Abstract
Publisher Summary This chapter focuses on the Ras regulation of Cyclin D 1 promoter. Cyclin D l, the regulatory subunit of cyclin-dependent kinases (CDK) 4 and 6, is required for, and capable of, shortening, the G j phase of the cell cycle through the formation of holoenzyme complexes (cyclin-CDK) that phosphorylate retinoblastoma protein (pRB). Ras transformation is inhibited by antisense to cyclin D1 mRNA. The Ras-related proteins, Rac and Rho, also induce the cyclin D1 promoter. Racl regulates several distinct pathways; no single Rac effect is necessary or sufficient for transformation. Platelet-derived growth factor (PDGF) activates the extracellular signal-regulated kinase (ERK) pathway, which has been shown to induce DNA synthesis, increase cyclin D1 protein levels, and stimulate the transcription of the cyclin D1 promoter. Therefore, Rac 1 is neither necessary nor sufficient to activate the ERK pathway, suggesting that Rac regulation of cyclin D1 is ERK independent. The cyclin DI promoter is used as a molecular probe of the signal transduction pathways involved in Ras signaling. The valid assessment of promoter activation by Ras requires the use of a reporter system that is not itself responsive to components of the Ras signaling pathway.
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