, F., additional, Fazal, L., additional, Polidano, E., additional, Merval, R., additional, Chatziantoniou, C., additional, Samuel, J., additional, Delcayre, C., additional, Mgandela, P., additional, Brooksbank, R., additional, Maswanganyi, T., additional, Woodiwiss, A., additional, Norton, G., additional, Makaula, S., additional, Bucciantini, M., additional, Spinelli, V., additional, Coppini, R., additional, Russo, E., additional, Stefani, M., additional, Sukumaran, V., additional, Watanabe, K., additional, Ma, M., additional, Thandavarayan, R., additional, Azrozal, W., additional, Sari, F., additional, Shimazaki, H., additional, Kobayashi, Y., additional, Roleder, T., additional, Golba, K., additional, Deja, M., additional, Malinowski, M., additional, Wos, S., additional, Grebe, M., additional, Preissner, K., additional, Ercan, E., additional, Guven, A., additional, Asgun, F., additional, Ickin, M., additional, Ercan, F., additional, Kaplan, A., additional, Yavuz, O., additional, Bagla, S., additional, Kuka, J., additional, Vilskersts, R., additional, Vavers, E., additional, Liepins, E., additional, Dambrova, M., additional, Duerr, G., additional, Suchan, G., additional, Heuft, T., additional, Klaas, T., additional, Zimmer, A., additional, Welz, A., additional, Fleischmann, B., additional, Dewald, O., additional, Voelkl, J., additional, Haubner, B., additional, Kremser, C., additional, Mayr, A., additional, Klug, G., additional, Reiner, M., additional, Pachinger, O., additional, Metzler, B., additional, Pisarenko, O., additional, Shulzhenko, V., additional, Pelogeykina, Y., additional, Khatri, D., additional, Studneva, I., additional, Bencsik, P., additional, Kocsis, G., additional, Shamloo, M., additional, Woodburn, K., additional, Szucs, G., additional, Kupai, K., additional, Csont, C., additional, Kocsisne Fodor, G., additional, Monostori, P., additional, and Turi, S., additional
- Published
- 2010
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24. Structure of 4-(4-tert-Butylbenzyl)-1-(7H-pyrrolo(2,3-d)pyrimidin-4- yl)piperidin-4-amine bound to PKB
- Author
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Davies, T.G., primary, McHardy, T., additional, Caldwell, J.J., additional, Cheung, K.M., additional, Hunter, L.J., additional, Taylor, K., additional, Rowlands, M., additional, Ruddle, R., additional, Henley, A., additional, Brandon, A.D., additional, Valenti, M., additional, Fazal, L., additional, Seavers, L., additional, Raynaud, F.I., additional, Eccles, S.A., additional, Aherne, G.W., additional, Garrett, M.D., additional, and Collins, I., additional
- Published
- 2010
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25. Structure of 4-Amino-N-(4-chlorobenzyl)-1-(7H-pyrrolo(2,3-d)pyrimidin- 4-yl)piperidine-4-carboxamide bound to PKB
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Davies, T.G., primary, McHardy, T., additional, Caldwell, J.J., additional, Cheung, K.M., additional, Hunter, L.J., additional, Taylor, K., additional, Rowlands, M., additional, Ruddle, R., additional, Henley, A., additional, Brandon, A.D., additional, Valenti, M., additional, Fazal, L., additional, Seavers, L., additional, Raynaud, F.I., additional, Eccles, S.A., additional, Aherne, G.W., additional, Garrett, M.D., additional, and Collins, I., additional
- Published
- 2010
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26. A phase I study of AT9283, an aurora kinase inhibitor, in patients with refractory solid tumors
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Kristeleit, R., primary, Calvert, H., additional, Arkenau, H., additional, Olmos, D., additional, Adam, J., additional, Plummer, E. R., additional, Lock, V., additional, Squires, M., additional, Fazal, L., additional, and Judson, I., additional
- Published
- 2009
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27. I038 Influence des kinines sur les effets cardioet réno-vasculaires de la cyclosporine a
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Fazal, L., primary, Alhenc-Gelas, F., additional, and Pizard, A., additional
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- 2009
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28. Structure determination of Aurora Kinase in complex with inhibitor
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Howard, S., primary, Berdini, V., additional, Boulstridge, J.A., additional, Carr, M.G., additional, Cross, D.M., additional, Curry, J., additional, Devine, L.A., additional, Early, T.R., additional, Fazal, L., additional, Gill, A.L., additional, Heathcote, M., additional, Maman, S., additional, Matthews, J.E., additional, McMenamin, R.L., additional, Navarro, E.F., additional, O'Brien, M.A., additional, O'Reilly, M., additional, Rees, D.C., additional, Reule, M., additional, Tisi, D., additional, Williams, G., additional, Vinkovic, M., additional, and Wyatt, P.G., additional
- Published
- 2009
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29. Fragment-Based Discovery of the Pyrazol-4-yl urea (AT9283), a Multi- targeted Kinase Inhibitor with Potent Aurora Kinase Activity
