scholarly journals Regulation of the Human Fc-Neonatal Receptor alpha-Chain Gene FCGRT by MicroRNA-3181

2018 ◽  
Vol 35 (1) ◽  
Author(s):  
Daniel C. Ferguson ◽  
Javier G. Blanco
Keyword(s):  
Chain Gene ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Receptor Alpha Chain

scholarly journals Delineation of an enhancerlike positive regulatory element in the interleukin-2 receptor alpha-chain gene.

1990 ◽  
Vol 10 (2) ◽  
pp. 850-853 ◽  
Author(s):  
B B Lin ◽  
S L Cross ◽  
N F Halden ◽  
D G Roman ◽  
M B Toledano ◽  
...  
Keyword(s):  
Regulatory Element ◽  
Interleukin 2 ◽  
Chain Gene ◽  
Enhancer Activity ◽  
Enhancer Element ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Interleukin 2 Receptor ◽  
Positive Regulatory Element ◽  
Receptor Alpha Chain

We have delineated a positive regulatory element in the interleukin-2 receptor alpha-chain gene (IL-2R alpha) between positions -299 and -243 that can potently activate a heterologous (herpesvirus thymidine kinase [tk]) promoter in phorbol myristate acetate (PMA)-induced Jurkat T cells and is functional when cloned in either orientation. This enhancerlike element contains a site (-268/-257) that can bind NF-kappa B; however, unlike the immunoglobulin kappa gene kappa B enhancer element, the IL-2R alpha kappa B-like site alone can only weakly activate a heterologous promoter. Adjacent 5' and 3' sequences also weakly activate the tk-CAT vector, but constructs combining the IL-2R alpha kappa B-like site plus adjacent 5' and 3' sequences potently activate gene expression. This combination of regions is essential for potent PMA-induced transcription from the tk promoter. Experiments using constructs in which IL-2R alpha upstream sequences are sequentially deleted suggested that there is a region 5' of position -299 which can suppress IL-2R alpha promoter and/or enhancer activity. Thus, it is possible that both positive and negative elements may be important in the regulation of IL-2R alpha gene transcription.

scholarly journals Kappa B site-dependent activation of the interleukin-2 receptor alpha-chain gene promoter by human c-Rel.

1992 ◽  
Vol 12 (9) ◽  
pp. 4067-4075 ◽  
Author(s):  
T H Tan ◽  
G P Huang ◽  
A Sica ◽  
P Ghosh ◽  
H A Young ◽  
...  
Keyword(s):  
T Cell Activation ◽  
Interleukin 2 ◽  
Regulatory Elements ◽  
Chain Gene ◽  
Nf Kappa B ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Interleukin 2 Receptor ◽  
Alpha Gene ◽  
Receptor Alpha Chain

The cis-acting control elements of the interleukin-2 receptor alpha-chain (IL-2R alpha) gene contain a potent kappa B-like enhancer whose activity can be induced by various mitogenic stimuli. Recent cloning of the p50 and p65 subunits of the kappa B-binding protein NF-kappa B complex revealed a striking sequence homology of these proteins with the c-rel proto-oncogene product (c-Rel). On the basis of this homology, we examined the potential role of c-Rel in controlling IL-2R alpha transcription. We now demonstrate that the recombinant human c-Rel protein binds to the kappa B element in the IL-2R alpha promoter and results in alteration of the DNA structure in the adjacent downstream regulatory elements containing the CArG box and the GC box. We found that human c-Rel can activate transcription from the IL-2R alpha promoter, but not the kappa B-containing human immunodeficiency virus type 1 promoter, upon cotransfection into Jurkat T cells. Furthermore, truncation of the carboxyl terminus of c-Rel results in a c-Rel mutant (RelNA) that (i) localizes exclusively in the nucleus and (ii) acts in synergy with wild-type c-Rel in activating transcription from the kappa B site of the IL-2R alpha promoter. Finally, induction of surface IL-2R alpha expression coincides with the induced levels of endogenous c-Rel and induced c-Rel binding to the IL-2R alpha kappa B site. Our study identified c-Rel as one component of the Rel/NF-kappa B-family proteins involved in the kappa B-dependent activation of IL-2R alpha gene expression. Furthermore, our results suggest that a Re1NA-like cellular factor (e.g., NF-kappa B p50 or p49 subunit) acts in synergy with c-Re1 during T-cell activation.

