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Myocyte enhancer factor 2A is transcriptionally autoregulated 总被引:1,自引:0,他引:1
Ramachandran B Yu G Li S Zhu B Gulick T 《The Journal of biological chemistry》2008,283(16):10318-10329
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A Zarain-Herzberg D H MacLennan M Periasamy 《The Journal of biological chemistry》1990,265(8):4670-4677
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Kurose K Ikeda S Koyano S Tohkin M Hasegawa R Sawada J 《Molecular and cellular biochemistry》2006,281(1-2):35-43
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Lu SY Sontag DP Detillieux KA Cattini PA 《American journal of physiology. Cell physiology》2008,294(5):C1242-C1249
FGF-16 has been reported to be preferentially expressed in the adult rat heart. We have investigated the expression of FGF-16 in the perinatal and postnatal heart and its functional significance in neonatal rat cardiac myocytes. FGF-16 mRNA accumulation was observed by quantitative RT-PCR between neonatal days 1 and 7, with this increased expression persisting into adulthood. FGF-2 has been shown to increase neonatal rat cardiac myocyte proliferative potential via PKC activation. Gene array analysis revealed that FGF-16 inhibited the upregulation by FGF-2 of cell cycle promoting genes including cyclin F and Ki67. Furthermore, the CDK4/6 inhibitor gene Arf/INK4A was upregulated with the combination of FGF-16 and FGF-2 but not with either factor on its own. The effect on Ki67 was validated by protein immunodetection, which also showed that FGF-16 significantly decreased FGF-2-induced Ki67 labeling of cardiac myocytes, although it alone had no effect on Ki67 labeling. Inhibition of p38 MAPK potentiated cardiac myocyte proliferation induced by FGF-2 but did not alter the inhibitory action of FGF-16. Receptor binding assay showed that FGF-16 can compete with FGF-2 for binding sites including FGF receptor 1. FGF-16 had no effect on activated p38, ERK1/2, or JNK/SAPK after FGF-2 treatment. However, FGF-16 inhibited PKC-alpha and PKC-epsilon activation induced by FGF-2 and, importantly, IGF-1. Collectively, these data suggest that expression and release of FGF-16 in the neonatal myocardium interfere with cardiac myocyte proliferative potential by altering the local signaling environment via modulation of PKC activation and cell cycle-related gene expression. 相似文献
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Xu J Gong NL Bodi I Aronow BJ Backx PH Molkentin JD 《The Journal of biological chemistry》2006,281(14):9152-9162
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T G Parker K L Chow R J Schwartz M D Schneider 《The Journal of biological chemistry》1992,267(5):3343-3350
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