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Howard, S., primary, Berdini, V., additional, Boulstridge, J.A., additional, Carr, M.G., additional, Cross, D.M., additional, Curry, J., additional, Devine, L.A., additional, Early, T.R., additional, Fazal, L., additional, Gill, A.L., additional, Heathcote, M., additional, Maman, S., additional, Matthews, J.E., additional, McMenamin, R.L., additional, Navarro, E.F., additional, O'Brien, M.A., additional, O'Reilly, M., additional, Rees, D.C., additional, Reule, M., additional, Tisi, D., additional, Williams, G., additional, Vinkovic, M., additional, and Wyatt, P.G., additional
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- 2009
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30. 147 POSTER AT13387, a fragment derived clinical candidate is active in lung and melanoma models
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Lyons, J., primary, Graham, B., additional, Curry, J., additional, Reule, M., additional, Smyth, T., additional, Fazal, L., additional, Williams, B., additional, Yule, M., additional, Squires, M., additional, and Thompson, N., additional
- Published
- 2008
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31. 287 POSTER Fragment-based discovery of AT9283; a multi-targeted kinase inhibitor with potent Aurora kinase activity
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Howard, S., primary, Berdini, V., additional, Curry, J., additional, Gill, A.L., additional, Richardson, C.J., additional, Rees, D., additional, Reule, M., additional, Tisi, D., additional, Wyatt, P., additional, and Fazal, L., additional
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- 2008
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32. Phase I and pharmacodynamic trial of AT9283, an aurora kinase inhibitor, in patients with refractory leukemia
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Foran, J. M., primary, Ravandi, F., additional, O'Brien, S. M., additional, Borthakur, G., additional, Rios, M., additional, Boone, P., additional, Worrell, J., additional, Mallett, K. H., additional, Squires, M., additional, Fazal, L. H., additional, and Kantarjian, H. M., additional
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- 2008
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33. Tackling security vulnerabilities in VPN-based wireless deployments
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Fazal, L., primary, Ganu, S., additional, Kappes, M., additional, Krishnakumar, A.S., additional, and Krishnan, P., additional
- Published
- 2004
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34. TARGET: Two-way Web Service Router Gateway.
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Feng Liu, Gesan Wang, Wu Chou, Fazal, L., and Li Li
- Published
- 2006
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35. 060 - Roles and Mechanisms of Action of Aldehydes Produced by Monoamine Oxidase-A in Cardiomyocyte Death and Heart Failure.
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Santin, Y., Sicard, P., Yücel Yücel, Y., Fazal, L., Sainte-Marie, Y., Dutaur, M., Maggiorani, D., Vindis, C., Parini, A., Lezoualc’h, F., and Mialet-Perez, J.
- Published
- 2017
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36. P610 Akt-mediated cardioprotective effects of aldosterone in type 2 diabetic mice.
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Fazal, L, Azibani, F, Coutance, G, Birhy, N, Polidano, E, Merval, R, Vodovar, N, Launay, JM, Delcayre, C, and Samuel, JL
- Subjects
- *
CARDIOTONIC agents , *ALDOSTERONE , *TYPE 2 diabetes , *NEOVASCULARIZATION , *CARDIOVASCULAR diseases , *LABORATORY mice - Abstract
Purpose: Studies have shown that aldosterone would have angiogenic effects, and therefore would be beneficial in the context of cardiovascular diseases. We thus investigated the potential involvement of aldosterone in triggering a cardiac angiogenic response in the context of type-2 diabetes, and the molecular pathways involved.Procedure: 3 week-old male mice, overexpressing aldosterone-synthase (AS), and their controls littermates (WT) were fed with a standard or high fat, high sucrose (HFHS) diet. After 6 months of diet, mice were sacrificed and cardiac samples were assayed by RT-PCR, immuno-blotting and -histology.Findings: HFHS-diet induced type-2 diabetes (D) in WT and AS mice. VEGFa mRNAs were decreased in WT-D (-43%, P<0.05 vs. WT) while increased in AS-D mice (+236%, P<0.01 vs. WT-D). In WT-D hearts, the proapoptotic p38-MAPK was activated (P<0.05 vs. WT and AS-D) whereas Akt activity decreased. The AS-mice, that exhibited a cardiac upregulation of IGF1-R, showed an increase in Akt phosphorylation when diabetic (P<0.05 vs. WT and AS-D). Contrary to WT-D, AS-D hearts did not express inflammatory markers and exhibited a normal capillary density (P<0.05 vs. WT-D)Conclusions: To our knowledge, this is the first study providing new insights into the mechanisms whereby aldosterone prevents diabetes-induced cardiac disorders. [ABSTRACT FROM PUBLISHER]
- Published
- 2014
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37. P598 Deleterious effects of cardiac aldosterone and exercise in type 2 diabetic mice.
