CLP-1 plays a pivotal role in regulating RNA transcript elongation during cardiac hypertrophy by interacting with the P-TEFb complex.
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Suggests hypertrophic transcriptional control in animals; leaves open CLP-1 targeting for human disease.
CLP-1 expression in developing heart and isolated post-natal cardiomyocytes colocalizes with P-TEFb expression and therefore has the potential to regulate RNA transcript elongation by controlling P-TEFb cdk9 kinase activity in heart. We further conclude that the dissociation of CLP-1 from P-TEFb is responsive to hypertrophic stimuli transduced by cellular signal transduction pathways. This process may be part of the genomic stress response resulting in increased RNA transcript synthesis in hypertrophic cardiomyocytes.
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Espinoza‐Derout et al. (2007) studied this question.
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