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At first glance, it may seem surprising that such different stimuli activate similar AP-1 complexes that are then responsible for stimulation of hypertrophy or apoptosis. It is found to be elevated after myocardial infarction [30] and is known to contribute to the remodeling process by enhancement of cardiac fibrosis [31].



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These examples show that AP-1 can serve as a mediator of either hypertrophy or apoptosis in one and the same cell type, i. Cardiomyocytes were preincubated with nM decoy oligonucleotides containing either specific binding sites for SMAD or AP-1 or the respective mutant binding sites Mut. In a first approach, we analyzed whether AP-1 composition differs under hypertrophic and apoptotic conditions. Oxidative stress induces DNA fragmentation and caspase activation via the c-Jun NH2-terminal kinase pathway in H9c2 cardiac muscle cells.


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There is a putative NFAT binding site in the SMMHC promoter enhancer (GGAAAA), at −/− relative to the transcriptional start site as well as a GATA-6 binding site at −/− To begin to address these complex issues, we recently developed a unique embryonic stem cell . E&A is a planning, engineering, environmental and field services company with roots planted firmly in the Midwest. As a company, we take pride in our responsibility to create and support the infrastructure and landscapes our families, friends and neighbors enjoy.


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AP-1 has been shown recently, and also in this study, to be involved in both pathways [1,2,6].




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