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Fazal, L, Polidano, E, Merval, R, Coutance, G, Delcayre, C, and Samuel, JL
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- *
TYPE 2 diabetes , *EXERCISE , *RENIN-angiotensin system , *HEART failure , *HYPERALDOSTERONISM , *LABORATORY mice - Abstract
Introduction: Scarcity of microvessels and deregulation of the renin-angiotensin-aldosterone system contribute to the development of heart failure in diabetes. We showed that cardiac aldosteronism inhibits the onset of cardiomyopathy in type 1 diabetic mice by preventing capillary rarefaction (Messaoudi, 2009). Another promising therapeutic approach to prevent diabetic heart disease is exercise training (Ex). Exercise is beneficial in diabetic cardiomyopathy in human and experimentally. Thus, the objective of the study was to determine whether cardiac aldosterone-induced angiogenesis in type 2 diabetes (D) is used to meet the energy demand associated with Ex, and to identify the mechanisms involved.Methods: 3 weeks old mice overexpressing cardiac aldosterone system (AS) and their controls (WT) were made diabetic by enriched fat and sucrose diet. After 4 months of diet, diabetic mice and their controls were subjected to 2 months of Ex on treadmill (3 sessions/week). Results: Cardiac function was not affected by Ex. The Ex led to cardiac hypertrophy in AS-D-Ex mice (+15 % in AS-D-Ex vs AS-D, P<0.01) while it improved the basic parameters of WT-D-Ex vs WT-D (body weight: -15 %, blood glucose: -15%, resistance to insulin:-50%). Interestingly, the Ex revealed a defect in AS mice: the cumulative distance traveled by AS mice, with or without type 2 D was 30% lower than in WT mice (p < 0.01). In addition, a 75% mortality was observed in AS mice (diabetic or not) submitted to the Ex, in contrast to WT mice. These results demonstrate that AS mice, unfit to Ex, developed a pathological hypertrophy. In contrast to the observed baseline responses, the Ex did not phosphorylate and thus did not activated the Akt pathway in AS-D-Ex mice (NS vs AS-D), signing the absence of activation of the physiological pathway of cardiac hypertrophy.Conclusion: These results demonstrate a deleterious effect of cardiac aldosteronism in response to Ex, regardless of diabetic context, thus underlining that the microangiogenesis observed in the AS-D mice prevented neither the inability to Ex nor mortality. This suggests that the proangiogenic effect of cardiac hyperaldosteronism associated with type 2 diabetes is not enough to cope with this overload of cardiac output associated with the physical exercise. [ABSTRACT FROM AUTHOR]
- Published
- 2014
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38. P720 Notch3 is an important mediator of cardiac adaptation to pressure overload.
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Ragot, H, Merval, R, Baudet, M, Fazal, L, Polidano, E, Delcayre, C, Chatziantoniou, C, and Samuel, J-L
- Subjects
PHYSIOLOGICAL effects of pressure ,VASCULAR smooth muscle ,CELL differentiation ,HYPERTENSION ,GENE expression ,CARDIAC hypertrophy - Abstract
Notch3, a receptor expressed in vascular smooth muscle cells (VSMC) and pericytes, has a key role in the integrity of resistance arteries by controlling the maturation of VSMC and the arterial differentiation. The goal of the study was to decipher the role of Notch3 in the normal heart and in the response to pressure overload.To reach our objectives, we used adult male C57Bl/6J mice lacking expression of the Notch3 gene (N3-/-). Hypertension was induced by continuous infusion of Angiotensin II (AngII) for 28 days (1μg/kg/min) in WT and N3-/- mice (n>13). The analysis combined with echocardiography analysis, mRNA quantification, western-blot, immuno- and/or histo-morphometry.In basal conditions, N3-/- mice exhibited cardiac hypertrophy (+20%, p<0.001 vs Wild Type, WT) combined with defects at the structure of coronary artery as evidenced by decreased F-actin content in the media (-20%, p<0.05) and decreased density of arterioles (p<0.05).The AngII -induced Hypertension is lower inN3-/- mice (-20%, p<0.05 vs WT +AngII). Despite this blunted systemic effect, N3-/- mice developed a more severe heart failure (HF) compared to WT+AngII mice with lower shortening fraction (-20%, p<0.01), higher cardiac hypertrophy (+35%, p<0.05), and enhanced markers of fibrosis and inflammation [induction of galectin-3 (x3.5, p<0.01)]. The results in N3-/- +AngII mice, which combined the induction of Angiopoïetin 2 mRNA (+70%, p<0.05) and the repression of VEGFa (p<0.05) are in favour of coronary artery destabilization. Interestingly, coronary vessels did not show medial hypertrophy and this lack of adaptive response to hypertension was accompanied by a decreased expression of F-actin and SM actin mRNA (-50%, p<0.01). Moreover a treatment by Notch3 antisens oligonucleotides (ON) of WT +AngII mice impair coronary artery network as suggested by Angiopoïetin 2 induction (p<0.05 vs WT+AngII+ scrambled ON).Altogether, we provide lines of evidence that alterations of Notch3 signaling pathway in the coronary arteries might play a role in the occurrence of HF in response to chronic increase in blood pressure. [ABSTRACT FROM PUBLISHER]
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- 2014
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39. 162 Poster - Combined inhibition of SHP2 and ERK enhances anti-tumour effects in preclinical models.
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Smyth, T., Brothwood, J., Fazal, L., Hearn, K., Hindley, C., Johnson, C., Jones, M., Kandola, N., Lyons, J., Martins, V., Miyadera, K., Muench, S., Munck, J., Nakatsuru, Y., Ochiiwa, H., Saini, H., Shah, A., Wagner, S., Wilsher, N., and Wallis, N.
- Subjects
- *
ANTINEOPLASTIC agents , *CONFERENCES & conventions , *DRUG design , *CLINICAL drug trials , *PHOSPHATASES , *PROTEIN-tyrosine kinases , *CHEMICAL inhibitors - Published
- 2020
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40. A commentary on the use of pharmacoenhancers in the pharmaceutical industry and the implication for DMPK drug discovery strategies.
