|
|
|
| Untersuchte Arbeit: Seite: 7, Zeilen: 13-22 |
Quelle: van Rooij et al 2002 Seite(n): 48617, Zeilen: 0 |
|---|---|
| Molkentin et al. (1998) and De Windt et al (2000) generated several lines of transgenic mice expressing activated forms of either calcineurin or NFATc4 in a cardiac-selective manner, which developed robust hypertrophy that quickly transitioned to ventricular dilation and overt heart failure. Hearts from transgenic mice expressing MCIP1, a dominant negative calcineurin mutant, or the calcineurin inhibitory domains of Cain or AKAP79, were largely resistant to pleiotropic, hypertrophic stimuli (Zou et al., 2001; Rothermel et al., 2001; De Windt et al., 2001). Adenoviral-mediated gene transfer of dominant negative NFAT in cultured cardiomyocytes efficiently inhibited calcineurin- and agonist induced cardiomyocyte hypertrophy (Rooij et al., 2002).
De Windt LJ, Lim HW, Taigen T, Wencker D, Condorelli G, Dorn GW, Kitsis RN and Molkentin JD (2000) Calcineurin-mediated hypertrophy protects cardiomyocytes from apoptosis in vitro and in vivo. Circ Res 86: 255-263. De Windt LJ, Lim HW, Bueno OF, Liang Q, Delling U, Braz JC, Glascock BJ, Kimball TF, Del Monte F, Hajjar RJ, and Molkentin JD (2001) Targeted inhibition of calcineurin attenuates cardiac hypertrophy in vivo. Proc Natl Acad Sci USA 98: 3322-3327. Molkentin JD, Lu JR, Antos CL, Markham B, Richardson J, Robbins J, Grant SR and Olson EN (1998) A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell 93: 215-228. Rothermel BA, McKinsey TA, Vega RB, Nicol RL, Mammen P, Yang J, Antos CL, Shelton JM, Bassel-Duby R, Olson EN and Williams RS (2001) Myocyteenriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo. Proc Natl Acad Sci USA 98: 3328-3333. Van Rooij E, Doevendans PA, de Theije CC, Babiker FA, Molkentin JD, and De Windt LJ (2002) Requirement of nuclear factor of activated T-cells in calcineurinmediated cardiomyocyte hypertrophy. J Biol Chem 277: 48617-48626. Zou Y, Hiroi Y, Uozumi H, Takimoto E, Toko H, Zhu W, Kudoh S, Mizukami M, Shimoyama M, Shibasaki F, Nagai R, Yazaki Y, and Komuro I (2001) Calcineurin plays a critical role in the development of pressure overload-induced cardiac hypertrophy. Circulation 104: 97-101. |
[Seite 48617]
Molkentin et al. (10, 11) generated several lines of transgenic mice expressing activated mutants of either calcineurin or NFATc4 in a cardiac-selective manner, which developed robust hypertrophy that quickly transitioned to ventricular dilation and overt heart failure. [Seite 48618] A central role for calcineurin in the cardiac hypertrophic response was substantiated by the observation that hearts from transgenic mice expressing either MCIP1, a dominant negative calcineurin mutant, or the calcineurin inhibitory domains of Cain or AKAP79, were largely resistant to pleiotropic, hypertrophic stimuli (14–16). [...] Adenoviralmediated gene transfer of dominant negative NFAT in cultured cardiomyocytes efficiently inhibited calcineurin- and agonistinduced cardiomyocyte hypertrophy. 10. Molkentin, J. D., Lu, J. R., Antos, C. L., Markham, B., Richardson, J., Robbins, J., Grant, S. R., and Olson, E. N. (1998) Cell 93, 215–228 11. De Windt, L. J., Lim, H. W., Taigen, T., Wencker, D., Condorelli, G., Dorn, G. W., 2nd, Kitsis, R. N., and Molkentin, J. D. (2000) Circ. Res. 86, 255–263 14. Zou, Y., Hiroi, Y., Uozumi, H., Takimoto, E., Toko, H., Zhu, W., Kudoh, S., Mizukami, M., Shimoyama, M., Shibasaki, F., Nagai, R., Yazaki, Y., and Komuro, I. (2001) Circulation 104, 97–101 15. Rothermel, B. A., McKinsey, T. A., Vega, R. B., Nicol, R. L., Mammen, P., Yang, J., Antos, C. L., Shelton, J. M., Bassel-Duby, R., Olson, E. N., and Williams, R. S. (2001) Proc. Natl. Acad. Sci. U. S. A. 98, 3328–3333 16. De Windt, L. J., Lim, H. W., Bueno, O. F., Liang, Q., Delling, U., Braz, J. C., Glascock, B. J., Kimball, T. F., del Monte, F., Hajjar, R. J., and Molkentin, J. D. (2001) Proc. Natl. Acad. Sci. U. S. A. 98, 3322–3327 |
Patchwork aus wortwörtlich übernommenen Texten, ohne dass die Übernahmen gekennzeichnet worden wären. |
|