scholarly journals T-cell activation signals and human T-cell leukemia virus type I-encoded p40x protein activate the mouse granulocyte-macrophage colony-stimulating factor gene through a common DNA element.

1988 ◽  
Vol 8 (12) ◽  
pp. 5581-5587 ◽  
Author(s):  
S Miyatake ◽  
M Seiki ◽  
M Yoshida ◽  
K Arai
Keyword(s):  
T Cell ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Jurkat Cells ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Gm Csf ◽  
Human T Cell

Activation of T cells by an antigen, a mitogen, or a combination of a phorbol ester (12-O-tetradecanoylphorbol-13-acetate [TPA]) and a calcium ionophore (A23187) leads to induction of a set of lymphokine genes. Treatment of human T-cell leukemia line Jurkat by a mitogen or p40x, a transactivator protein encoded by human T-cell leukemia virus type I, activates many transfected lymphokine genes in a transient transfection assay. To study the mechanism of lymphokine gene induction, we examined the effects of mitogen stimulation and p40x on the gene for the mouse granulocyte-macrophage colony-stimulating factor (GM-CSF) in Jurkat cells. Deletion and mutation analyses showed that the 5'-flanking region of the gene for the GM-CSF is composed of two types of regulatory elements. One sequence, located at positions -95 to -73, determines response to stimulation by either TPA-A23187 or p40x. This region contains conserved lymphokine element 2, which appears in the gene for interleukin 3 (IL-3) and is followed by a GC-rich stretch. This GC-rich stretch alone specifies inducible response to p40x but not to TPA-A23187. Another sequence, located at positions -113 to -96 upstream of a TATA-like sequence, mediates inducible response to p40x but not to TPA-A23187. This sequence includes conserved lymphokine element 1, which appears in several lymphokine-cytokine genes, such as those for IL-3, G-CSF, and IL-2. We previously showed that the simian virus 40 early region promoter was also induced by a mitogen or p40x in Jurkat cells. Deletion analysis showed that the minimum region require for stimulation by both signals are identical. These results, which indicate that p40(x) stimulates transcription of the gene for the GM-CSF or the simian virus 40 early region promoter through the same DNA element or an overlapping DNA element required for induction by a mitogen, lend further support to the notion that p40(x) can exert its function by activating a component(s) of the T-cell signal transduction pathway which is activated by an antigen or a mitogen.

T-cell activation signals and human T-cell leukemia virus type I-encoded p40x protein activate the mouse granulocyte-macrophage colony-stimulating factor gene through a common DNA element

1988 ◽  
Vol 8 (12) ◽  
pp. 5581-5587
Author(s):  
S Miyatake ◽  
M Seiki ◽  
M Yoshida ◽  
K Arai
Keyword(s):  
T Cell ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Jurkat Cells ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Gm Csf ◽  
Human T Cell

Activation of T cells by an antigen, a mitogen, or a combination of a phorbol ester (12-O-tetradecanoylphorbol-13-acetate [TPA]) and a calcium ionophore (A23187) leads to induction of a set of lymphokine genes. Treatment of human T-cell leukemia line Jurkat by a mitogen or p40x, a transactivator protein encoded by human T-cell leukemia virus type I, activates many transfected lymphokine genes in a transient transfection assay. To study the mechanism of lymphokine gene induction, we examined the effects of mitogen stimulation and p40x on the gene for the mouse granulocyte-macrophage colony-stimulating factor (GM-CSF) in Jurkat cells. Deletion and mutation analyses showed that the 5'-flanking region of the gene for the GM-CSF is composed of two types of regulatory elements. One sequence, located at positions -95 to -73, determines response to stimulation by either TPA-A23187 or p40x. This region contains conserved lymphokine element 2, which appears in the gene for interleukin 3 (IL-3) and is followed by a GC-rich stretch. This GC-rich stretch alone specifies inducible response to p40x but not to TPA-A23187. Another sequence, located at positions -113 to -96 upstream of a TATA-like sequence, mediates inducible response to p40x but not to TPA-A23187. This sequence includes conserved lymphokine element 1, which appears in several lymphokine-cytokine genes, such as those for IL-3, G-CSF, and IL-2. We previously showed that the simian virus 40 early region promoter was also induced by a mitogen or p40x in Jurkat cells. Deletion analysis showed that the minimum region require for stimulation by both signals are identical. These results, which indicate that p40(x) stimulates transcription of the gene for the GM-CSF or the simian virus 40 early region promoter through the same DNA element or an overlapping DNA element required for induction by a mitogen, lend further support to the notion that p40(x) can exert its function by activating a component(s) of the T-cell signal transduction pathway which is activated by an antigen or a mitogen.

scholarly journals trans-activation of the simian virus 40 enhancer by a pX product of human T-cell leukemia virus type I.

