human adenovirus 12
Recently Published Documents


TOTAL DOCUMENTS

18
(FIVE YEARS 0)

H-INDEX

8
(FIVE YEARS 0)

Virology ◽  
2015 ◽  
Vol 475 ◽  
pp. 120-128 ◽  
Author(s):  
Chengjun Wu ◽  
Lufeng Bai ◽  
Zhiqun Li ◽  
Charles E. Samuel ◽  
Göran Akusjärvi ◽  
...  

1986 ◽  
Vol 6 (10) ◽  
pp. 3550-3554 ◽  
Author(s):  
J Vogel ◽  
M Kress ◽  
G Khoury ◽  
G Jay

The major histocompatibility complex class I antigens play an indispensable role in cell-cell interactions. Perturbation of their expression has been shown to have deleterious physiological consequences, including the escape of transformed cells from immune detection. In an attempt to understand how class I genes are regulated, we dissected the Ld gene to identify potential control regions. By using a test vector containing the simian virus 40 early promoter placed upstream of the bacterial chloramphenicol acetyltransferase (cat) gene, we demonstrated the presence of a transcriptional enhancer within the 5'-flanking region. The sequence is functional in both orientations and has been mapped within 350 base pairs upstream of the Ld transcriptional start site. Although human adenovirus 12 can suppress endogenous class I genes, it cannot down-regulate the activity of the transiently transfected cat gene which has been placed under the control of the Ld enhancer and promoter. Our results suggested that if the human adenovirus 12-induced function regulates the expression of class I genes by a trans mechanism, then its target site must not be within 1.9 kilobases of the 5'-flanking region. Treatment of cells with interferon increases the accumulation of class I transcripts. Expression of the cat gene under the control of the Ld enhancer and promoter also can be up-regulated by interferon. Our study shows that the target sequence required for this enhancement resides, at least in part, within the same 350-base pair segment which contains the transcriptional enhancer.


1986 ◽  
Vol 6 (10) ◽  
pp. 3550-3554
Author(s):  
J Vogel ◽  
M Kress ◽  
G Khoury ◽  
G Jay

The major histocompatibility complex class I antigens play an indispensable role in cell-cell interactions. Perturbation of their expression has been shown to have deleterious physiological consequences, including the escape of transformed cells from immune detection. In an attempt to understand how class I genes are regulated, we dissected the Ld gene to identify potential control regions. By using a test vector containing the simian virus 40 early promoter placed upstream of the bacterial chloramphenicol acetyltransferase (cat) gene, we demonstrated the presence of a transcriptional enhancer within the 5'-flanking region. The sequence is functional in both orientations and has been mapped within 350 base pairs upstream of the Ld transcriptional start site. Although human adenovirus 12 can suppress endogenous class I genes, it cannot down-regulate the activity of the transiently transfected cat gene which has been placed under the control of the Ld enhancer and promoter. Our results suggested that if the human adenovirus 12-induced function regulates the expression of class I genes by a trans mechanism, then its target site must not be within 1.9 kilobases of the 5'-flanking region. Treatment of cells with interferon increases the accumulation of class I transcripts. Expression of the cat gene under the control of the Ld enhancer and promoter also can be up-regulated by interferon. Our study shows that the target sequence required for this enhancement resides, at least in part, within the same 350-base pair segment which contains the transcriptional enhancer.


1984 ◽  
Vol 50 (1) ◽  
pp. 132-136 ◽  
Author(s):  
Y Fukui ◽  
K Shiroki ◽  
I Saito ◽  
H Shimojo

Science ◽  
1980 ◽  
Vol 210 (4473) ◽  
pp. 1023-1025 ◽  
Author(s):  
N Mukai ◽  
S. Kalter ◽  
L. Cummins ◽  
V. Matthews ◽  
T Nishida ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document