| First Author | Fernandez-Sanchez ME | Year | 2009 |
| Journal | Mol Cell Biol | Volume | 29 |
| Issue | 23 | Pages | 6182-91 |
| PubMed ID | 19805518 | Mgi Jnum | J:154987 |
| Mgi Id | MGI:4412119 | Doi | 10.1128/MCB.00973-09 |
| Citation | Fernandez-Sanchez ME, et al. (2009) S-adenosyl homocysteine hydrolase is required for Myc-induced mRNA cap methylation, protein synthesis, and cell proliferation. Mol Cell Biol 29(23):6182-91 |
| abstractText | 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. |
