Projects per year
Abstract
The c-Myc proto-oncogene promotes mRNA cap methylation, which is essential for almost all mRNA translation. The mRNA cap methylation reaction produces an inhibitory byproduct, S-adenosyl homocysteine. Here we report that Myc promotes upregulation of S-adenosyl homocysteine hydrolase (SAHH), an enzyme which hydrolyzes S-adenosyl homocysteine, thus neutralizing its inhibitory effects, and this is required for c-Myc-induced mRNA cap methylation. c-Myc-induced mRNA cap methylation was repressed by inhibiting the expression or activity of SAHH, whereas the same treatments did not have a significant effect on c-Myc-induced transcription or other c-Myc-dependent methylation events. The selective inhibition of mRNA cap methylation afforded by SAHH repression revealed that c-Myc-induced cap methylation could be correlated with the core c-Myc functions of protein synthesis, cell proliferation, and cell transformation.
Original language | English |
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Pages (from-to) | 6182-6191 |
Number of pages | 10 |
Journal | Molecular and Cellular Biology |
Volume | 29 |
Issue number | 23 |
DOIs | |
Publication status | Published - 1 Dec 2009 |
Keywords
- CARBOXY-TERMINAL DOMAIN
- POLYMERASE-II
- CAPPING ENZYME
- C-MYC
- ADENOSYLHOMOCYSTEINE HYDROLASE
- GENOMIC TARGETS
- XENOPUS-LAEVIS
- TRANSCRIPTION
- METHYLTRANSFERASE
- TRANSLATION
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- 1 Finished
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Aref#d: 19352. The Mechanism of Myc function in cell proliferation and cancer (Career Development Fellowship)
Cowling, V. (Investigator)
3/12/07 → 2/01/14
Project: Research