| First Author | Rapicavoli NA | Year | 2013 |
| Journal | Elife | Volume | 2 |
| Pages | e00762 | PubMed ID | 23898399 |
| Mgi Jnum | J:330516 | Mgi Id | MGI:6207894 |
| Doi | 10.7554/eLife.00762 | Citation | Rapicavoli NA, et al. (2013) A mammalian pseudogene lncRNA at the interface of inflammation and anti-inflammatory therapeutics. Elife 2:e00762 |
| abstractText | Pseudogenes are thought to be inactive gene sequences, but recent evidence of extensive pseudogene transcription raised the question of potential function. Here we discover and characterize the sets of mouse lncRNAs induced by inflammatory signaling via TNFalpha. TNFalpha regulates hundreds of lncRNAs, including 54 pseudogene lncRNAs, several of which show exquisitely selective expression in response to specific cytokines and microbial components in a NF-kappaB-dependent manner. Lethe, a pseudogene lncRNA, is selectively induced by proinflammatory cytokines via NF-kappaB or glucocorticoid receptor agonist, and functions in negative feedback signaling to NF-kappaB. Lethe interacts with NF-kappaB subunit RelA to inhibit RelA DNA binding and target gene activation. Lethe level decreases with organismal age, a physiological state associated with increased NF-kappaB activity. These findings suggest that expression of pseudogenes lncRNAs are actively regulated and constitute functional regulators of inflammatory signaling. DOI:http://dx.doi.org/10.7554/eLife.00762.001. |
