Abstract
Abstract We have recently reported the characterization of RBEL1 proteins, a novel subfamily of the Ras/Rab-like GTPases. Our studies demonstrate that RBEL1 proteins have Ras-like GTPase activity and differentially regulate the ERK signaling pathway. Our studies also demonstrate that RBEL1A is overexpressed in the majority of breast cancers and a large segment of colon cancers. Knockdown of RBEL1A negatively affects cell growth and induces apoptosis, suggesting that RBEL1A is critical for regulation of cell growth and survival. To investigate the molecular mechanisms by which RBEL1A mediates its function, we have studied a number of RBEL1A-interacting proteins. Our results indicate that RBEL1A interacts with p53 and negatively regulates p53 function via a proteasome-dependent pathway. We have also examined the molecular interactions between RBEL1A and p53 and our results demonstrate that RBEL1A is an important negative regulator of p53 that affects p53-mediated functions. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3841. doi:10.1158/1538-7445.AM2011-3841
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