In tumors with RASSF1 CGI methylation, an alternative isoform, RASSF1C, is expressed from an internal promoter and has been suggested to promote motility and invasive disease [ 26, 27].
The eight genes are usually co-transcribed by sigma A. When sigma B is activated in response to heat stress, it promotes transcription of the sigB regulon from the internal promoter, resulting in a shorter TU, rsbV-W-sigB rsbX.
In addition, in an orientation-dependent manner, the 0.25-kb core element significantly increased transgene expression from an internal promoter due to improved transcriptional termination.
Furthermore, we show that overexpression of a short PAX6 isoform derived from an internal promoter in a multicopy YAC transgenic line results in a microphthalmia phenotype.
This mechanism becomes predominant when the enhancer activity of the internal promoter is shielded by the presence of a synthetic chromatin insulator cassette.
These results demonstrate that neighboring gene activation can be limited by using internal promoter(s) lacking enhancer activity, especially when present in an FV vector backbone that prevents read‐through transcription.
HIV and FV proviruses containing an internal MLV long‐terminal repeat (LTR) promoter also had significant enhancer activity, which was not observed with an internal promoter from the murine phosphoglycerate kinase‐1 gene, PGK.
Design of vectors in which the enhancer element of retroviral LTR has been deleted and an internal promoter added (self-inactivated vectors) could provide both safe and efficient gene transfer as being presently tested.
SIN vectors carry a deleted LTR (Long Terminal Repeat) promoter that results in transcriptional initiation exclusively from the internal promoter.
The structural proteins are translated from the subgenomic 26S mRNA, which is transcribed from an internal promoter present in the minus strand RNA [1].
This mRNA corresponds to the 3' third of the genome and is transcribed from an internal promoter present on the minus strand RNA [2], [3].