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Martins V, Fazal L, Oganesian A, Shah A, Stow J, Walton H, and Wilsher N
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- Humans, Drug Industry, Myotonin-Protein Kinase, COVID-19, Drug Discovery, Ritonavir
- Abstract
Paxlovid, a drug combining nirmatrelvir and ritonavir, was designed for the treatment of COVID-19 and its rapid development has led to emergency use approval by the FDA to reduce the impact of COVID-19 infection on patients.In order to overcome potentially suboptimal therapeutic exposures, nirmatrelvir is dosed in combination with ritonavir to boost the pharmacokinetics of the active product.Here we consider examples of drugs co-administered with pharmacoenhancers.Pharmacoenhancers have been adopted for multiple purposes such as ensuring therapeutic exposure of the active product, reducing formation of toxic metabolites, changing the route of administration, and increasing the cost-effectiveness of a therapy.We weigh the benefits and risks of this approach, examining the impact of technology developments on drug design and how enhanced integration between cross-discipline teams can improve the outcome of drug discovery.
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- 2022
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41. Discovery of ASTX029, A Clinical Candidate Which Modulates the Phosphorylation and Catalytic Activity of ERK1/2.
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Heightman TD, Berdini V, Bevan L, Buck IM, Carr MG, Courtin A, Coyle JE, Day JEH, East C, Fazal L, Griffiths-Jones CM, Howard S, Kucia-Tran J, Martins V, Muench S, Munck JM, Norton D, O'Reilly M, Palmer N, Pathuri P, Peakman TM, Reader M, Rees DC, Rich SJ, Shah A, Wallis NG, Walton H, Wilsher NE, Woolford AJ, Cooke M, Cousin D, Onions S, Shannon J, Watts J, and Murray CW
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- Animals, Antineoplastic Agents chemical synthesis, Antineoplastic Agents metabolism, Antineoplastic Agents pharmacokinetics, Crystallography, X-Ray, Dogs, Humans, Indoles chemical synthesis, Indoles metabolism, Indoles pharmacokinetics, Male, Mice, Inbred BALB C, Mitogen-Activated Protein Kinase 1 chemistry, Mitogen-Activated Protein Kinase 1 metabolism, Molecular Structure, Phosphorylation drug effects, Protein Binding, Protein Kinase Inhibitors chemical synthesis, Protein Kinase Inhibitors metabolism, Protein Kinase Inhibitors pharmacokinetics, Proto-Oncogene Mas, Pyrimidines chemical synthesis, Pyrimidines metabolism, Pyrimidines pharmacokinetics, Rats, Sprague-Dawley, Rats, Wistar, Structure-Activity Relationship, Xenograft Model Antitumor Assays, Mice, Rats, Antineoplastic Agents therapeutic use, Indoles therapeutic use, Mitogen-Activated Protein Kinase 1 antagonists & inhibitors, Neoplasms drug therapy, Protein Kinase Inhibitors therapeutic use, Pyrimidines therapeutic use
- Abstract
Aberrant activation of the mitogen-activated protein kinase pathway frequently drives tumor growth, and the ERK1/2 kinases are positioned at a key node in this pathway, making them important targets for therapeutic intervention. Recently, a number of ERK1/2 inhibitors have been advanced to investigational clinical trials in patients with activating mutations in B-Raf proto-oncogene or Ras. Here, we describe the discovery of the clinical candidate ASTX029 ( 15 ) through structure-guided optimization of our previously published isoindolinone lead ( 7 ). The medicinal chemistry campaign focused on addressing CYP3A4-mediated metabolism and maintaining favorable physicochemical properties. These efforts led to the identification of ASTX029, which showed the desired pharmacological profile combining ERK1/2 inhibition with suppression of phospho-ERK1/2 (pERK) levels, and in addition, it possesses suitable preclinical pharmacokinetic properties predictive of once daily dosing in humans. ASTX029 is currently in a phase I-II clinical trial in patients with advanced solid tumors.
- Published
- 2021
- Full Text
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42. Structure-Based Design of Potent and Orally Active Isoindolinone Inhibitors of MDM2-p53 Protein-Protein Interaction.
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Chessari G, Hardcastle IR, Ahn JS, Anil B, Anscombe E, Bawn RH, Bevan LD, Blackburn TJ, Buck I, Cano C, Carbain B, Castro J, Cons B, Cully SJ, Endicott JA, Fazal L, Golding BT, Griffin RJ, Haggerty K, Harnor SJ, Hearn K, Hobson S, Holvey RS, Howard S, Jennings CE, Johnson CN, Lunec J, Miller DC, Newell DR, Noble MEM, Reeks J, Revill CH, Riedinger C, St Denis JD, Tamanini E, Thomas H, Thompson NT, Vinković M, Wedge SR, Williams PA, Wilsher NE, Zhang B, and Zhao Y
- Subjects
- Animals, Antineoplastic Agents chemical synthesis, Antineoplastic Agents metabolism, Bone Neoplasms drug therapy, Cell Line, Tumor, Cell Proliferation drug effects, Crystallography, X-Ray, Drug Stability, Female, Humans, Isoindoles chemical synthesis, Isoindoles metabolism, Macaca fascicularis, Male, Mice, Inbred BALB C, Mice, Nude, Microsomes, Liver metabolism, Molecular Structure, Protein Binding, Structure-Activity Relationship, Xenograft Model Antitumor Assays, Mice, Antineoplastic Agents pharmacology, Isoindoles pharmacology, Osteosarcoma drug therapy, Protein Multimerization drug effects, Proto-Oncogene Proteins c-mdm2 metabolism, Tumor Suppressor Protein p53 metabolism
- Abstract
Inhibition of murine double minute 2 (MDM2)-p53 protein-protein interaction with small molecules has been shown to reactivate p53 and inhibit tumor growth. Here, we describe rational, structure-guided, design of novel isoindolinone-based MDM2 inhibitors. MDM2 X-ray crystallography, quantum mechanics ligand-based design, and metabolite identification all contributed toward the discovery of potent in vitro and in vivo inhibitors of the MDM2-p53 interaction with representative compounds inducing cytostasis in an SJSA-1 osteosarcoma xenograft model following once-daily oral administration.
