Differentially-Expressed Pseudogenes in HIV-1 Infection
AbstractNot all pseudogenes are transcriptionally silent as previously thought. Pseudogene transcripts, although not translated, contribute to the non-coding RNA pool of the cell that regulates the expression of other genes. Pseudogene transcripts can also directly compete with the parent gene transcripts for mRNA stability and other cell factors, modulating their expression levels. Tissue-specific and cancer-specific differential expression of these “functional” pseudogenes has been reported. To ascertain potential pseudogene:gene interactions in HIV-1 infection, we analyzed transcriptomes from infected and uninfected T-cells and found that 21 pseudogenes are differentially expressed in HIV-1 infection. This is interesting because parent genes of one-third of these differentially-expressed pseudogenes are implicated in HIV-1 life cycle, and parent genes of half of these pseudogenes are involved in different viral infections. Our bioinformatics analysis identifies candidate pseudogene:gene interactions that may be of significance in HIV-1 infection. Experimental validation of these interactions would establish that retroviruses exploit this newly-discovered layer of host gene expression regulation for their own benefit. View Full-Text
- Supplementary File 1:
Supplementary (PDF, 667 KB)
Scifeed alert for new publicationsNever miss any articles matching your research from any publisher
- Get alerts for new papers matching your research
- Find out the new papers from selected authors
- Updated daily for 49'000+ journals and 6000+ publishers
- Define your Scifeed now
Gupta, A.; Brown, C.T.; Zheng, Y.-H.; Adami, C. Differentially-Expressed Pseudogenes in HIV-1 Infection. Viruses 2015, 7, 5191-5205.
Gupta A, Brown CT, Zheng Y-H, Adami C. Differentially-Expressed Pseudogenes in HIV-1 Infection. Viruses. 2015; 7(10):5191-5205.Chicago/Turabian Style
Gupta, Aditi; Brown, C. T.; Zheng, Yong-Hui; Adami, Christoph. 2015. "Differentially-Expressed Pseudogenes in HIV-1 Infection." Viruses 7, no. 10: 5191-5205.