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| Untersuchte Arbeit: Seite: 13, Zeilen: 17-22 |
Quelle: Vlasblom et al 2004 Seite(n): 537, 538, 543, Zeilen: S.537,24-25 und S.538, li.Sp. 19-22 und S.543, re.Sp. 17-20 |
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| In myocardial hypertrophy induced by calcineurin over expression, both a fall in SERCA2a mRNA (Molkentin et al 1998) and a rise in SERCA2a protein (Chu et al., 2002) have been observed. In neonatal cardiomyocytes an up-regulation of SERCA2a mRNA expression was found in absence of contractile activity. This is likely due to calcineurin signaling and synergistic stimulation of the SERCA2a promoter by NFATc4 and MEF2c.
Chu G, Carr AN, Young KB, Lester JW, Yatani A, Sanbe A, et al. (2002) Enhanced myocyte contractility and Ca2+ handling in a calcineurin transgenic model of heart failure. Cardiovasc. Res 54: 105–116. 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. |
[Seite 537]
Conclusion: Following contractile arrest with BDM, upregulation of SERCA2a mRNA expression by CN/CAMK-II signaling becomes evident. [Seite 538] In myocardial hypertrophy induced by CN overexpression, both a fall in SERCA2a mRNA [12] and a rise in SERCA2a protein [16] have been observed. [Seite 543] 5. Conclusions [...] Both CN and CAMK-II pathways are involved in the calcium-dependent upregulation, most likely due to synergistic stimulation of the SERCA2a promoter by NFATc4 and MEF2c. [12] Molkentin JD, Lu JR, Antos CL, Markham B, Richardson J, Robbins J, et al. A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell 1998;93:215–28. [16] Chu G, Carr AN, Young KB, Lester JW, Yatani A, Sanbe A, et al. Enhanced myocyte contractility and Ca2+ handling in a calcineurin transgenic model of heart failure. Cardiovasc Res 2002;54:105– 16. |
Patchwork: vielfach identisch bis hin zu den Literaturverweisen. Übernahmen bleiben ungekennzeichnet. |
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