- Published
- 2021
- Full Text
- View/download PDF
43. Mitochondrial 4-HNE derived from MAO-A promotes mitoCa 2+ overload in chronic postischemic cardiac remodeling.
- Author
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Santin Y, Fazal L, Sainte-Marie Y, Sicard P, Maggiorani D, Tortosa F, Yücel YY, Teyssedre L, Rouquette J, Marcellin M, Vindis C, Shih JC, Lairez O, Burlet-Schiltz O, Parini A, Lezoualc'h F, and Mialet-Perez J
- Subjects
- Animals, Calcium metabolism, Cells, Cultured, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Rats, Ventricular Remodeling, Aldehydes metabolism, Heart Failure metabolism, Mitochondria, Heart metabolism, Monoamine Oxidase metabolism, Myocardial Infarction metabolism, Myocytes, Cardiac metabolism, Myocytes, Cardiac pathology
- Abstract
Chronic remodeling postmyocardial infarction consists in various maladaptive changes including interstitial fibrosis, cardiomyocyte death and mitochondrial dysfunction that lead to heart failure (HF). Reactive aldehydes such as 4-hydroxynonenal (4-HNE) are critical mediators of mitochondrial dysfunction but the sources of mitochondrial 4-HNE in cardiac diseases together with its mechanisms of action remain poorly understood. Here, we evaluated whether the mitochondrial enzyme monoamine oxidase-A (MAO-A), which generates H
2 O2 as a by-product of catecholamine metabolism, is a source of deleterious 4-HNE in HF. We found that MAO-A activation increased mitochondrial ROS and promoted local 4-HNE production inside the mitochondria through cardiolipin peroxidation in primary cardiomyocytes. Deleterious effects of MAO-A/4-HNE on cardiac dysfunction were prevented by activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2), the main enzyme for 4-HNE metabolism. Mechanistically, MAO-A-derived 4-HNE bound to newly identified targets VDAC and MCU to promote ER-mitochondria contact sites and MCU higher-order complex formation. The resulting mitochondrial Ca2+ accumulation participated in mitochondrial respiratory dysfunction and loss of membrane potential, as shown with the protective effects of the MCU inhibitor, RU360. Most interestingly, these findings were recapitulated in a chronic model of ischemic remodeling where pharmacological or genetic inhibition of MAO-A protected the mice from 4-HNE accumulation, MCU oligomer formation and Ca2+ overload, thus mitigating ventricular dysfunction. To our knowledge, these are the first evidences linking MAO-A activation to mitoCa2+ mishandling through local 4-HNE production, contributing to energetic failure and postischemic remodeling.- Published
- 2020
- Full Text
- View/download PDF
44. Identification of a pharmacological inhibitor of Epac1 that protects the heart against acute and chronic models of cardiac stress.
- Author
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Laudette M, Coluccia A, Sainte-Marie Y, Solari A, Fazal L, Sicard P, Silvestri R, Mialet-Perez J, Pons S, Ghaleh B, Blondeau JP, and Lezoualc'h F
- Subjects
- Animals, Cell Death drug effects, Chronic Disease, Disease Models, Animal, Fibrosis, G-Protein-Coupled Receptor Kinase 5 metabolism, Guanine Nucleotide Exchange Factors genetics, Guanine Nucleotide Exchange Factors metabolism, HEK293 Cells, Histone Deacetylases metabolism, Humans, MEF2 Transcription Factors metabolism, Mice, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Myocardial Infarction genetics, Myocardial Infarction metabolism, Myocardial Infarction physiopathology, Myocardial Reperfusion Injury genetics, Myocardial Reperfusion Injury metabolism, Myocardial Reperfusion Injury physiopathology, Myocytes, Cardiac metabolism, Myocytes, Cardiac pathology, Rats, Signal Transduction, Ventricular Dysfunction, Left genetics, Ventricular Dysfunction, Left metabolism, Ventricular Dysfunction, Left physiopathology, Cardiovascular Agents pharmacology, Guanine Nucleotide Exchange Factors antagonists & inhibitors, Myocardial Infarction prevention & control, Myocardial Reperfusion Injury prevention & control, Myocytes, Cardiac drug effects, Ventricular Dysfunction, Left drug therapy, Ventricular Function, Left drug effects, Ventricular Remodeling drug effects
- Abstract