1988 ◽  
Vol 62 (2) ◽  
pp. 644-648 ◽  
Author(s):  
S Saito ◽  
M Nakamura ◽  
K Ohtani ◽  
M Ichijo ◽  
K Sugamura ◽  
...  
Keyword(s):  
T Cell ◽  
Virus Type ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Type I ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus

Comparison of the trans-activation capabilities of the human T-cell leukemia virus type I and II chi proteins

1986 ◽  
Vol 6 (11) ◽  
pp. 3626-3631
Author(s):  
N P Shah ◽  
W Wachsman ◽  
A J Cann ◽  
L Souza ◽  
D J Slamon ◽  
...  
Keyword(s):  
T Cell ◽  
Mammalian Cells ◽  
Leukemia Virus ◽  
Mammalian Species ◽  
Cellular Transformation ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell

The mechanism of cellular transformation by the human T-cell leukemia viruses (HTLVs) is thought to involve a novel retrovirus gene known as chi. The chi gene is essential for HTLV replication and acts by enhancing transcription from the viral long terminal repeat. By using the HTLV type I and II chi gene-coding regions inserted into a highly efficient expression vector, we directly compared the efficiencies of the two chi proteins to trans activate the HTLV type I and II long terminal repeats. We demonstrate that the two chi proteins have different patterns of trans activation. The patterns were highly reproducible in all mammalian cells tested. A different pattern of activation was observed in avian cells. These results suggest that the mechanism of trans activation involves specific cellular factors that are highly conserved throughout mammalian species but different in avian cells. Understanding the mechanism of trans activation by the chi gene product may provide insights into mechanisms of cellular transformation by HTLV.

scholarly journals Human T-cell Leukemia Virus Type I p30 Nuclear/Nucleolar Retention Is Mediated through Interactions with RNA and a Constituent of the 60 S Ribosomal Subunit

2006 ◽  
Vol 281 (48) ◽  
pp. 37150-37158 ◽  
Author(s):  
Sofiane Ghorbel ◽  
Uma Sinha-Datta ◽  
Miroslav Dundr ◽  
Megan Brown ◽  
Genoveffa Franchini ◽  
...  
Keyword(s):  
T Cell ◽  
Virus Type ◽  
Leukemia Virus ◽  
Ribosomal Subunit ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus

scholarly journals Cytokine Expression and Tumorigenicity of Large Granular Lymphocytic Leukemia Cells From Mice Transgenic for the tax Gene of Human T-Cell Leukemia Virus Type I

Blood ◽  
1997 ◽  
Vol 90 (2) ◽  
pp. 783-794 ◽  
Author(s):  
William J. Grossman ◽  
Lee Ratner
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Leukemia Virus ◽  
Transgenic Animal ◽  
Type I ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Gm Csf ◽  
Human T Cell ◽  
T Cell Leukemia Virus

The human T-cell leukemia virus type I (HTLV-I) regulatory protein, Tax, has been speculated to play a major role in HTLV-I leukemogenesis. Indeed, several studies have suggested that upregulation of various cellular oncogenes and cytokines by Tax may explain the pathogenesis observed in HTLV-I–infected individuals, as well as several Tax-transgenic animal models. We report here the analysis of cytokine expression in a Tax-transgenic animal model with large granular lymphocytic (LGL) leukemia. Two different transgenic mice showed identical expression of interleukin-1α (IL-1α), IL-1β, interferon γ (IFNγ), and granulocyte-macrophage colony-stimulating factor (GM-CSF ) in peripheral tail tumors. Interestingly, LGL cell lines derived from these same tumors expressed high levels of both IFNγ and GM-CSF, which correlated with the level of Tax expression. These same LGL cell lines also expressed high levels of lymphocyte function-associated antigen-1 (LFA-1) and intracellular adhesion molecule-1 (ICAM-1). Engraftment of these LGL cell lines into severe combined immunodeficient (SCID) mice led to the development of leukemia and lymphomas. Examination of these SCID mice showed that their pathology was nearly identical to that observed in the original Tax-transgenic mouse model. Both the Tax-transgenic and engrafted SCID mouse models allow for the analysis of cellular events that are required for tumor development associated with HTLV infection and suggest that Tax expression may be responsible for the upregulation of certain cytokines and adhesion molecules that affect the infiltrating capabilities of HTLV-I–infected cells.

scholarly journals Adult T-cell leukemia/lymphoma not associated with human T-cell leukemia virus type I.

1986 ◽  
Vol 83 (12) ◽  
pp. 4524-4528 ◽  
Author(s):  
M. Shimoyama ◽  
Y. Kagami ◽  
K. Shimotohno ◽  
M. Miwa ◽  
K. Minato ◽  
...  
Keyword(s):  
T Cell ◽  
Virus Type ◽  
Leukemia Virus ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Adult T Cell Leukemia ◽  
Human T Cell ◽  
T Cell Leukemia Virus
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