期刊
MOLECULAR CELL
卷 74, 期 4, 页码 701-+出版社
CELL PRESS
DOI: 10.1016/j.molcel.2019.03.006
关键词
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资金
- NIH Director's Pioneer Award [DP1-GM123454]
- Damon Runyon Innovator Award
- Pershing Square Sohn Cancer Research Alliance
- NCI Cancer Center Support Grant [P30 CA008748]
Alternative 3' untranslated regions (3' UTRs) are wide-spread, but their functional roles are largely unknown. We investigated the function of the long BIRC33' UTR, which is upregulated in leukemia. The 3' UTR does not regulate BIRC3 protein localization or abundance but is required for CXCR4-mediated B cell migration. We established an experimental pipeline to study the mechanism of regulation and used mass spectrometry to identify BIRC3 protein interactors. In addition to 3'-UTR-independent interactors involved in known BIRC3 functions, we detected interactors that bind only to BIRC3 protein encoded from the mRNA with the long 3' UTR. They regulate several functions, including CXCR4 trafficking. We further identified RNA-binding proteins differentially bound to the alternative 3' UTRs and found that cooperative binding of Staufen and HuR mediates 3'-UTR-dependent complex formation. We show that the long 3' UTR is required for the formation of specific protein complexes that enable additional functions of BIRC3 protein beyond its 3'-UTR-independent functions.
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