First Author | Higuchi T | Year | 2008 |
Journal | Biochim Biophys Acta | Volume | 1780 |
Issue | 2 | Pages | 274-81 |
PubMed ID | 18078822 | Mgi Jnum | J:133419 |
Mgi Id | MGI:3778554 | Doi | 10.1016/j.bbagen.2007.11.005 |
Citation | Higuchi T, et al. (2008) U7 snRNA acts as a transcriptional regulator interacting with an inverted CCAAT sequence-binding transcription factor NF-Y. Biochim Biophys Acta 1780(2):274-81 |
abstractText | An inverted CCAAT sequence is recognized by both transcription factors NF-Y and DNA/RNA binding protein YB-1. In the process of examining the effect of nuclear RNA on an inverted CCAAT-containing promoter of MDR1 gene, we found that U7 snRNA inhibits NF-Y and suppresses the promoter activity both in vitro and in NG108-15 tumor cells. Analysis using a designed RNA, which was structurally unrelated to U7 snRNA, revealed that RNA binding by YB-1 is not specific and that the protein is not involved in the transcription. Furthermore, we demonstrated that in the nucleus of doxorubicin-treated cells, DNA binding by NF-Y and transcriptional activity of the promoter were inhibited without either a decrease of NF-Y or an increase of the p53 tumor suppressor, which is known to inhibit DNA binding by NF-Y. In these cells, U7 snRNA was specifically increased and associated with NF-Y, and treatment with RNase A eliminated the inhibition of NF-Y activity. These results suggest that U7 snRNA has a novel function as a transcriptional regulator to control NF-Y. |