HIV-1 integration sites are flanked by potential MARs that alone can act as promoters

Identification of a potent MAR element from the mouse genome and assessment of its activity in stable and transient transfections

“…In general, it has been reported that MAR elements do not increase expression significantly in transient transfections, possibly because transgene genomic integration and/or changes in chromatin structure are not prominent in transient transfections. However, there have been a few reports of MAR increasing transgene expression within 48 h of transfection (Chancham et al, 2003;Kulkarni et al, 2004). We have also shown that the 1-68 MAR was able to improve retroviral vector titers in transient transfections in the human embryo HEK293 cell line (Buceta et al, 2011).…”

“…Moreover, as MAR do not usually function as enhancers, they are not expected to increase transgene expression in transient transfections. However, under certain circumstances MAR were shown to be able to increase transgene expression in transient transfections (Chancham et al, 2003;Kulkarni et al, 2004), and at least one MAR (huIFN-␤ MAR) is also capable of maintaining a plasmid in an episomal state when it is transcribed (Jenke et al, 2004). This effect, however, may be due to unique features of this particular MAR and vector, as a stressinduced duplex destabilization (SIDD) profile analysis found that maintenance and replicative potential of the episome was dependent on a specific SIDD profile that could be altered by MAR or other vector components (Giannakopoulos et al, 2009).…”

KRAB Can Repress Lentivirus Proviral Transcription Independently of Integration Site

“…A series of studies have revealed that lentiviral integration favors active transcription units as well as Alu elements and regions that correlate with high gene density and have a high GC content (8,13,14). Lentiviral integration sites are apparently also often flanked by matrix attachment regions, which are cis-regulatory elements involved in stabilizing gene expression (15). In contrast, heterochromatic centromeres and telomeres are disfavored for HIV integration (14).…”

Nuclear Matrix Protein SMAR1 Represses c-Fos-mediated HPV18 E6 Transcription through Alteration of Chromatin Histone Deacetylation

“…Recently the contribution of SMAR1 in regulating transcription of HIV genes has been accredited (21,29), but its effect on HPV18 oncogenes is not yet known. To address the role of SMAR1 in regulation of HPV18 E6, we first deciphered their relationship, if any.…”

“…Culminating the results above, it can be suggested that proper functioning of p53-SMAR1 loop is indispensable for E6 repression and reinstalling apoptosis in HPV18-infected cervical cancer cells. (29), but the mechanism by which they elicit these effects is not yet understood. In the previous sections, we observed SMAR1-mediated suppression of the HPV18 oncogene E6 and restoration of the apoptotic machinery.…”