Discordance of the T-cell receptor alpha-chain gene in familial multiple sclerosis

Neurology ◽  
1992 ◽  
Vol 42 (4) ◽  
pp. 839-839 ◽  
Author(s):  
S. G. Lynch ◽  
J. W. Rose ◽  
J. H. Petajan ◽  
M. Leppert
Keyword(s):  
Multiple Sclerosis ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Chain Gene ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Receptor Alpha Chain ◽  
Cell Receptor Alpha

Delineation of an enhancerlike positive regulatory element in the interleukin-2 receptor alpha-chain gene

1990 ◽  
Vol 10 (2) ◽  
pp. 850-853
Author(s):  
B B Lin ◽  
S L Cross ◽  
N F Halden ◽  
D G Roman ◽  
M B Toledano ◽  
...  
Keyword(s):  
Regulatory Element ◽  
Interleukin 2 ◽  
Chain Gene ◽  
Enhancer Activity ◽  
Enhancer Element ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Interleukin 2 Receptor ◽  
Positive Regulatory Element ◽  
Receptor Alpha Chain

We have delineated a positive regulatory element in the interleukin-2 receptor alpha-chain gene (IL-2R alpha) between positions -299 and -243 that can potently activate a heterologous (herpesvirus thymidine kinase [tk]) promoter in phorbol myristate acetate (PMA)-induced Jurkat T cells and is functional when cloned in either orientation. This enhancerlike element contains a site (-268/-257) that can bind NF-kappa B; however, unlike the immunoglobulin kappa gene kappa B enhancer element, the IL-2R alpha kappa B-like site alone can only weakly activate a heterologous promoter. Adjacent 5' and 3' sequences also weakly activate the tk-CAT vector, but constructs combining the IL-2R alpha kappa B-like site plus adjacent 5' and 3' sequences potently activate gene expression. This combination of regions is essential for potent PMA-induced transcription from the tk promoter. Experiments using constructs in which IL-2R alpha upstream sequences are sequentially deleted suggested that there is a region 5' of position -299 which can suppress IL-2R alpha promoter and/or enhancer activity. Thus, it is possible that both positive and negative elements may be important in the regulation of IL-2R alpha gene transcription.

Kappa B site-dependent activation of the interleukin-2 receptor alpha-chain gene promoter by human c-Rel

1992 ◽  
Vol 12 (9) ◽  
pp. 4067-4075
Author(s):  
T H Tan ◽  
G P Huang ◽  
A Sica ◽  
P Ghosh ◽  
H A Young ◽  
...  
Keyword(s):  
T Cell Activation ◽  
Interleukin 2 ◽  
Regulatory Elements ◽  
Chain Gene ◽  
Nf Kappa B ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Interleukin 2 Receptor ◽  
Alpha Gene ◽  
Receptor Alpha Chain

The cis-acting control elements of the interleukin-2 receptor alpha-chain (IL-2R alpha) gene contain a potent kappa B-like enhancer whose activity can be induced by various mitogenic stimuli. Recent cloning of the p50 and p65 subunits of the kappa B-binding protein NF-kappa B complex revealed a striking sequence homology of these proteins with the c-rel proto-oncogene product (c-Rel). On the basis of this homology, we examined the potential role of c-Rel in controlling IL-2R alpha transcription. We now demonstrate that the recombinant human c-Rel protein binds to the kappa B element in the IL-2R alpha promoter and results in alteration of the DNA structure in the adjacent downstream regulatory elements containing the CArG box and the GC box. We found that human c-Rel can activate transcription from the IL-2R alpha promoter, but not the kappa B-containing human immunodeficiency virus type 1 promoter, upon cotransfection into Jurkat T cells. Furthermore, truncation of the carboxyl terminus of c-Rel results in a c-Rel mutant (RelNA) that (i) localizes exclusively in the nucleus and (ii) acts in synergy with wild-type c-Rel in activating transcription from the kappa B site of the IL-2R alpha promoter. Finally, induction of surface IL-2R alpha expression coincides with the induced levels of endogenous c-Rel and induced c-Rel binding to the IL-2R alpha kappa B site. Our study identified c-Rel as one component of the Rel/NF-kappa B-family proteins involved in the kappa B-dependent activation of IL-2R alpha gene expression. Furthermore, our results suggest that a Re1NA-like cellular factor (e.g., NF-kappa B p50 or p49 subunit) acts in synergy with c-Re1 during T-cell activation.

scholarly journals Cloning and comparative analysis of the human pre-T-cell receptor alpha-chain gene.

1995 ◽  
Vol 92 (26) ◽  
pp. 12105-12109 ◽  
Author(s):  
P. Del Porto ◽  
L. Bruno ◽  
M. G. Mattei ◽  
H. von Boehmer ◽  
C. Saint-Ruf
Keyword(s):  
Comparative Analysis ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Chain Gene ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Receptor Alpha Chain ◽  
Cell Receptor Alpha

Haplotypes of the interleukin-4 receptor alpha chain gene associate with susceptibility to and severity of atopic asthma

2004 ◽  
Vol 34 (10) ◽  
pp. 1570-1575 ◽  
Author(s):  
A.-M. Hytonen ◽  
O. Lowhagen ◽  
M. Arvidsson ◽  
B. Balder ◽  
A. L. Bjork ◽  
...  
Keyword(s):  
Atopic Asthma ◽  
Interleukin 4 ◽  
Chain Gene ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Interleukin 4 Receptor ◽  
Receptor Alpha Chain
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