Aims: Recent studies reported that cAMP-binding protein Epac1-deficient mice were protected against various forms of cardiac stress, suggesting that pharmacological inhibition of Epac1 could be beneficial for the treatment of cardiac diseases. To test this assumption, we characterized an Epac1-selective inhibitory compound and investigated its potential cardioprotective properties., Methods and Results: We used the Epac1-BRET (bioluminescence resonance energy transfer) for searching for non-cyclic nucleotide Epac1 modulators. A thieno[2,3-b]pyridine derivative, designated as AM-001 was identified as a non-competitive inhibitor of Epac1. AM-001 has no antagonist effect on Epac2 or protein kinase A activity. This small molecule prevents the activation of the Epac1 downstream effector Rap1 in cultured cells, in response to the Epac1 preferential agonist, 8-CPT-AM. In addition, we found that AM-001 inhibited Epac1-dependent deleterious effects such as cardiomyocyte hypertrophy and death. Importantly, AM-001-mediated inhibition of Epac1 reduces infarct size after mouse myocardial ischaemia/reperfusion injury. Finally, AM-001 attenuates cardiac hypertrophy, inflammation and fibrosis, and improves cardiac function during chronic β-adrenergic receptor activation with isoprenaline (ISO) in mice. At the molecular level, ISO increased Epac1-G protein-coupled receptor kinase 5 (GRK5) interaction and induced GRK5 nuclear import and histone deacetylase type 5 (HDAC5) nuclear export to promote the activity of the prohypertrophic transcription factor, myocyte enhancer factor 2 (MEF2). Inversely, AM-001 prevented the non-canonical action of GRK5 on HDAC5 cytoplasmic shuttle to down-regulate MEF2 transcriptional activity., Conclusion: Our study represents a 'proof-of-concept' for the therapeutic effectiveness of inhibiting Epac1 activity in cardiac disease using small-molecule pharmacotherapy., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)
- Published
- 2019
- Full Text
- View/download PDF
45. Fragment-Based Discovery of a Potent, Orally Bioavailable Inhibitor That Modulates the Phosphorylation and Catalytic Activity of ERK1/2.
- Author
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Heightman TD, Berdini V, Braithwaite H, Buck IM, Cassidy M, Castro J, Courtin A, Day JEH, East C, Fazal L, Graham B, Griffiths-Jones CM, Lyons JF, Martins V, Muench S, Munck JM, Norton D, O'Reilly M, Palmer N, Pathuri P, Reader M, Rees DC, Rich SJ, Richardson C, Saini H, Thompson NT, Wallis NG, Walton H, Wilsher NE, Woolford AJ, Cooke M, Cousin D, Onions S, Shannon J, Watts J, and Murray CW
- Subjects
- Administration, Oral, Animals, Biological Availability, Cell Line, Tumor, Humans, Mice, Mitogen-Activated Protein Kinase 1 chemistry, Mitogen-Activated Protein Kinase 3 chemistry, Models, Molecular, Phosphorylation drug effects, Protein Conformation, Protein Kinase Inhibitors administration & dosage, Protein Kinase Inhibitors chemistry, Protein Kinase Inhibitors pharmacokinetics, Biocatalysis drug effects, Drug Discovery, Mitogen-Activated Protein Kinase 1 antagonists & inhibitors, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinase 3 antagonists & inhibitors, Mitogen-Activated Protein Kinase 3 metabolism, Protein Kinase Inhibitors pharmacology
- Abstract
Aberrant activation of the MAPK pathway drives cell proliferation in multiple cancers. Inhibitors of BRAF and MEK kinases are approved for the treatment of BRAF mutant melanoma, but resistance frequently emerges, often mediated by increased signaling through ERK1/2. Here, we describe the fragment-based generation of ERK1/2 inhibitors that block catalytic phosphorylation of downstream substrates such as RSK but also modulate phosphorylation of ERK1/2 by MEK without directly inhibiting MEK. X-ray crystallographic and biophysical fragment screening followed by structure-guided optimization and growth from the hinge into a pocket proximal to the C-α helix afforded highly potent ERK1/2 inhibitors with excellent kinome selectivity. In BRAF mutant cells, the lead compound suppresses pRSK and pERK levels and inhibits proliferation at low nanomolar concentrations. The lead exhibits tumor regression upon oral dosing in BRAF mutant xenograft models, providing a promising basis for further optimization toward clinical pERK1/2 modulating ERK1/2 inhibitors.
