Measurement of the concentration of serum soluble interleukin-2 receptor alpha chain in dogs with lymphoma

2020 ◽  
Vol 225 ◽  
pp. 110054
Author(s):  
Noriyuki Mizutani ◽  
Yuko Goto-Koshino ◽  
Keigo Kurata ◽  
Aki Fujiwara-Igarashi ◽  
Masahiro Sakaguchi ◽  
...  
Keyword(s):  
Interleukin 2 ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Interleukin 2 Receptor ◽  
Soluble Interleukin 2 Receptor ◽  
Receptor Alpha Chain

Interleukin-2 receptor alpha-chain (CD25) expression on leukaemic blasts is predictive for outcome and level of residual disease in AML

2009 ◽  
Vol 45 (9) ◽  
pp. 1692-1699 ◽  
Author(s):  
Monique Terwijn ◽  
Nicole Feller ◽  
Anna van Rhenen ◽  
Angèle Kelder ◽  
Guus Westra ◽  
...  
Keyword(s):  
Residual Disease ◽  
Interleukin 2 ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Cd25 Expression ◽  
Interleukin 2 Receptor ◽  
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.

scholarly journals HTLV-1 p27rex stabilizes human interleukin-2 receptor alpha chain mRNA.

1990 ◽  
Vol 9 (12) ◽  
pp. 4161-4166 ◽  
Author(s):  
H. Kanamori ◽  
N. Suzuki ◽  
H. Siomi ◽  
T. Nosaka ◽  
A. Sato ◽  
...  
Keyword(s):  
Interleukin 2 ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Interleukin 2 Receptor ◽  
Receptor Alpha Chain

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.

Interaction between NF-kappa B- and serum response factor-binding elements activates an interleukin-2 receptor alpha-chain enhancer specifically in T lymphocytes

1993 ◽  
Vol 13 (4) ◽  
pp. 2536-2545
Author(s):  
A A Kuang ◽  
K D Novak ◽  
S M Kang ◽  
K Bruhn ◽  
M J Lenardo
Keyword(s):  
T Cells ◽  
Serum Response Factor ◽  
Interleukin 2 ◽  
Response Factor ◽  
Nf Kappa B ◽  
Receptor Alpha ◽  
Alpha Chain ◽  
Interleukin 2 Receptor ◽  
Serum Response ◽  
Receptor Alpha Chain

We find that a short enhancer element containing the NF-kappa B binding site from the interleukin-2 receptor alpha-chain gene (IL-2R alpha) is preferentially activated in T cells. The IL-2R alpha enhancer binds NF-kappa B poorly and is only weakly activated by the NF-kappa B site alone. Serum response factor (SRF) binds to a site adjacent to the NF-kappa B site in the IL-2R enhancer, and both sites together have strong transcriptional activity specifically in T cells. Surprisingly, the levels of SRF constitutively expressed in T cells are consistently higher than in other cell types. Overexpression of SRF in B cells causes the IL-2R enhancer to function as well as it does in T cells, suggesting that the high level of SRF binding in T cells is functionally important.

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