期刊
NATURE STRUCTURAL & MOLECULAR BIOLOGY
卷 14, 期 6, 页码 511-518出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb1249
关键词
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资金
- NCI NIH HHS [R01 CA052443, R01 CA052443-14, CA052443] Funding Source: Medline
(A+U)-rich elements (AREs) within 3 untranslated regions are signals for rapid degradation of messenger RNAs encoding many oncoproteins and cytokines. The ARE-binding protein AUF1 contributes to their degradation. We identified MYC proto-oncogene mRNA as a cellular AUF1 target. Levels of MYC translation and cell proliferation were proportional to AUF1 abundance but inversely proportional to the abundance of the ARE-binding protein TIAR, a MYC translational suppressor. Both AUF1 and TIAR affected MYC translation via the ARE without affecting mRNA abundance. Altering association of one ARE-binding protein with MYC mRNA in vivo reciprocally affected mRNA association with the other protein. Finally, genetic experiments revealed that AUF1 and TIAR control proliferation by a MYC-dependent pathway. Together, these observations suggest a novel regulatory mechanism where tuning the ratios of AUF1 and TIAR bound to MYC mRNA permits dynamic control of MYC translation and cell proliferation.
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