- Published
- 2018
- Full Text
- View/download PDF
46. Beneficial effects of exercise training in heart failure are lost in male diabetic rats.
- Author
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Boudia D, Domergue V, Mateo P, Fazal L, Prud'homme M, Prigent H, Delcayre C, Cohen-Solal A, Garnier A, Ventura-Clapier R, and Samuel JL
- Subjects
- Animals, Diet, High-Fat, Disease Models, Animal, Echocardiography, Energy Metabolism, Heart physiopathology, Male, Myocardial Infarction physiopathology, Random Allocation, Rats, Rats, Wistar, Signal Transduction, Stress, Physiological, Diabetes Mellitus, Experimental physiopathology, Heart Failure physiopathology, Physical Conditioning, Animal
- Abstract
Exercise training has been demonstrated to have beneficial effects in patients with heart failure (HF) or diabetes. However, it is unknown whether diabetic patients with HF will benefit from exercise training. Male Wistar rats were fed either a standard (Sham, n = 53) or high-fat, high-sucrose diet ( n = 66) for 6 mo. After 2 mo of diet, the rats were already diabetic. Rats were then randomly subjected to either myocardial infarction by coronary artery ligation (MI) or sham operation. Two months later, heart failure was documented by echocardiography and animals were randomly subjected to exercise training with treadmill for an additional 8 wk or remained sedentary. At the end, rats were euthanized and tissues were assayed by RT-PCR, immunoblotting, spectrophotometry, and immunohistology. MI induced a similar decrease in ejection fraction in diabetic and lean animals but a higher premature mortality in the diabetic group. Exercise for 8 wk resulted in a higher working power developed by MI animals with diabetes and improved glycaemia but not ejection fraction or pathological phenotype. In contrast, exercise improved the ejection fraction and increased adaptive hypertrophy after MI in the lean group. Trained diabetic rats with MI were nevertheless able to develop cardiomyocyte hypertrophy but without angiogenic responses. Exercise improved stress markers and cardiac energy metabolism in lean but not diabetic-MI rats. Hence, following HF, the benefits of exercise training on cardiac function are blunted in diabetic animals. In conclusion, exercise training only improved the myocardial profile of infarcted lean rats fed the standard diet. NEW & NOTEWORTHY Exercise training is beneficial in patients with heart failure (HF) or diabetes. However, less is known of the possible benefit of exercise training for HF patients with diabetes. Using a rat model where both diabetes and MI had been induced, we showed that 2 mo after MI, 8 wk of exercise training failed to improve cardiac function and metabolism in diabetic animals in contrast to lean animals.
- Published
- 2017
- Full Text
- View/download PDF
47. Imbalanced Angiogenesis in Peripartum Cardiomyopathy - Diagnostic Value of Placenta Growth Factor.
- Author
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Mebazaa A, Seronde MF, Gayat E, Tibazarwa K, Anumba DOC, Akrout N, Sadoune M, Sarb J, Arrigo M, Motiejunaite J, Laribi S, Legrand M, Deschamps L, Fazal L, Bouadma L, Collet C, Manivet P, Solal AC, Launay JM, Samuel JL, and Sliwa K
- Subjects
- Cardiomyopathies diagnosis, Female, Heart Failure diagnosis, Humans, Peripartum Period, Pregnancy, Cardiomyopathies blood, Neovascularization, Pathologic blood, Placenta Growth Factor blood, Vascular Endothelial Growth Factor Receptor-1 blood
- Abstract
Background: Concentrations of the anti-angiogenic factor soluble fms-like tyrosine kinase-1 (sFlt-1) are altered in peripartum cardiomyopathy (PPCM). In this study we investigated changes in the angiogenesis balance in PPCM.Methods and Results:Plasma concentrations of sFlt-1 and the pro-angiogenic placenta growth factor (PlGF) were determined in patients with PPCM during the post-partum phase (n=83), in healthy women at delivery (n=30), and in patients with acute heart failure (AHF; n=65). Women with cardiac failure prepartum or associated with any form of hypertension, including pre-eclampsia, were excluded. Compared with non-pregnant women, in women with AHF and PPCM, median PlGF concentrations were greater (19 [IQR 16-22] and 98 [IQR 78-126] ng/mL, respectively; P<0.001) and the sFlt-1/PlGF ratio was lower (9.8 [6.6-11.3] and 1.2 [0.9-2.8], respectively; P<0.001). The sFlt-1/PlGF ratio was lower in PPCM than in normal deliveries (1.2 [0.9-2.8] vs. 94.8 [68.8-194.1], respectively; P<0.0001). The area under the curve for PlGF (cut-off value: 50ng/mL) and/or the sFlt-1/PlGF ratio (cut-off value: 4) to distinguish PPCM from either normal delivery or AHF was >0.94. Median plasma concentrations of the anti-angiogenic factor relaxin-2 were lower in PPCM and AHF (0.3 [IQR 0.3-1.7] and 0.3 [IQR 0.3-1] ng/mL, respectively) compared with normal deliveries (1,807 [IQR 1,101-4,050] ng/mL; P<0.001)., Conclusions: Plasma of PPCM patients shows imbalanced angiogenesis. High PlGF and/or low sFlt-1/PlGF may be used to diagnose PPCM.
