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| Content Provider | PubMed Central |
|---|---|
| Author | Kumar, G. Renuka Glaunsinger, Britt A. |
| Copyright Year | 2010 |
| Abstract | Poly(A) tail length is emerging as an important marker of mRNA fate, where deviations from the canonical length can signal degradation or nuclear retention of transcripts. Pathways regulating polyadenylation thus have the potential to broadly influence gene expression. Here we demonstrate that accumulation of cytoplasmic poly(A) binding protein (PABPC) in the nucleus, which can occur during viral infection or other forms of cellular stress, causes mRNA hyperadenylation and nuclear accumulation of poly(A) RNA. This inhibits gene expression but does not affect mRNA stability. Unexpectedly, PABPC-induced hyperadenylation can occur independently of mRNA 3′-end processing yet requires the canonical mRNA poly(A) polymerase II. We find that nuclear PABPC-induced hyperadenylation is triggered by multiple divergent viral factors, suggesting that altering the subcellular localization of PABPC may be a commonly used mechanism to regulate cellular gene expression in a polyadenylation-linked manner. |
| Related Links | http://dx.doi.org/10.1128/mcb.00600-10 |
| Ending Page | 5008 |
| Page Count | 13 |
| Starting Page | 4996 |
| File Format | |
| ISSN | 02707306 |
| e-ISSN | 10985549 |
| Journal | Molecular and Cellular Biology |
| Issue Number | 21 |
| Volume Number | 30 |
| Language | English |
| Publisher | American Society for Microbiology (ASM) |
| Publisher Date | 2010-11-01 |
| Access Restriction | Open |
| Rights Holder | American Society for Microbiology (ASM) |
| Subject Keyword | Cell Biology Molecular Biology Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Molecular Biology |
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