Keywords :
Animals; Cardiomegaly/genetics/metabolism/pathology; Extracellular Signal-Regulated MAP Kinases/metabolism; Genotype; Humans; Mice; Mice, Knockout; Myocardium/metabolism/pathology; Neoplasms/genetics/metabolism/pathology; Phenotype; Protein Conformation; Proto-Oncogene Proteins c-raf/metabolism; Signal Transduction/genetics; Structure-Activity Relationship; Tumor Suppressor Proteins/chemistry/deficiency/genetics/metabolism; ras Proteins/metabolism
Abstract :
[en] The close relationship between signaling pathways regulating tumor growth and cardiac hypertrophy has attracted considerable interest. Although the involvement of proto-oncogenes in positively modulating myocardial hypertrophy has long been recognized, little is known about factors that counterregulate them. In this article, we review the novel tumor suppressor Ras-association domain family protein isoform 1A (RASSF1A), which strongly inhibits the prohypertrophic Ras-Raf1-ERK1/2 pathway in the heart. RASSF1A interacts with a number of important signaling molecules regulating cell growth, survival, and apoptosis; therefore, it serves as a key adaptor molecule that integrates the upstream stimuli and transduces them to the selective downstream effectors.
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