- Published
- 2017
- Full Text
- View/download PDF
48. Multifunctional Mitochondrial Epac1 Controls Myocardial Cell Death.
- Author
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Fazal L, Laudette M, Paula-Gomes S, Pons S, Conte C, Tortosa F, Sicard P, Sainte-Marie Y, Bisserier M, Lairez O, Lucas A, Roy J, Ghaleh B, Fauconnier J, Mialet-Perez J, and Lezoualc'h F
- Subjects
- Animals, Animals, Newborn, Cell Death physiology, Cells, Cultured, Heart Failure metabolism, Heart Failure pathology, Humans, Male, Membrane Microdomains metabolism, Membrane Microdomains pathology, Mice, Mice, Knockout, Mitochondria, Heart pathology, Myocytes, Cardiac pathology, Rats, Guanine Nucleotide Exchange Factors biosynthesis, Mitochondria, Heart metabolism, Myocytes, Cardiac metabolism
- Abstract
Rationale: Although the second messenger cyclic AMP (cAMP) is physiologically beneficial in the heart, it largely contributes to cardiac disease progression when dysregulated. Current evidence suggests that cAMP is produced within mitochondria. However, mitochondrial cAMP signaling and its involvement in cardiac pathophysiology are far from being understood., Objective: To investigate the role of MitEpac1 (mitochondrial exchange protein directly activated by cAMP 1) in ischemia/reperfusion injury., Methods and Results: We show that Epac1 (exchange protein directly activated by cAMP 1) genetic ablation ( Epac1
-/- ) protects against experimental myocardial ischemia/reperfusion injury with reduced infarct size and cardiomyocyte apoptosis. As observed in vivo, Epac1 inhibition prevents hypoxia/reoxygenation-induced adult cardiomyocyte apoptosis. Interestingly, a deleted form of Epac1 in its mitochondrial-targeting sequence protects against hypoxia/reoxygenation-induced cell death. Mechanistically, Epac1 favors Ca2+ exchange between the endoplasmic reticulum and the mitochondrion, by increasing interaction with a macromolecular complex composed of the VDAC1 (voltage-dependent anion channel 1), the GRP75 (chaperone glucose-regulated protein 75), and the IP3R1 (inositol-1,4,5-triphosphate receptor 1), leading to mitochondrial Ca2+ overload and opening of the mitochondrial permeability transition pore. In addition, our findings demonstrate that MitEpac1 inhibits isocitrate dehydrogenase 2 via the mitochondrial recruitment of CaMKII (Ca2+ /calmodulin-dependent protein kinase II), which decreases nicotinamide adenine dinucleotide phosphate hydrogen synthesis, thereby, reducing the antioxidant capabilities of the cardiomyocyte., Conclusions: Our results reveal the existence, within mitochondria, of different cAMP-Epac1 microdomains that control myocardial cell death. In addition, our findings suggest Epac1 as a promising target for the treatment of ischemia-induced myocardial damage., (© 2017 American Heart Association, Inc.)- Published
- 2017
- Full Text
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49. Loss of Notch3 Signaling in Vascular Smooth Muscle Cells Promotes Severe Heart Failure Upon Hypertension.
- Author
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Ragot H, Monfort A, Baudet M, Azibani F, Fazal L, Merval R, Polidano E, Cohen-Solal A, Delcayre C, Vodovar N, Chatziantoniou C, and Samuel JL
- Subjects
- Adaptation, Physiological, Animals, Mice, Mice, Knockout, Oxidative Stress, Signal Transduction, Coronary Vessels, Heart Failure etiology, Heart Failure metabolism, Heart Failure physiopathology, Hypertension complications, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular physiopathology, Receptor, Notch3 metabolism, Tunica Media metabolism, Tunica Media pathology
- Abstract
Hypertension, which is a risk factor of heart failure, provokes adaptive changes at the vasculature and cardiac levels. Notch3 signaling plays an important role in resistance arteries by controlling the maturation of vascular smooth muscle cells. Notch3 deletion is protective in pulmonary hypertension while deleterious in arterial hypertension. Although this latter phenotype was attributed to renal and cardiac alterations, the underlying mechanisms remained unknown. To investigate the role of Notch3 signaling in the cardiac adaptation to hypertension, we used mice with either constitutive Notch3 or smooth muscle cell-specific conditional RBPJκ knockout. At baseline, both genotypes exhibited a cardiac arteriolar rarefaction associated with oxidative stress. In response to angiotensin II-induced hypertension, the heart of Notch3 knockout and SM-RBPJκ knockout mice did not adapt to pressure overload and developed heart failure, which could lead to an early and fatal acute decompensation of heart failure. This cardiac maladaptation was characterized by an absence of media hypertrophy of the media arteries, the transition of smooth muscle cells toward a synthetic phenotype, and an alteration of angiogenic pathways. A subset of mice exhibited an early fatal acute decompensated heart failure, in which the same alterations were observed, although in a more rapid timeframe. Altogether, these observations indicate that Notch3 plays a major role in coronary adaptation to pressure overload. These data also show that the hypertrophy of coronary arterial media on pressure overload is mandatory to initially maintain a normal cardiac function and is regulated by the Notch3/RBPJκ pathway., (© 2016 American Heart Association, Inc.)
- Published
- 2016
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- View/download PDF
50. Cyclic AMP Sensor EPAC Proteins and Their Role in Cardiovascular Function and Disease.
- Author
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Lezoualc'h F, Fazal L, Laudette M, and Conte C
- Subjects
- Animals, Cardiovascular Diseases pathology, Humans, Second Messenger Systems physiology, Cardiovascular Diseases metabolism, Cardiovascular Physiological Phenomena, Cyclic AMP physiology, Guanine Nucleotide Exchange Factors physiology
- Abstract
cAMP is a universal second messenger that plays central roles in cardiovascular regulation influencing gene expression, cell morphology, and function. A crucial step toward a better understanding of cAMP signaling came 18 years ago with the discovery of the exchange protein directly activated by cAMP (EPAC). The 2 EPAC isoforms, EPAC1 and EPAC2, are guanine-nucleotide exchange factors for the Ras-like GTPases, Rap1 and Rap2, which they activate independently of the classical effector of cAMP, protein kinase A. With the development of EPAC pharmacological modulators, many reports in the literature have demonstrated the critical role of EPAC in the regulation of various cAMP-dependent cardiovascular functions, such as calcium handling and vascular tone. EPAC proteins are coupled to a multitude of effectors into distinct subcellular compartments because of their multidomain architecture. These novel cAMP sensors are not only at the crossroads of different physiological processes but also may represent attractive therapeutic targets for the treatment of several cardiovascular disorders, including cardiac arrhythmia and heart failure., (© 2016 American Heart Association, Inc.)
- Published
- 2016
- Full Text
- View/download PDF
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